Donna A. Sanzari Women's Hospital
Obstetric Research Division
Obstetric research in the Center for Abnormal Placentation (CAP) at Hackensack University Medical Center focuses on the human placenta and its crucial role in supporting fetal growth and development over the nine months of pregnancy. We have two types of projects: molecular (basic science) and clinical-translational (improving diagnostic imaging methods, diagnostic or preventative approaches, and disseminating clinical information that improves care).
We have known for some time that the appropriate implantation of the placenta into the wall of the uterus is vital to a successful pregnancy. Implantation means the process whereby the embryo attaches to the mother’s uterus and the placenta develops. Both the location in the uterus where the placenta develops and how deep into the uterus it invades influence the risk of pregnancy complications that could harm mother or baby. Human placentas invade the uterine wall more deeply than any other mammalian species. The invasion process remodels maternal blood vessels to ensure an adequate blood supply to the developing baby. Several major pregnancy pathologies begin with abnormal implantation and subsequent abnormal placental invasion.
|Fetus and placenta in the uterus at term, showing the maternal and fetal circulations supplying blood to the placenta.|
Abnormally invasive placenta (AIP), also known as placenta accreta spectrum (PAS) or placenta accreta, is an “over-invasion” pathology that can lead to significant maternal risk of bleeding. In contrast, preeclampsia and intrauterine growth restriction are “under-invasion” pathologies of the placenta. All three pathologies carry risks for both mother and baby, including uterine rupture and/or massive blood loss (AIP), maternal hypertension (high blood pressure) and organ damage (preeclampsia), greater risk of future cardiovascular disease, prematurity, and poor fetal growth (preeclampsia) due to inadequate blood flow and fetal nutrition. Poor fetal growth then confers an increased risk of metabolic or cardiovascular disease during adulthood in babies who were growth-restricted.
CAP research examines placental invasion, blood flow, and function through an integrated approach, encompassing molecular through clinical investigations. We are developing studies at a very basic level examining the invasion process, the factors that control it, and the changes that occur in these pregnancy pathologies. Simultaneously, we are performing studies designed to improve ultrasound imaging technology so we can examine blood flow and placental growth, structure, and function during the first-trimester standard ultrasound screening examination. This is the key time period during human placentation. Only by combining basic science and clinical-translational approaches can we develop therapies for the detection, amelioration, and prevention of abnormal placentation in women at high risk for these pathologies.
The Obstetric Research Division is focused on building the Center for Abnormal Placentation as the site of major translational research efforts within the Department of Obstetrics and Gynecology in the Hackensack Meridian Health network. This involves several research ventures, the most important of which are the program to investigate placenta accreta-related pathologies, programs to explore the relationship between invasion and pregnancy outcomes, and the program examining the mechanisms and regulation of uterine invasion by trophoblast (placental) cells. All of these relate to our current network-wide efforts to understand how COVID-19 impacts pregnancy and neonatal health.
We are developing and testing novel methods for ultrasound-based assessment of placental development, structure, and function. These tests are designed for first-trimester diagnosis of any pregnant woman. At the same time, we work on improving maternal care via assessment of outcomes after changes in care are instituted. We are developing biomarkers for placental disease that can be used to detect placental problems early, in the clinic.
With the advent of COVID-19, Hackensack Meridian Health is following all pregnant women tested and delivering within the network during the pandemic. Our team is examining how silent infection (no symptoms) and infection requiring medical treatment might impact pregnancy outcome and neonatal health. In prior pandemics of respiratory viral diseases, pregnant women suffered more than non-pregnant women of similar age, with more preterm births, pregnancy losses, and higher rates of maternal hospitalization and death.
The initial research in this program involved a retrospective study of all AIP cases over a ten-year period to evaluate whether CAP has improved maternal outcomes. Our data, published in 2014 (Ref. 1) shows that outcomes — most especially the mother’s blood loss during surgery — improved dramatically when an expert team approach is employed. In collaboration with researchers at Oxford University in the United Kingdom, we have shown that an area of confluent blood vessels at the interface between the mother’s uterus and the placenta accurately diagnoses AIP in 100% of at-risk mothers at 32 weeks of pregnancy. It is predictive of whether an individual case will require caesarean/hysterectomy at delivery (Ref. 2).
These improvements in imaging technology are now part of a much larger National Institutes of Health (NIH)-funded collaborative study with Oxford University. It is designed to advance imaging of the placenta at the standard, first-trimester ultrasound examination used for women all over the world. The goal is to be able to diagnose AIP, preeclampsia, and the risk of intrauterine growth failure with 100% accuracy as early as possible, allowing physicians to intervene and save the pregnancy or reduce the impact of a complication on mother and baby.
We are taking advantage of the advances we have made in first-trimester imaging to explore how infection with SARS-CoV-2 (the novel coronavirus causing COVID-19 disease) might impact pregnancy and neonatal outcomes. In addition, we are responsible for monitoring pregnancy and neonatal health outcomes in women who were infected during pregnancy across the Hackensack-Meridian Health network, which delivers 20% of all babies born in New Jersey every year.
Funding: National Institutes of Health, Office of the Director and the Eunice Kennedy Shriver Institute for Child Health and Human Development Human Placenta Project
New ultrasound techniques have been tested in our ultrasound facilities to measure placental volume, shape, vascular development, and blood flow at the end of the first trimester in pregnancy. This is when all women receive their first screening ultrasound, called the nuchal translucency. The data from the ultrasound measurements will be paired with the corresponding birth outcomes to test whether we can observe signs of abnormal placentation at this key milestone in placental development. We anticipate that the continuing development of new analytical software by the bioengineering group in Oxford will enable us to detect quantitative measures of abnormal placentation early enough to institute significant therapeutic remedies. The graphic below is an example of the kind of imaging we are working on. It shows how we can isolate and measure the shape, size, and volume of the placenta, and the size and location of the maternal arteries that supply the placenta and fetus. These are called “spiral arteries,” and they are remodeled by placenta to ensure enough oxygen and nutrients are conveyed to the developing fetus.
The video shows a 3D Power Doppler ultrasound volume visualized with the camera rotating around the center of the placenta (cyan) with single 2D B-Mode slice shown for scale. 3D Power Doppler of maternal vessels and umbilical cord are rendered illustrating the vessels supplying the organ. As we rotate around, the placental volume is removed and replaced with a curved surface representing the Power Doppler data found 2mm into the placenta and away from the utero-placental interface (UPI). Individual ingress/jets of vascularity entering the placenta are outlined automatically (multicolor).
Funding: Hackensack Meridian Health network, pending NIH: Impact of SARS-CoV-2 (COVID-19) on pregnancy and neonatal outcomes
We are comparing pregnancy outcomes and neonatal health in women who were infected with the novel coronavirus during their pregnancy. We will use the first-trimester ultrasounds from our ongoing NIH studies as well. We are investigating whether or not first trimester infection with the novel coronavirus affects the developing placenta and results in differences in fetal growth or rates of pregnancy complications.
- Yurteri-Kaplan L, Saber S, Zamudio S, Srinivasan D, Nyirenda T, Alvarez M, Al-Khan, A. Brain Natriuretic Peptide in term pregnancy. Reproductive Sciences. 2012;19(5):520-5. UI: 22547689
- Al-Khan A, Gupta V, Illsley NP, Mannion C, Koenig C, Bogomol A, Alvarez M, Zamudio S. Maternal and Fetal Outcomes in Placenta Accreta After Institution of Team-Managed Care. Reproductive Sciences. 2014;21(6):761-71. UI: 24336676
- Timor-Tritsch IE. Monteagudo A. Cali G. Vintzileos A. Viscarello R. Al-Khan A. Zamudio S. Mayberry P. Cordoba MM. Dar P. Cesarean scar pregnancy is a precursor of morbidly adherent placenta. Ultrasound in Obstetrics & Gynecology. 2014;44(3):346-53. UI: 24890256
- Odibo IN, Zamudio S, Young JM, Magann EF, Williams SF. Patient Awareness of Untoward Effects of Smoking on Fetal and Maternal Well-being During Pregnancy: A Pilot Study. Journal of Addiction Medicine. 2015;9(3):211-6. UI: 25918967
- Collins SL, Stevenson GN, Al-Khan A, Illsley NP, Impey L, Pappas L, Zamudio S. Three-dimensional Power Doppler ultrasonography for diagnosing abnormally invasive placenta and quantifying the risk. Obstetrics and Gynecology. 2015;126(3):645-653. UI: 26214694 PMID: 26214694
- Ilekis JV, Tsilou E, Fisher S, Abrahams VM, Soares MJ, Cross JC, Zamudio S, Illsley NP, Myatt L, Colvis C, Costantine MM, Haas DM, Sadovsky Y, Weiner C, Rytting E, Bidwell G. Placental origins of adverse pregnancy outcomes: potential molecular targets: an Executive Workshop Summary of the Eunice Kennedy Shriver National Institute of Child Health and Human Development. American Journal Obstetrics and Gynecology. 2016;215(1 Suppl):S1-46. UI: 26972897
- Rubenstein AF, Zamudio S, Al-Khan A, Douglas C, Sledge S, Tully G, Thurer RL. Clinical experience with the implementation of accurate measurement of blood loss during Cesarean delivery: Influences on hemorrhage recognition and allogenic transfusion. American Journal of Perinatology. (e-pub ahead of print Dec. 5) 2017. American Journal Perinatology. 2018;35(7):655–659. PMID: 29207419
- Maynard H, Zamudio S, Jauniuax E, Collins SL. The importance of bladder volume in the ultrasound diagnosis of placenta accreta spectrum disorders (AIP). International Journal of Obstetrics and Gynecology. 2018;140(3):332-337. UI: 29086915
- Rubenstein AF, Block M, Zamudio S, Douglas C, Sledge S, Tully G, Thurer RL. Accurate Assessment of Blood Loss During Cesarean Delivery Improves Estimation of Postoperative Hemoglobin. American Journal Perinatology. 2018;36(4): 434-439. doi: 10.1055/s-0038-1669397 PMID: 30142649
- Kuhn T, Martimucci K, Al-Khan A, Bilinski R, Zamudio S, Alvarez M, Alvarez-Perez J. Prophylactic hypogastric artery ligation during Placenta Percreta Surgery: A Retrospective Cohort Study. American Journal Perinatology 2018;8(2):e142-e145. PMID: 29977660
- DeMeritt J, Wajswol E, Wattamwar A, Litkouhi B, Vaidya A, Sbarra M, Zamudio S, Pozzi RA, Canning A, Woytanowski J, Al-Khan A. Serial uterine artery embolization for the treatment of placenta percreta in the first trimester: A case report. Cardiovascular and Interventional Radiology. 2018;41(8):1280-1284. PMID: 29556708
- Spillane N, Zamudio S, Alvarez-Perez J, Andrews T, Nyirenda T, Alvarez M, Al-Khan A. Increased incidence of Respiratory Distress Syndrome in neonates of mothers with abnormally invasive placentation. PLoS One. 2018;13(7):e0201266. PMID: 30048504
- Al-Khan A, Guirguis G, Zamudio, S, Alvarez, M, Martimucci K, Luke D, Alvarez-Perez J. Preoperative cystoscopy could determine the severity of Placenta Accreta Spectrum disorders: an observational study. In press, Journal of Obstetrics and Gynecology Research online publication 2018;Aug 23. UI: 30136333 PMID: 30136333
- DeMeritt J, Wajswol E, Wattamwar A, Chervoni-Knapp T, Zamudio S. Duplicated prostate artery central gland blood supply: Functional vascular anatomy and relevance for prostate artery embolization. Journal of Vascular and Interventional Radiology. 2018;29:1595-1600. PMID: 30293730
- Martimucci K, Kuhn T, Perez A, Alvarez M, Al-Khan A, Zamudio S, Alvarez-Perez J. Interpregnancy interval and Abnormally Invasive Placentation. Acta Obstetrica et Gynecologica Scandinavica. 2019;98(2):183-187. PMID: 30288733
- Rubenstein AF, Zamudio S, Douglas C, Sledge S, Tully G, Thurer RL. Automated Quantification of Blood Loss versus Visual Estimation in 274 Vaginal Deliveries. American Journal Perinatology. 2019 [Epub ahead of print] doi: 10.1055/s-0040-1701507
- Al-Khan A, Youseff YH, Feldman KM, Illsley NP, Remache Y, Alvarez-Perez J, Mannion C, Zamudio S. 2020 Biomarkers of abnormally invasive placenta. Placenta. 2020;91(1):37-42. doi.org/10.1016/j.placenta.2020.01.007
- Romagano MP, Guerrero K, Spillane S, Kayaalp E, Smilen SW, Alvarez M, Alvarez-Perez J, Kim AF, Aschner J, Al-Khan A, Perinatal outcomes in critically ill pregnant women with coronavirus disease American Journal of Obstetrics & Gynecology 2019, MFM 2020 (in press). doi.org/10.1016/j.ajogmf.2020.100151
Molecular (Basic Science) Investigations
Funding: two prior NIH awards. Molecular investigations of abnormal placentation
This program is complementary to the clinical, translational studies described above. We are discovering the basic mechanisms responsible for transforming noninvasive, placental cytotrophoblast cells (the parent cells of the very early developing placenta) into invasive extravillous trophoblast cells. These cells anchor the placenta to the uterine wall and eventually invade and remodel the spiral arteries of the mother. Comparison of these two cell types from first trimester placenta showed clearly that the mechanism was a highly conserved evolutionary process called an epithelial-mesenchymal transition (EMT). It is common in early intrauterine development, cancer, and wound healing. It occurs when anchored and polarized epithelial cells lose their cell-cell adhesion molecules and transform into anchorage-independent, non-polar, migratory cells (Ref. 3 and DaSilva-Arnold). In developmental and cancer biology, this molecular mechanism enables cells to convert from an epithelial to mesenchymal phenotype.
We showed this large change in first trimester cells is blunted in normal third trimester cells, consistent with the loss of invasive capability later in pregnancy (see figure below). Analysis of extravillous trophoblast cells from AIP (over-invasion) pregnancies shows that these cells retain more of the mesenchymal, invasive characteristics observed in the first trimester compared to normal third trimester cells. In contrast, extravillous trophoblast cells from preeclamptic (under-invasion) pregnancies have more epithelial characteristics compared to normal third trimester cells, consistent with a reduced invasive potential. These data allow us to place these cells on an EMT spectrum where the extent of the EMT regulates the degree of invasiveness.
|This figure shows the relative position on the EMT (phenotypic) spectrum for cytotrophoblast cells (CTB) and extravillous trophoblast cells (EVT) from normal first trimester and third trimester pregnancies. It also shows the position of extravillous trophoblast cells from preeclamptic and AIP pregnancies.|
We discovered a candidate for regulation of the EMT in the human placenta: a DNA-binding factor named ZEB2, which controls the transcription of DNA into RNA for a host of genes involved in the EMT process. It has been described as an EMT “master regulator” in a variety of other cellular processes in which the EMT mechanism is involved. Our studies examine ZEB2 in model epithelial trophoblast cell lines, from abnormal and normal pregnancies and in a 3D bioprinted model developed in the CAP labs with collaborators from the engineering departments at the Stevens Institute of Technology.
|Figure shows loss of occludin, a cell adhesion protein, following overexpression of the ZEB2 transcription factor and EMT “master regulator” in a model trophoblast cell line.|
It is probable that the extent of EMT and invasiveness is regulated, at least in part, by the uterine environment. As the mechanism becomes clearer and better defined, we will be exploring the potential regulators of the transformation process, looking for the means to detect pathological changes and to derive possible therapeutic modalities for ameliorating pathological consequences.
Basic Science/Molecular Placental Development Publications
- Illsley NP, Caniggia I, Zamudio S. Placental metabolic reprogramming: do changes in the mix of energy-generating substrates modulate fetal growth? International Journal of Developmental Biology. 2010;54(2-3):409-19. PMCID: PMC4497569
- Zamudio S, Torricos T, Fik E, Oyalo M, Echalar L, Pullockaran J, Tutino E, Martin B, Belliappa S, Balanza E, Illsley NP. Hypoglycemia and the origin of hypoxia-induced reduction in fetal growth. PLoS One. 2010;5(1):e8551. PMID: 20049329
- Al-Khan A, Aye IL, Barsoum I, Borbely A, Cebral E, et. al. IFPA Meeting 2010 Workshops Report II: Placental pathology; trophoblast invasion; fetal sex; parasites and the placenta; decidua and embryonic or fetal loss; trophoblast differentiation and syncytialisation.Placenta. 2011;32 Suppl 2:S90-9.
- Brown, K, Heller DH, Zamudio S, Illsley NP. Glucose transporter 3 (GLUT3) protein expression in human placenta across gestation. Placenta. 2011;32(12): 1041-1049.
- Bibee KP, Illsley NP, Moley KH Asymmetric syncytial expression of GLUT9 splice variants in human term placenta and alterations in diabetic pregnancies. Reproductive Sciences. 2011;18:20-27.
- Williams SF, Fik E, Zamudio S, Illsley NP. Protein synthesis in human syncytiotrophoblast is resistant to inhibition by hypoxia. 2012;33(1):31-38. PMID: PMC3422675
- Al-Khan A, Bulmer JN, Chantraine F, Chen CP, Chen Q, Collins S, Cotechini T, Fitzgerald JS, He M, Holland O, Hung TH, Illsley NP, Ino K, Iwaki T, Kanayama N, Kaneki E, Katabuchi H, Kobayashi Y, Kondo A, Masuzaki H, Matjila M, Miura K, Mori A, Murthi P, Nagahashi K, Nie G, Ohba T, Sood R, Sugimura M, Takizawa T, Usui H, Velicky P, Lash GE IFPA Meeting 2012 Workshop Report III: trophoblast deportation, gestational trophoblastic disease, placental insufficiency and fetal growth restriction, trophoblast over-invasion and accreta-related pathologies, placental thrombosis and fibrinolysis. 2013;34 Suppl:S11-6. doi: 10.1016/j.placenta.2012.11.018. PMID:23257209.
- Zamudio S, Kovalenko O, Echalar L, Torricos T, Al-Khan A, Alvarez M, Illsley NP. Evidence for extraplacental sources of circulating angiogenic growth effectors in human pregnancy. Placenta. 2013;34(12):1170-1176. PMID: 24161217.
- Ackerman WE 4th, Adamson L, Carter AM, Collins S, Cox B, Elliot MG, Ermini L, Gruslin A, Hoodless PA, Huang J, Kniss DA, McGowen MR, Post M, Rice G, Robinson W, Sadovsky Y, Salafia C, Salomon C, Sled JG, Todros T, Wildman DE, Zamudio S, Lash GE. IFPA Meeting 2013 Workshop Report II: Use of ‘omics’ in understanding placental development bioinformatics tools for gene expression analysis, planning and coordination of placenta research network, placental imaging, evolutionary approaches to understanding preeclampsia. 2014;35 Suppl:S10-4. UI: 24315655
- Zamudio S, Borges M, Echalar L, Kovalenko O, Vargas E, Torricos T, Al-Khan A, Alvarez M, Illsley NP. Maternal and fetoplacental hypoxia do not alter circulating angiogenic growth effectors during human pregnancy. Biology of Reproduction. 2014;90(2):42. UI: 24352559
- Baumann MU, Schneider H, Malek A, Palta V, Surbek DV, Sager R, Zamudio S, Illsley NP. Regulation of human trophoblast GLUT1 glucose transporter by insulin-like growth factor I (IGF-I). PLoS One. 2014;9(8):e106037. UI: 25157747
- DaSilva-Arnold S, James JL, Al-Khan A, Zamudio S, Illsley NP. Differentiation of first trimester cytotrophoblast to extravillous trophoblast involves an epithelial to mesenchymal transition. 2015;36(12):1412-8. PMID: 26545962
- Francois LN, Gorczyca L, Du J, Bircsak KM, Yen E, Wen X, Tu MJ, Yu AM, Illsley NP, Zamudio S, Aleksunes LM. Down-regulation of the placental BCRP/ABCG2 transporter in response to hypoxia signaling. 2017;51:57-63. PMID: 28292469.
- Ihde ES, Zamudio S, Loh JM, Zhu Y, Woytanowski J, Rosen L, Liu M, Buckley B. Application of a novel assay to examine exposure to Bisphenol-A and common substitutes in a maternal fetal cohort. Human and Ecological Risk Assessment: An International Journal. 2018;24:2:331-346. PMID: 30462321
- DaSilva-Arnold S, Al-Khan A, Zamudio S, Alvarez M, Mannion C, Koenig C, Petroff M, Illsley NP. Human trophoblast epithelial-mesenchymal transition in abnormally invasive placenta. Biology of Reproduction. 2018;99(2):409-421. PMID: 29438480
- Albrecht C, Chamley L, Charnock-Jones DS, Collins S, Fujiwara H, Golos T, Grayo S, Hannan N, Harris L, Ichizuka K, Illsley NP, Iwashita M, Kallol S, Al-Khan A, Lash G, Nagamatsu T, Nakashima A, Niimi K, Nomoto M, Redman C, Saito S, Tanimura K, Tomi M, Usui H, Vatish M, Wolfe B, Yamamoto E, O’Tierney-Ginn P IFPA meeting 2018 workshop report II: Abnormally invasive placenta; inflammation and infection; preeclampsia; gestational trophoblastic disease and drug delivery. 2019;84:9-13. doi: 10.1016/j.placenta.2019.02.006. PMID: 30773233.
- DaSilva-Arnold, Kuo C-Y, Viralkumar D, Remache Y, Kim PCW, Fisher JP, Zamudio S, Al-Khan A, Birge R, Illsley NP. ZEB2, a master regulator of the epithelial-mesenchymal transition, mediates trophoblast differentiation. Molecular Human Reproduction. 2019;25(2):61-75. PMID 30462321
- Borges MH, Pullockaran J, Catalano PM, Baumann MU, Zamudio S, Illsley NP. Human placental GLUT1 glucose transporter expression and the fetal insulin-like growth factor axis in pregnancies complicated by diabetes. BBA – Molecular Basis of Disease. 2019;1865(9):2411-2419. UI 31175930
- Ding H, Illsley NP, Chang R. 3D Bioprinted GelMA based models for the study of trophoblast cell invasion. Scientific Reports. 2019;9. 18854 org/10.1038/s41598-019-55052-7.
- lllsley NP, Baumann MU. Human placental glucose transport in fetoplacental growth and metabolism. BBA – Molecular Basis of Disease. 2020;1866(2). 165359. doi: 10.1016/j.bbadis.2018.12.010. PMID: 30593896
- Do C, Dumont ELP, Salas M, Castano A, Mujahed H, Maldonado L, Singh A, DaSilva-Arnold SC, Bhagat G, Lehman S, Christano AM, Madhavan S, Nagy PL, Green PHR, Feinman R, Trimble C, Illsley NP, Marder K, Honig L, Monk C, Goy A, Chow K, Goldlust S, Kaptain G, Siegel D, Tycko B. Allele-specific DNA methylation is increased in cancers and its dense mapping in normal plus neoplastic cells increases the yield of disease-associated regulatory SNPs. Genome Biology. 2020;21: doi.org/10.1186/s13059-020-02059-3
- Illsley NP, DaSilva-Arnold SC, Zamudio S, Alvarez M, Al-Khan A. Trophoblast invasion: lessons from abnormally invasive placenta (placenta accreta). Trophoblast Research. 2020 (in press). doi.org/10.1016/j.placenta.2020.01.004
Changing Health Care
Our eventual goal is to combine both lines of our research to develop therapies for the detection, amelioration and prevention of abnormal placentation in high-risk women.
Our Research Scientists
Stacy Zamudio, Ph.D.
Senior Scientist, Director of Research, Department of Obstetrics and Gynecology
Academic Title: Adjunct Associate Professor of Preventive Medicine and Community Health, Rutgers-New Jersey Medical School
Education: B.A., M.A., University of California, Los Angeles; Ph.D., University of Colorado, Boulder
Dr. Zamudio has published more than 80 articles on maternal and fetal physiology, genetics, epidemiology, and clinical outcomes. She studies what goes wrong with the placenta in pregnancies with complications like placenta accreta and preeclampsia. Her work has been funded by the National Institutes of Health (NIH), the National Science Foundation, the American Heart Association, and the Fogarty International Research Collaborative. She is a leader in the field, serving or having served on three scientific journal editorial boards, on the Council of the Society for Reproductive Investigation, as President of the Perinatal Research Society, and as Chair of the NIH Obstetrics and Maternal-Fetal Biology study section (OMFB). OMFB evaluates training grants in reproductive biology/medicine, clinical trials, and transition to independence award for junior faculty. In this capacity, Dr. Zamudio helps to shape the future of research in obstetrics and gynecology and the next generation of scientists.
Her past and current funding have focused the effects of hypoxia (high altitude) on the placenta and pregnancy outcomes, rates of pregnancy complications, and how the placental genome has evolved to protect fetuses from the adverse effects of hypoxia. Her work on placenta accreta has several goals: to develop a diagnostic test that can be used early in pregnancy; to improve the ability to discriminate between mild, moderate, and severe disease via diagnostic imaging; and to learn how the cells of the placenta are permitted to invade tissues they normally do not invade. She is the principal investigator on the NIH U01 study to develop new ultrasound measures of placental structure and function early in pregnancy.
Nicholas P. Illsley, D.Phil.
Senior Scientist, Department of Obstetrics and Gynecology
Academic Title: Adjunct Professor of Pharmacology, Physiology and Neuroscience, Rutgers-New Jersey Medical School
Education: B.Sc. (Hons) in Biochemistry, University of Bristol, U.K.; D.Phil., University of Oxford, U.K.
Dr. Illsley came to Hackensack University Medical Center in 2012, following positions at the U.K. Medical Research Council’s Clinical Research Centre in London, the Department of Obstetrics, Gynecology and Reproductive Sciences at the University of California San Francisco, and the Department of Obstetrics, Gynecology and Women’s Health at UMDNJ-New Jersey Medical School. His research focuses on the human placenta, its mechanisms of maternal to fetal transport, metabolism, and role in the regulation of fetal growth. He has studied diabetic pregnancy, fetal growth restriction, preeclampsia, and pregnancies subject to chronic hypoxia. He has published more than 80 articles in scientific journals on these topics. He has been awarded multiple research grants, primarily from the NIH, with continuous funding since 1988. Dr. Illsley has been instrumental in developing and promoting the NIH Human Placenta Project, a 10-year effort to devise real-time methods for examining placental function.
Dr. Illsley is a leader in his field, helping to found both the Placenta Association of the Americas — for which he served as the first President (2001-2011) — and the International Federation of Placenta Associations, for which he is completing a five-year term as President. He has served on several journal editorial boards and on the Council of the Society for Gynecologic Investigation and Perinatal Research Society. He was a charter member of the NIH Human Embryology and Development Study Section and continues to serve on multiple NIH study sections, reviewing research in perinatal medicine. Dr. Illsley has now put this experience and expertise to use in a new role: leading investigations for the Center for Abnormal Placentation. In collaboration with Dr. Zamudio and Dr. Al-Khan, he is developing new research to investigate the molecular biology that underlies placental invasion into the uterus in both normal and abnormal pregnancies. He is particularly interested in abnormally invasive placenta (placenta accreta) and preeclampsia.
If you want to participate in our research …
Our NIH-funded ultrasound study of the placenta needs your help. If you are in early pregnancy (less than or equal to 11 weeks gestation) you may be having a nuchal translucency ultrasound scan, a standard clinical screening procedure performed for most pregnant women. This procedure uses ultrasound to measure the thickness of the fluid buildup at the back of the developing baby’s neck. If this area is thicker than normal, it can be an early sign of Down syndrome, trisomy 18, or heart problems. If you are having this procedure performed at Hackensack University Medical Center, you will also have two other scans as standard of care, to measure placental volume and uterine artery blood flow. We would like to make use of these ultrasound scans in our research on placental implantation and pregnancy outcomes. This will be anonymous; we will assign a ID code to your information which will be used throughout the research.