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A critical role for adiponectin-mediated development of endometrial luminal epithelial cells during the peri-implantation period of pregnancy

Authors
Lim, WhasunChoi, Myung JinBae, HyocheolBazer, Fuller W.Song, Gwonhwa
Issue Date
11월-2017
Publisher
WILEY
Keywords
adiponectin; cell proliferation; ER stress; peri-implantation period of pregnancy; uterine epithelial cells
Citation
JOURNAL OF CELLULAR PHYSIOLOGY, v.232, no.11, pp.3146 - 3157
Indexed
SCIE
SCOPUS
Journal Title
JOURNAL OF CELLULAR PHYSIOLOGY
Volume
232
Number
11
Start Page
3146
End Page
3157
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/81666
DOI
10.1002/jcp.25768
ISSN
0021-9541
Abstract
Adiponectin is one of the adipokines in the collagen superfamily. It is secreted primarily by white adipocytes and influences reproductive processes including ovarian and uterine functions. Adiponectin regulates energy homeostasis, insulin sensitivity, and is anti-inflammatory in various tissues. Its receptors (ADIPOR1 and ADIPOR2) are widely expressed in mammalian tissues, including porcine conceptuses and endometrial during the estrous cycle and peri-implantation period of pregnancy. However, regulatory effects of adiponectin on endometrial epithelial cells are unknown. Therefore, we investigated the effects of parity on expression of ADIPOR1 and ADIPOR2 and the effects of adiponectin in the porcine endometrium during early pregnancy. Results of this study revealed robust expression of ADIPOR1 and ADIPOR2 in uterine luminal (LE) and glandular (GE) epithelia during early pregnancy and expression decreased as with increasing parity. For porcine luminal epithelial (pLE) cells, adiponectin enhanced proliferation, and increased phosphorylation of AKT, P70S6K, S6, ERK1/2, JNK, P38, and P90RSK in a time-dependent manner. Moreover, the abundance of adiponectin-activated signaling molecules were suppressed by pharmacological inhibitors including wortmannin, U0126, SP600125, and SB203580, respectively, in pLE cells. Furthermore, inhibition of each targeted signal transduction molecule influenced proliferation of adiponectin-stimulated pLE cells. In addition, adiponectin inhibited tunicamycin-induced endoplasmic reticulum (ER)-stress through effects on ER stress regulated proteins in pLE cells. Collectively, these results suggest that adiponectin affects development of porcine uterine epithelia and reproductive performance through modulation of PI3K/AKT and MAPK cell signaling pathways.
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