Department of Physiology, Cardiovascular Health Cluster
Interests: The role of prenatal and postnatal environments and the mechanisms involved in the programming of hypertension, diabetes & obesity.
Keywords: Fetus, newborn, programming, adult disease, diabetes, hypertension, growth & development, lactation.
Associate Professor Mary Wlodek
+61 3 8344 8801
+61 3 8344 9671
+61 3 8344 5818
Printer friendly version of text [PDF (155KB)]
Our Research Focus
Small size at birth for gestational age occurs in 10% of human pregnancies in developed societies. This results from restricted growth of the fetus, which primarily reflects a poor environment within the uterus, commonly due to placental insufficiency. Recent human studies have confirmed that being born small is associated with the increased risk of developing adult diseases such as insulin resistance, cardiovascular disease and type 2 diabetes. Growing evidence suggests that the nutrition provided to the baby via the mother’s milk during lactation, and rapid growth of the baby after birth, are both critical factors influencing the programming of adult disease.
Our laboratory has made novel and significant contributions to understanding the importance of the nutritional environment provided by the placenta to the baby before birth and that of the mother’s milk after birth in the programming of adult diseases. We are the first to demonstrate that placental compromise in rats, which causes slow fetal growth, also adversely affects breast development, milk quality and supply, which further impair growth after birth.
We are exploring how a reduction in the number of functioning units (nephrons) of the kidney, alterations in key genes involved in kidney and heart development and changes in blood vessel reactivity are associated with rat offspring born small developing hypertension and cardiovascular disease. Exploring the development of the pancreas and mitochondria of small pups will further our understanding of how and when these offspring develop insulin resistance and diabetes. We are able to manipulate nutrition for a rat pup born small after birth by altering the quality and quantity of nutrition they consume after birth (by cross-fostering) and subsequently exploring disease consequences. We are also exploring the mechanisms that result in abnormal mammary development leading to low milk quality and quantity and aim to develop treatments to improve milk production and growth of offspring.
We aim to identify developmental stages during which nutritional or other interventions may have beneficial consequences. These studies will enable us to identify individuals at increased risk of developing later diseases and provide the scientific basis for the design and testing of appropriately targeted early life interventions. Identification of groups of individuals at risk of developing adult diseases will become increasingly important due to the ever-increasing incidence and earlier age at onset of these diseases.
|Mary Wlodek||Assoc Prof||Head of email@example.com|
|Andrew Siebel||Dr||NH&MRC Peter Doherty Fellow||
|Kerryn Westcott||Mrs||Senior Research Officer (0.8)||
|Andrew Jefferies||Mr||Research Assistant||
|Rachael O'Dowd||Ms||PhD student||
|Lenka Vodstrcil||Ms||PhD student||
|Marc Mazzuca||Mr||PhD student||
|Wlodek, Tare, Moritzfirstname.lastname@example.org|
|Tania Romano||Ms||PhD student||
|Rhianna Laker||Ms||PhD student||
|Wlodek, McConell, Wadleyemail@example.com|
|Yu May Soh||Ms||PhD student||
|Parry, Wlodek, Conradfirstname.lastname@example.org|
|Linda Gallo||Ms||Honours student||
|Siebel, Wlodek, McConellemail@example.com|
|Emma Simpson||Ms||Honours student||
|Wlodek, Parry, Westcott|
|Brianne Lauritz||Ms||Honours student||
Achievements of Current Research Group Members
Assoc Prof Mary Wlodek – Recent Invited International / National Presentations
|2008||What happens when you are born small? Health and Medical Sciences Conference & International Postgraduate Convention. Penang, Malaysia.|
|What are the critical nutritional environments for small babies in the programming of growth and disease? Fetal Physiology Symposium; Society For Gynecological Investigation. San Diego, CA, USA.|
|2007||Role of the perinatal environment in the programming of adult diseases. Perinatal Society of Australia and New Zealand. Melbourne, Australia.|
|2007||The postnatal environment is critical for the programming of adult diseases. International Congress on Developmental Origins of Health and Disease. Perth, Australia.|
|2006||Placental effects on lactation, growth and adult diseases. Experimental Biology 2006, American Society for Nutrition Presidential Symposium on Novel concepts in the developmental origins of adult health and disease. San Francisco, USA.|
|2006||The role of the prenatal and postnatal environments in the programming of growth and cardiovascular disease. International Society of Hypertension Satellite Symposium, International Symposium on Lifestyle Related Diseases- Perspectives for Primary Prevention and Treatment in Animal Models and Humans, Nishinomiya, Japan.|
|2005||Effect of uteroplacental insufficiency on mammary function, milk composition and neonatal growth and their consequences for growth and adult disease development. Society For Gynecological Investigation Minisymposium on Regulation of Breast Development and Lactational Function. Los Angeles, CA, USA.|
|2005||Placental and mammary programming adult diseases. International Union of Physiological Sciences (IUPS) Satellite Symposia on The prenatal environment, programming and postnatal consequences. San Diego, CA, USA.|
Department of Pathology, The University of Melbourne, Australia
Department of Anatomy & Cell Biology, The University of Melbourne, Australia
Department of Physiology, The University of Melbourne, Melbourne, Australia
Mothers & Babies Research Centre, University of Newcastle, Newcastle, Australia
Department of Anatomy and Cell Biology, Monash University, Melbourne, Australia
Centre for Obesity Research and Education, Monash Univ, Melbourne, Australia
Department of Physiology, Monash University, Melbourne, Australia
Department of Zoology, The University of Melbourne, Australia
Perinatal Society of Australia and New Zealand Thorburn Visiting Professor Symposium on Fetal Growth: An experimental and clinical workshop, Melbourne, Australia
Garvan Institute of Medical Research, Sydney, Australia
Assoc Prof Mary Wlodek – Other Achievements
Associate Dean, Melbourne School of Graduate Research (Oct 2007 – Dec 2009)
Chair of newly formed Central University Committee Melbourne School of Graduate Research Supervisor Programs Advisory Committee
Re-elected University Research Higher Degrees Committee 2007-2009
Elected to Departmental Committee 2007
Co-Convenor Post Graduate Students 2007
Evidence of National and International research profile is provided by meetings at which staff and students have presented abstracts with oral presentations indicated.
Conference Abbreviations: Australian Health and Medical Research Council (AHMRC); Australian Society for Medical Research (ASMR); Developmental Origins of Health and Disease (DOHAD); US Endocrine Society (ENDO); Endocrine Society of Australia (ESA); Fetal and Neonatal Physiology Symposium (FNPS); International Congress on Obesity (ICO); International Symposium on Resistance Arteries (ISRA); Network for Genes & Environment in Development (NGED); Perinatal Society of Australia and New Zealand (PSANZ); Society for Gynecologic Investigation (SGI); Society for Reproductive Biology (SRB); Society for the Study of Reproduction (SSR).
Dr Andrew Siebel
- NHMRC Peter Doherty Fellowship 2005 – 2009
- Chair - Early Career Researcher Committee of ARC Research Network in Genes Environment in Development 2006-2007
- Chair organizing committee for NGED ECR Conference, North Stradbroke Island, November 2007
- NGED Travel Award: SGI 2007 ($1,000)
- Coordinator Postdoctoral Group, Department of Physiology
- Finalist in President’s Poster session (top 8% of posters), International Congress on Obesity, 2006
- National competitive grant - ANZ Trusts William Buckland Foundation for 2007
- Two successful University of Melbourne ECR grants in 2006 & 2008
- CASS Foundation Travel Grant $3,500 & ESA-Ipsen International Travel Award $3,500 San Francisco & Los Angeles 2008
Abstracts – DOHAD 2005; ICO 2006; SGI 2007; PSANZ oral 2007; DOHAD oral 2007; NGED oral 2007; ENDO 2008
Publication – J. Am. Soc. Nephrol. 2007; Endocrinology 2008; Am. J. Physiol. 2008; Kidney Int. 2008; Reprod Sci 2008
Mrs Kerryn Westcott
- Promotion from Research Assistant to Senior Research Officer in 2006 based on her significant contributions to research, role in supervision of research students and leadership within the laboratory group
- First senior author publication in press
- NGED Travel Award: DOHAD 2007 ($500)
Abstracts – ASMR 2003; ESA oral 2006; DOHAD oral 2007
Publications – J. Endocrinol. 2003; Placenta 2004; Am. J. Physiol. 2005; Physiol. Behav. 2005; Clin. Exp. Pharmacol. Physiol. 2006; Kidney Int. 2008; Endocrinology 2008; Neuroendocrinology 2008 (Westcott as first author); Reprod Sci 2008
Ms Rachael O’Dowd
- Finalist, Novartis Junior Investigator Oral Session (top 10% of abstracts) , Endocrine Society of Australia, 2006. Postnatal growth is improved by cross-fostering a pup born small onto a mother with normal lactation by altering alveolar area, milk production and milk protein gene expression
- Writing PhD thesis (working full-time in Department of Anatomy & Cell Biology)
Abstracts – PSANZ oral 2004; PSANZ oral 2005; FNPS oral 2005; ESA oral 2006
Publications – Am. J. Physiol. 2007; Am. J. Physiol. 2008; Reprod. Fert. Develop; Reprod Sci 2008
Ms Lenka Vodstrcil
- NH&MRC Dora Lush Postgraduate Scholarship 2006 – 2008
- NGED Travel Award: SGI 2007 ($1,000)
- John and Allan Gilmour Award from the Faculty of Science 2008 ($4,500)
Abstracts – SGI 2005; SRB oral 2006; SGI 2007; PSANZ 2007; SRB oral 2007; NGED oral 2007; Relaxin 2008 oral & poster; SSR 2008; SRB oral 2008 (Young Investigator Award session)
Publications – Reprod. Fert. Develop. 2007; Adv. Exp. Med. Biol. 2007
Mr Marc Mazzuca
- Kidney Health Australia Biomedical Research Scholarship 2007 – 2008
- Melbourne International Fee Remission Scholarship (MIFRS) 2006 – 2008
- SGI Medical and Graduate PhD Student Stipend for Research in Reproduction 2007
- NGED Travel Awards: SGI 2007 ($1,000); DOHAD 2007 ($500)
- New Investigator Award for the Best Oral Presentation in the Basic Science Discipline (student or <5 years post PhD), PSANZ 2007
- Bioline Student Award for best oral presentation, NGED ECR Conference 2007
- NGED Annual Forum 2008 - Invited Talk "NGED's contribution to my PhD and implications to my research" & ECR Forum: "Progressing through 1st and 2nd year of my PhD"
- International Symposium on Resistance Arteries (ISRA) - Oral presentation 2008
Abstracts – SGI 2007; PSANZ oral 2007; DOHAD 2007; NGED oral 2007; ISRA oral 2008
Ms Tania Romano
- Geoffrey Gardiner Dairy Foundation Scholarship 2007 – 2008
- MDHS Univ of Melbourne, Faculty Research Scholarship 2008
- NGED Travel Award: ANZBMS 2007 ($1,000)
- ANZBMS 2007 Student Travel Grant $552
- DOHAD 2007 Early Career Research Award for best abstract $500
Abstracts – AHMRC 2006; SGI 2007; PSANZ oral 2007; DOHAD oral 2007; NGED oral 2008
Ms Rhianna Laker
- Faculty of Medicine, Dentistry and Health Sciences, Univ of Melbourne, Lowe Scholarship 2007
- NHMRC/NHF Dora Lush Postgraduate Scholarship 2008 – 2010
- NGED Travel Award: DOHAD 2007 ($500)
Abstracts – DOHAD 2007
Ms Yu May Soh
- Melbourne International Fee Remission Scholarship (MIFRS) 2008 – 2011
- Science Faculty Scholarship (SFS) 2008 – 2011
Abstracts – Relaxin oral 2008; SRB oral 2008
Recent grant income (2006 - current)
|Description||Chief investigators||Granting body||Year(s)||Amount (AUD)|
|Intergenerational programming of cardiovascular disease for babies born small: pathways and prevention||
|March of Dimes Foundation||2008-2011||
|Are postnatal nutrition and the intrauterine environment important for early skeletal muscle development and function?||
|Diabetes Australia Research Trust||2008||
|Development of the endocrine pancreas is regulated by nutritional environments||AL Siebel||Uni of Melb ECR Grant Scheme||2008||
|Medical and Graduate PhD Student Stipend for Research in Reproduction||
|Society for Gynecologic Investigation||2007||
|Can exercise and improved nutrition normalise rat skeletal muscle mitochondrial biogenesis following growth restriction?||G McConell
|NH&MRC Project Grant||2007-2009||
|Can exercise and improved nutrition normalise myocardial mitochondrial biogenesis following fetal growth restriction in rats?||G Wadley
|National Heart Foundation||2007-2008||
|Being born small programs gestational diabetes and poor milk quality: mechanisms for the transmission of diabetes to the next generation||ME Wlodek
|Diabetes Australia Research Trust||2007||
|Optimising the bone response to dietary calcium: a physiological approach||ME Wlodek
|Geoffrey Gardiner Dairy Foundation||2007||
|Development and function of the pancreas is compromised in growth-restricted offspring||
|ANZ Trusts William Buckland Foundation||2007||
|Regulation of uterine artery function during pregnancy and impact on fetal development||LJ Parry
|University of Melbourne Research Grant||2007||
|Prenatal placental and postnatal mammary programming of cardiovascular and renal diseases||
|NH&MRC Project Grant||2006-2008||
|Perinatal and intergenerational influences on adult diabetes||ME Wlodek||NH&MRC Project Grant||2006-2008||
|Intrauterine growth restriction programs reduced bone growth and development in rats||
|Eli Lilly Endocrinology Research Grant||2006||
|Maternal calcium supplementation and prevention of diabetes in offspring born small||
|Diabetes Australia Research Trust||2006||
|Being born small and the intergenerational programming of diabetes||ME Wlodek||Melbourne Research Grants Scheme||2006||
|Diabetes is programmed in small babies by the nutritional environment||AL Siebel||MDHS Early Career Grant||2006||
Established Research Collaborations
- Perinatal Programming of Disease Research
Perinatal programming of adult metabolic diseases
Prof Julie Owens, Dept of Obstetrics and Gynaecology, Univ of Adelaide, SA
Placental & lactational restriction and the programming of hypertension – the role of the kidney
Dr Karen Moritz, Dept of Anatomy & Cell Biology, Monash Univ, Melbourne, VIC
Placental & lactational restriction and the programming of hypertension – Role of blood vessel stiffness & reactivity
Dr Marianne Tare and A/Prof Helena Parkington, Dept of Physiology, Monash Univ, Melbourne, VIC
Role of mitochondrial biogenesis in the programming of diabetes
Drs Glenn McConell and Glenn Wadley, Dept of Physiology, Univ of Melbourne, Melbourne, VIC
A/Prof Greg Cooney, Garvan Institute of Medical Research, Sydney, NSW
Placental & lactational restriction and the programming of reduced bone mineral density
Prof John Wark, Dept of Medicine, Univ of Melbourne, Melbourne, VIC
Prof Howard Morris, Hanson Institute, Adelaide, SA
Cardiomyocyte development in growth-restricted offspring
Dr Jane Black, Dept Anatomy & Cell Biology, Monash University, VIC
- Pregnancy, Lactation & Reproductive Research
The effect of placental restriction on mammary gland biology
Dr Kevin Nicholas, Dept of Zoology, Univ of Melbourne, Melbourne, VIC
Impact of placental restriction on reproductive relaxin and relaxin receptors
Dr Laura Parry, Dept of Zoology, Univ of Melbourne, Melbourne, VIC
Prof Kirk Conrad, Dept of Physiology and Functional Genomics, Univ of Florida, Florida, USA
Uterine and steroid regulation of reproductive relaxin and relaxin receptors
Prof Stephen Lye & Dr Oksana Shynlova, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Canada
Placental restriction alters fetal and neonatal brain neurosteoids
Dr Jon Hirst, School of Biomedical Sciences, Univ of Newcastle, NSW
A/Prof David Walker, Dept of Physiology, Monash Univ, Melbourne, VIC
Techniques & Facilities
In vivo & in vitro rat techniques
- Uteroplacental insufficiency surgery to induce fetal growth restriction
- Embryo transfer techniques (maternal vs fetal influences)
- Cross-foster techniques (prenatal vs postnatal influences)
- Measurement of postnatal milk intake and composition
- Measurement of growth, food intake and body composition
- Rat telemetry and tail-cuff blood pressure
- Intra-arterial & intra-peritoneal glucose tolerance testing and catheter surgery
- Exercise training
- 24 hour renal function studie
- Real-time PCR
- In vitro mammary cell culture
- Unbiased sterology to determine nephron number (off-site)
- Vessel stiffness & reactivity measures (off-site)
- DXA & pQCT bone analysis (off-site)
- Hormone, metabolite, electrolyte, growth factor measurements
- Experimental model
Perturbations of the environment in early life, including both the prenatal and postnatal environments, alter growth and functional development and have a major impact on life long health and disease risk. Our laboratory has made novel and significant contributions to understanding the importance of both prenatal placental and postnatal lactational environments in the programming of perinatal growth restriction and accelerated growth following placental restriction in an established rat model. Reduced placental blood flow is a major cause of fetal growth restriction and is implicated in programming adult disease. Uteroplacental insufficiency and fetal growth restriction is induced in Wistar-Kyoto rats by ligating the uterine vessels on day 18 of pregnancy. We are the first to demonstrate that placental compromise in rats also adversely affects breast development, milk quality and supply, which further impair growth during lactation. This is followed by accelerated growth after weaning, programming more adverse outcomes. The consequences of the perinatal growth restriction on adult hypertension, diabetes and obesity are also being explored.
We have found that cross-fostering small rat pups onto mothers with normal lactation improves growth during lactation. Manipulations of postnatal nutrition (by cross-fostering) and other interventions will help us to identify a developmental stage during which nutritional or other manipulations may have beneficial consequences for the health of the small infant.
- Fetal growth and placental function and the role of relaxin
A key feature of mammalian reproduction is the development of the embryo and fetus within the reproductive tract of the mother, giving the young better protection and allowing it to reach an optimal size at birth. Efficient placental function depends critically on the unrestricted flow of maternal blood to the placenta. Disruption to placental blood flow can lead to restricted fetal growth and places the offspring at increased risk of developing adult diseases. The consequences of placental restriction on placental growth factors, fetal growth and calcium homeostasis are all research focuses of the lab. Using embryo transfer techniques we have identified the key roles of the embryo versus the intrauterine environment in programming growth in the rat.
Surprisingly few studies have investigated the acute effects of restricting maternal blood flow to the placenta on the ovary and uterus during pregnancy. As the ovary and maintenance of a viable uterine environment are both crucial aspects of pregnancy, disruption to either could have a significant negative impact on the well-being of the fetus, including growth. We have recently showed that restricting placental blood flow in late pregnant rats leads to a decrease in the amount of relaxin (RLX - peptide hormone) protein in the ovary and an increase in the receptors for RLX in the uterus. These data provide new evidence to link restricted placental function with a disruption to both ovarian function (production and release of hormones) and expression of receptors in the uterus. The overall aim of this project is to demonstrate a role for an important growth factor, RLX, in maintaining adequate uteroplacental blood flow during pregnancy. It will also characterise changes in RLX-related ovarian and uterine physiology that could affect fetal growth in late gestation.
- Mammary gland development and function
The overall aim of this project is to identify genes that regulate mammary development as well as nutritional quality and quantity of milk and subsequently postnatal growth. Challenges exist for the development of markers of impaired lactation to identify neonates at risk demanding new and innovative basic science approaches. The majority of recent human and experimental research has focused on the prenatal environment as the key period for programming perinatal growth and adult diseases. We have recently identified the lactational environment as critical in programming postnatal growth restriction. We are establishing how poor placental function alters the interaction with the mammary gland to impair mammary development before birth and lactation after birth. We have shown in a novel rat placental restriction model that hormonal regulators of mammary development are reduced inducing premature lactogenesis (alteration in milk protein gene expression) which impairs lactation causing perinatal growth restriction. In addition, the role of parathyroid hormone-related peptide (PTHrP) in regulating calcium transfer to milk is being explored.
Using innovative cross-fostering techniques, we are establishing how these prenatal and postnatal environments separately and synergistically program growth after birth. Our model system of impaired lactation together with a program of gene discovery will enable development of markers of impaired lactation. These markers will be used in targeted treatments aiming to correct the deficiencies in mammary tissue in vitro and in the rat in vivo. Identification of markers of impaired lactation and low milk quality and quantity in humans will provide options for treatment to benefit neonatal health.
- Cardiovascular disease and the role of the heart, kidney and blood vessels
Being born small and the associated accelerated growth, independently predict adult hypertension and cardiovascular disease. Using our rat placental restriction model, we are determining whether restricting nutrition before birth via the placenta or after birth via lactation increases the risk of developing high blood pressure as well as heart, kidney and blood vessel dysfunction. Manipulations of nutrition after birth are achieved by cross-fostering studies. We have shown that growth-restricted pups fostered on to a mother with impaired lactation have a lower nephron number, high blood pressure and impaired vessel reactivity as adults when compared to Control – on – Control offspring. Most importantly, when these growth-restricted pups (compromised in utero environment) are cross-fostered on to Control mothers (normal lactational environment) they had restored nephron endowment, blood pressure and vessel reactivity. We will further establish whether a reduction in the number of functioning units (nephrons) in the kidney, alterations in key genes involved in kidney and heart development as well as adult renal and cardiovascular function and changes in blood vessel reactivity and stiffness are associated with developing cardiovascular disease. These studies will identify the mechanisms by which the kidney, heart and vasculature contribute to the programming of cardiovascular disease and the relative roles of the prenatal and postnatal environments.
- Programming of adult diabetes, obesity & osteoporosis
The aim of this aspect of our research is to determine the effects of restriction of nutrient supply before and after birth on growth and the development of adult onset diabetes, obesity and osteoporosis. Our novel findings suggest that uteroplacental insufficiency impairs milk quality and supply which limits overfeeding and accelerated growth initially, but on weaning, may independently lead to diabetes and obesity. We will determine if this is a direct result of poor nutrition and made worse by overfeeding in response to restored nutrition after birth or after weaning. We hypothesize that placental compromise permanently reduces an individual's metabolic capacity and that the extent of availability of nutrition after birth determines the consequences for insulin action and increased body fat. Our recent studies are exploring whether restriction nutrient supply before birth via the placenta, or after birth via the mother’s milk (by cross-fostering) increases the risk of reduced bone density and growth as well as increasing overall fat mass. The relationship between sex hormones and skeletal development and key bone markers will also be assessed to establish the link between programming bone growth and reproductive maturation with gender specific effects. Identification of novel populations at risk of developing osteoporosis, and increased incidence of bone fractures, is increasingly important due to the rising incidence of this under-diagnosed disorder.
Intrauterine growth restriction, commonly arising from a poorly functioning placenta, increases the risk of insulin resistance and adult diabetes. One of our aims is to determine the effect of placental restriction and its associated lactational restraint on glucose tolerance, insulin secretion and markers of adiposity and skeletal muscle mitochondrial biogenesis in adult offspring. We have found that placental restriction impairs adult glucose homeostasis and induces fasting and second phase hyperinsulinaemia. In males, placental restriction reduces key markers of mitochondrial biogenesis in skeletal muscle. Furthermore, our data highlight the importance of the postnatal lactational environment as a major determinant of later metabolic phenotype.
- Established that uteroplacental insufficiency in a rat model of growth restriction directly impairs mammary development during pregnancy, which consequently compromises milk quality and quantity after birth, further restricting postnatal growth for pups born small.
- Using a unique approach, our recent cross-fostering studies have unequivocally proven that both prenatal growth restriction and postnatal mammary function independently influence postnatal growth, the extent of accelerated growth following uteroplacental insufficiency and susceptibility to a host of adult diseases.
- Identified that sex differences and alterations in reproductive maturation play an important role in the programming of adult diseases (hypertension, obesity, diabetes and osteoporosis).
- Further characterize the mechanisms by which uteroplacental insufficiency impairs mammary development and identify additional markers of impaired lactation as well as developmental stages during which time interventions may have beneficial consequences for lactational performance.
- Identify the relative roles of the prenatal placental and postnatal lactational environments, using cross-fostering, in the programming of adult diseases including hypertension, obesity, osteoporosis and diabetes.
- Identify the role of the pancreas in programming insulin resistance and Type 2 diabetes.
- Identify potential interventions and treatments, as well as elucidate mechanisms, contributing to the programming of adult diseases (hypertension, diabetes, cardiovascular disease, osteoporosis and obesity).
Major Research Projects and Interests
Key Research Outcomes to Date
Wlodek, M.E., Ceranic, V., O’Dowd, R., Westcott, K.T., and Siebel, A.L. Maternal progesterone treatment rescues the mammary impairment following uteroplacental insufficiency and improves postnatal pup growth in the rat. Reprod Sci In press accepted July 8, 2008.
Pascoe K.C., Wlodek M.E. and Jones, G.T. Increased elastic tissue defect formation in the growth restricted Brown Norway rat: a potential link between in utero condition and cardiovascular disease? Pediatr Res 64:125-130, 2008.
Westcott, K.T., Hirst, J.J., Ciurej, I., Walker, D.W., Wlodek, M.E. Brain allopregnanolone concentrations in the fetal and postnatal rat fetus and pup in response to uteroplacental insufficiency. Neuroendocrinology DOI: 10.1159/000139771, 2008.
Siebel, A.L., Mibus, A.L., De Blasio, M.J., Westcott, K.T., Morris, M.J., Prior, L., Owens, J.A. and Wlodek, M.E. Improved lactational nutrition and postnatal growth ameliorates impairment of glucose tolerance by uteroplacental insufficiency in male rat offspring. Endocrinology 149:3067-3076, 2008.
Wadley, G.D., Siebel, A.L., Cooney, G.J., McConell, G.K., Wlodek, M.E. and Owens, J.A. Uteroplacental insufficiency and reducing litter size alters skeletal muscle mitochondrial biogenesis in a sex specific manner in the adult rat. Am J Physiol (Endocrinol Metab) 294:E861-E869, 2008.
Needham, B.E., Wlodek, M.E., Ciccotosto, G.D., Fam, B.C. Masters, C.L., Proietto, J. Andrikopoulos, S. Cappai, R. Identification of the Alzeimer’s disease amyloid precursor protein (APP) and its homolog APLP2 as essential modulators of glucose and insulin homeostatsis and growth. J Pathol 215:155-163, 2008.
O’Dowd, R., Wlodek, M.E. and Nicholas, K.R. Uteroplacental insufficiency alters the mammary gland response to lactogenic hormones in vitro. Reprod. Fert. Develop. 20:460-465, 2008.
Wlodek, M.E., Westcott, K.T., Siebel, A.L., Owens, J.A. and Moritz, K.A. Growth restriction induced before or after birth reduces nephron number and increases blood pressure in male rats. Kidney International 74:187-195, 2008.
O’Dowd, R.A., Kent, J.C., Moseley, J.M. and Wlodek, M.E. The effects of uteroplacental insufficiency and reducing litter size on maternal mammary function and postnatal offspring growth. Am J Physiol (Regul Integr Comp Physiol) 294: R539-R548, 2008 [PDF (1,500KB)].
Ping, S., Trieu, J., Wlodek, M. and Barrett, G. The effects of estrogen on basal forebrain cholinergic neurons and spatial learning. J Neurosci Res In Press accepted Oct 31, 2007.
Wlodek , M.E., Mibus, A.L., Tan, A., Siebel, A.L., Owens, J.A. and Moritz, K. A normal lactational environment restores nephron endowment and prevents hypertension after placental restriction in the rat. J Am Soc Nephrol 18:1688-1696, 2007 [PDF (185KB)]
Subject of “JASN This Month’s Highlights” J Am Soc Nephrol18:1617-1618, 2007 [PDF (110KB)] and the “JASN Editorial”J Am Soc Nephrol18:1626-1629, 2007 [PDF (56KB)].
Vodstrcil, L.A., Wlodek, M.E., Parry, L.J. The effects of uteroplacental restriction on the relaxin-family receptors, Lgr7 and Lgr8, in the uterus of late pregnant rats. Reprod Fert Develop 19:530-538, 2007 [PDF (303KB)].
Reti, N.G., Lappas, M., Berthold, H. Riley, C., Wlodek, M.E., Henschke, P., Permezel, M., Walker, S., Rice, G.E. The effect of high oxygen on placental function in short term explant cultures. Cell Tissue Res 328:607-616, 2007 [PDF (431KB)].
Reti, NG, Lappas, M, Riley, C, Wlodek, ME, Permezel, M, Walker, S, Rice, GE. Why do membranes rupture at term? Evidence of increased cellular apoptosis in the supra-cervical fetal membranes. Am J Obstet Gynecol 196: 484.e1-484.e10, 2007 [PDF (2,743KB)].
Di Nicolantonio, R, Koutsis, K, Westcott, KT and Wlodek, ME. Relative Contribution of the prenatal versus postnatal period on development of hypertension and growth rate of the Spontaneously Hypertensive Rat. Clin Exp Pharmacol Physiol 33:9-16, 2006 [PDF (194KB)].
Di Nicolantonio, R, Koutsis, K, Westcott, KT and Wlodek, ME. Lack of evidence for a role for either the in utero or suckling periods in the exaggerated salt preference of the Spontaneously Hypertensive Rat. Physiology & Behavior 86:500-507, 2005 [PDF (135KB)].
Wlodek, ME, Westcott, KT, O’Dowd, R, Serruto, A, Wassef, L, Moritz, KM and Moseley, JM. Uteroplacental restriction in the rat impairs fetal growth in association with alterations in placental growth factors including PTHrP. Am J Physiol (Regulatory) Jun;288(6):R1620-7, 2005 [PDF (653KB)].
Mathai, ML, Soueid, M, Chen, N, Jayasooriya, AP, Sinclair, AJ, Wlodek, ME, Weisinger, HS and Weisinger, RS. Does perinatal omega-3 polyunsaturated fatty acid deficiency increase appetite signalling? Obes Res Nov;12(11):1886-94, 2004 [PDF (116KB)].
Lappas, L, Permezel, M, Ho, PW, Moseley, JM, Wlodek, ME, and Rice, GE. Effect of nuclear factor kappa b inhibitors and peroxisome proliferator-activated receptor-gamma ligands on PTHrP release from human fetal membranes. Placenta 25:699-704, 2004 [PDF (151KB)].
Briscoe TA, Rehn AE, Dieni S, Duncan JR, Wlodek ME, Owens JA, Rees SM. Cardiovascular and renal disease in the adolescent guinea pig after chronic placental insufficiency. Am J Obstet Gynecol Sep;191(3):847-55, 2004 [PDF (552KB)].
Wlodek ME, Di Nicolantonio R, Westcott KT, Farrugia W, Ho PW, Moseley JM. PTH/PTHrP receptor and mid-molecule PTHrP regulation of intrauterine PTHrP: PTH/PTHrP receptor antagonism increases SHR fetal weight. Placenta Jan;25(1):53-61, 2004 [PDF (155KB)].
de Gooyer TE, Skinner SL, Wlodek ME, Kelly DJ, Wilkinson-Berka JL. Angiotensin II influences ovarian follicle development in the transgenic (mRen-2)27 and Sprague-Dawley rat. J Endocrinol Feb;180(2):311-24, 2004 [PDF (1,270KB)].
Macheda, M.L., Williams, E.D., Best, J.D., Wlodek, M.E. and Rogers, S. Expression and localisation of GLUT1 and GLUT12 glucose transporters in the pregnant and lactating rat mammary gland. Cell and Tissue Research 311:91-97, 2003 [PDF (412KB)].
Wlodek, M.E., Westcott, K.T., Serruto, A., O’Dowd, R., Wassef, L, Ho, P.W.M. and Moseley, J.M. Impaired mammary function and parathyroid hormone-related protein during lactation in growth restricted spontaneously hypertensive rats. J Endocrinol 178:233-245, 2003 [PDF (271KB)].
Wlodek, M.E., Koutsis, K., Westcott, K.T., Ho, P.W.M., Serruto, A., Di Nicolantonio, R. and Moseley, J.M. The spontaneously hypertensive rat fetus, not the mother, is responsible for its reduced amniotic fluid PTHrP and growth restriction. Placenta 22:646-651, 2001 [PDF (116KB)].
Di Nicolantonio, R., Koutsis, K. and Wlodek, M.E. Fetal versus maternal determinants of the reduced fetal and placental growth in SHR. J Hypertens 18:45-50, 2000.
Curtis, N.E., King, R.G., Moseley, J.M., Ho, P.W.M., Rice, G.E. and Wlodek, M.E. Preterm fetal growth restriction is associated with increased parathyroid hormone-related protein expression in the fetal membranes. Am J Obstet Gynecol 183:700-705, 2000.
Wlodek, M.E., Westcott, K.T., Ho, P.W.M., Serruto, A., Di Nicolantonio, R., Farrugia, W. and Moseley, J.M. Reduced fetal, placental and amniotic fluid PTHrP in the growth restricted spontaneously hypertensive rat. Am J Physiol (Regulatory) 279:R31-38, 2000 [PDF (629KB)].
Farrugia, W., Ho, P.W.M., Rice, G.E., Moseley, J.M., Permezel, M. and Wlodek, M.E. Parathyroid hormone-related protein (1-34) in gestational fluids and release from gestational tissues. J Endocrinol 165:657-662, 2000 [PDF (109KB)].
Carragounis, A., Koutsis, K., Wlodek, M.E., Berka, J.L.A. and Di Nicolantonio, R. First report of active renin in rat amniotic fluid. Clin Exp Pharmacol Physiol 27:631-633, 2000 [PDF (85KB)].
Farrugia, W., De Gooyer, T.E., Rice, G.E., Moseley, J.M. and Wlodek, M.E. Parathyroid hormone (1-34) and parathyroid hormone-related protein (1-34) stimulate calcium release from human syncytiotrophoblast basal membranes via a common receptor. J Endocrinol 166:689-695, 2000 [PDF (117KB)].
Study and Employment Opportunities
We have many opportunities for students to join our lab, including vacation scholarships, 3rd year, Honours and postgraduate research projects. We also take expressions of interest from potential post-doctoral fellows competitive for independent funding. Please contact Assoc Prof Mary Wlodek (firstname.lastname@example.org) or Dr Andrew Siebel (email@example.com) for more information.