A photo of Sanjoy Das.

Professor, UC Department of Pediatrics



Biography & Affiliation


In my laboratory, my colleagues and I focus our research mostly on molecular, genetic and epigenetic systems managing the features of uterine cell proliferation and differentiation during early pregnancy and the factors under the control of natural estrogen and xenoestrogens.

We are trying to solve two types of problems. First, we are mostly interested in addressing the genomic and epigenomic processes for natural estrogen-mediated and xenoestrogen-mediated actions in uterine cell biology. Second, our research explicitly studies the mechanism of cell cycle regulation to develop uterine stromal cell differentiation for decidualization in implantation.

Some of the most notable discoveries that my team and I have made in our laboratory include finding:

  • Epigenetic transformations through DNA methylation lead to uterine stromal cell decidualization
  • Estrogen-facilitated epithelial cell proliferation in the uterus is led by stroma-derived Fgf10 and Bmp8a
  • Factors that regulate uterine genes with estrogen
  • GPR30 activation resists estrogen-dependent uterine growth by hindering stromal ERK1/2 and estrogen receptor alpha (ERα) phosphorylation signals
  • High levels of cellular Bip determining estrogenic potency for xenoestrogen kepone in a mouse uterus
  • Nucleolar Sik-similar protein (Sik-SP) maintains a uterine estrogen signaling method via ERα
  • Over-expression of cyclin D3 enhances decidualization defects in Hoxa-10-/- mice
  • Polycomb repressive complex 1 directs uterine decidualization
  • The molecular link between the first and second phase estrogenic responses in the uterus
  • The role of FoxM1 downstream of Hoxa10 and cyclin D3

For more than 60 years, researchers have distinguished “early” and “late” phase uterine responses to estrogen even though the systems behind these fluctuating responses remain uncertain.

One branch of our research studies is the nongenomic actions of natural estrogen and xenoestrogens in the uterus, which is restricted toward known estrogen receptors. Endometrial stromal cells change into functionally and morphologically specified decidual cells, which is known as decidualization.

Decidualization takes place in women during the secretory phase of the menstrual cycle and during pregnancy in rodents. Uterine decidualization after embryo implantation is needed for establishing pregnancy and placentation. The progression of decidualization is portrayed by widespread endometrial stromal cell proliferation and differentiation throughout the decidual bed at the location of early implantation.

Yet, acquiring decidual cell polyploidy via terminal differentiation occurs within the decidual bed at the anti-mesometrial and lateral region of the implantation site. Research using a genetic mouse model has illustrated that polyploidy growth is specifically involved with effective decidualization in early embryo implantation.

The molecular systems regulating this program for regional decidual growth remain insufficiently understood. As such, today’s research specifically concentrates on the functions of cMet, imprinting gene H19, and epigenetic regulation via DNA methylation and PRC1 regulators in the midst of decidual development.

While fertility rates worldwide have remained the same over the last two decades, 50 million couples worldwide face fertility difficulties. A vital determinant of this condition is failure of early pregnancy events, which lead to 50 to 75 percent of all preclinical pregnancy irregularities.

We observed that effective embryo implantation needs two-way interaction between the implantation-competent blastocyst and the receptive endometrium. This interaction includes complex systems that lead to cellular, molecular and physiological differences in the embryo and endometrium.

During early pregnancy, the endometrial decidualization becomes a dynamic gatekeeper to implantation. Abnormal decidualization due to ineffective hormone responsiveness and impaired endometrial decidual cell growth regularly links with various endometrial and pregnancy complexities, including preeclampsia, premature birth, intrauterine growth retardation, unexplained infertility and recurrent spontaneous abortion as well as other gynecological conditions such as endometriosis and endometrial cancer.

In recent years, major progress has taken place in uncovering the features of implantation. However, there is a significant need to discover the molecular complications of the regulatory mechanisms during the onset of embryo implantation and decidualization. An enhanced understanding of the molecular system behind the early uterine implantation procedures is essential to confirm a healthy pregnancy outcome and address vital matters regarding female fertility conditions.

Throughout my career, I have gained numerous recognitions, including becoming a(n):

  • Associate Editor for Molecular Reproduction and Development
  • Associate Editor-in-Chief for Asian Pacific Journal of Reproduction
  • Recipient of the Israel Science Foundation (ISF) grant (2010)
  • Member of the editorial board for Biology of Reproduction
  • Member of the Special Emphasis Panel/Scientific Review, Xenobiotic and Nutrient Disposition and Action (2007 and 2009)

I have more than 30 years of experience in the field of reproductive sciences and began working at the Cincinnati Children’s Hospital Medical Center in 2008. My research has been published in numerous journals, such as Scientific Reports, Biology of Reproduction and the Journal of Molecular Endocrinology.

Research Interests

Characterization of non-genomic actions of natural estrogen and xenoestrogens in the uterus without involving the nuclear ERa and ERb; aspects of uterine cell cycle regulation for decidualization in implantation

Academic Affiliation

Professor, UC Department of Pediatrics

Research Divisions

Reproductive Sciences


PhD: Biochemistry, University of Calcutta, Calcutta, India.

MSc: Biochemistry, University of Calcutta, Calcutta, India.

BSc: Chemistry (Honors), University of Calcutta, Calcutta, India.


Extraembryonic heparin-binding epidermal growth factor-like growth factor deficiency compromises placentation in mice. Liu, Z; Skafar, DF; Kilburn, B; Das, SK; Armant, DR. Biology of Reproduction. 2019; 100:217-226.