Research highlights  

Our laboratory is pursuing research on physiology and cell biology of ovarian function with emphasis on folliculogenesis, signal transduction, apoptosis, and regulation of corpus luteum function.

During the periovulatory period, the mammalian ovary is the site of dramatic structural and functional changes leading to oocyte maturation, follicle rupture and corpus luteum formation. Our main goal is to understand these processes at physiological, morphological and molecular levels. We are currently employing various experimental animal model systems to understand these processes, which to a large extent, result from changes in the transcriptome/ proteome of various ovarian cell types by employing a variety of molecular biology tools such as differential display, DNA array technology, proteomics etc., Recently, we have standardized an animal model system in which an single follicle could be developed to ovulate for purposes of studying global gene expression profiling prior to and at different time intervals after administration of an ovulatory dose of gonadotropins to delineate different biochemical pathways associated with oocyte maturation, follicular rupture and tissue remodeling. Expressions of around 4000 genes have been identified to be up- or down-regulated in the follicular granulosa cells before and after exposure to gonadotropins, and analysis are underway to catalog changes in gene expression into different cell functions. In parallel with this work, we are pursuing research on delineating signal transduction pathways associated with apoptosis of ovarian somatic cells during follicular atresia. Also, using genomic data base of different species, efforts are underway to identify and map quantitative trait loci associated with milk production and reproductive efficiency in domestic animals. Another area of research being pursued in the laboratory is the elucidation of molecular mechanisms regulating the primate corpus luteum function.  

Corpus luteum is the transient endocrine organ formed from postovulatory ovarian follicle in most vertebrates. Its secretion of progesterone is essential for establishment and, in some species, the maintenance of pregnancy in mammals. In several non-primate species, prostaglandin F2α has been recognized as a chief luteolysin responsible for regression of corpus luteum (by ovary of apoptosis) at the end of a non-fertile cycle. On the other hand, the role of prostaglandin F2α during luteolysis in higher primates is questionable since prostaglandin F2α of uterine source has no role in higher primates. Whether prostaglandin F2α from intra-luteal source might participate in the luteal regression during non-fertile cycles in primates remains to be investigated, although presence of prostaglandin, its receptors and its effect have been demonstrated. We have recently standardized a model system in which prostaglandin F2α has been observed to function as luteolysin in macaques, a representative higher primate. Also, another important aspect of research is being pursued on corpus luteum is on elucidation of signaling pathways that regulate its function, since control of its function occupies a central position in reproduction both in sucess or failures of conception and pregnancy. In this regard, our laboratory demonstrated for the first time the presence of CREB, an transcription factor, required for mediating the nuclear actions of LH via cAMP-PKA pathway. Efforts are also underway to catalog multiple signaling pathways activated by trophic factors required for regulation of corpus luteum function.