DEEPAK MODI
Articles written in Journal of Biosciences
Volume 38 Issue 1 March 2013 pp 85-92 Articles
Cellular ontogeny of RBMY during human spermatogenesis and its role in sperm motility
Shadaan Abid Vrushali Sagare-Patil Jyotsna Gokral Deepak Modi
The Y-chromosome-encoded gene
Volume 42 Issue 1 March 2017 pp 69-80 Article
SANIYA LAHERI DEEPAK MODI PURVI BHATT
Oviductal glycoprotein 1 (OVGP1), also called oviductin, is an oviduct-specific protein and is suggested to play a rolein fertilization. Traditionally, Ovgp1 has been shown to be exclusively expressed by the oviduct; however, recentstudies have demonstrated its expression in some cancers. This observation led us to hypothesize that Ovgp1 mighthave some extra-oviductal expression. In the current study, we evaluated the mRNA and protein expression of Ovgp1in normal reproductive tissues of male and female mice. For the first time, we demonstrate that beyond the oviduct,Ovgp1 mRNA is expressed in the testis, epididymis and ovary, but not in the uterus, cervix, vagina, breast, seminalvesicles and prostate gland. In the testis, Ovgp1 mRNA was localized in the cells at the base of seminiferous tubules(most likely, Sertoli cells), while the protein was detected in the round and elongating spermatids. In the epididymis,Ovgp1 transcripts were localized in epididymal epithelium of the caput but not the corpus and cauda; OVGP1 proteinwas, however, not detected in any of the segments but was present in the epididymal sperm. In the ovary, Ovgp1transcripts and protein were detected in the surface epithelium, granulosa cells of the preantral and the antral folliclesand corpus luteum. In both, the ovary and oviduct, the expression of Ovgp1 was found to be higher at estrus stage thanat diestrus stage. To the best of our knowledge, this is the first study demonstrating the extra-oviductal expression ofOvgp1. Our data suggests that, beyond fertilization, Ovgp1 might have specific roles in gonadal physiology.
Volume 45 All articles Published: 13 August 2020 Article ID 0105 Article
ANURADHA MISHRA MOSAMI GALVANKAR SHANTASHRI VAIDYA UDDHAV CHAUDHARI DEEPAK MODI
Endometriosis is a common disorder of unknown etiology, and non-surgical therapies are still a challenge. Tounderstand the pathogenesis and preclinical testing of drugs for endometriosis, animal models are highlydesirous. Herein, we carried out longitudinal characterization of a mouse model for endometriosis whereuterine tissue was transplanted onto the intestinal mesentery. During the course of lesion development from day15 to 60 post-induction, the ectopic endometrium became pale, fluid-filled and the animals developed peritonealadhesions. Most lesions resembled a well-differentiated type of endometriosis and ~13% of animalshad mixed type of lesions. There was extensive stromal compaction in the ectopic tissue. During the progressionof endometriosis, there was increased proliferation of epithelial and stromal cells as evident by PCNAstaining. Cyp19a1 (aromatase) mRNA was detected in the ectopic lesions on day 15 and 30 post-induction ofendometriosis, by day 60 the expression was reduced. As compared to the control endometrium, the mRNAlevels of Esr1 progressively reduced while the levels of inflammation associated genes (Esr2, Ifng, Tnf andIl1b) increased in the ectopic lesions. Infiltration of macrophages and polymorphonuclear leucocytes was alsoobserved in the ectopic lesions indicative of inflammation. As compared to control, there was no change inlevels of Cytokeratin and E-cadherin in the epithelial cells of ectopic endometrium. We did not observeexcessive collagen deposition or alpha-SMA positive myofibroblasts in the stroma of the ectopic endometrium.Thus, epithelial-to-mesenchymal transition and fibrosis are not detected in the mouse model of endometriosis.Our results show that the mouse model of endometriosis mimics some but not all the features of humanendometriosis.
Volume 45, 2020
All articles
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