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Cell survival effect of activin against heat shock stress on OVCAR3.

  • Fukuda, J
  • Ito, I
  • Tanaka, T
  • Leung, P C
Published Article
Life Sciences
Publication Date
Jan 01, 1998
PMID: 9870706


Activin has been known as the hormone protein which regulates either cell proliferation or cell differentiation. Recently, it has also been reported that activin may have cell survival function. In this study, we have investigated, 1) the expression of inhibin subunits and activin receptors (ActRs) in ovarian carcinoma cell line (OVCAR3), 2) the binding property between activin and its receptors under the exposure to stress, and 3) the effect of activin on cell proliferation. All of inhibin subunits and ActR Ia, IIa and IIb mRNA were amplified by RT-PCR in OVCAR3. By Western blot analysis, ActR IIa and IIb proteins were detected. The binding property between activin and ActRs was analyzed with the fixed complex, using chemical cross linker. The bigger molecular weight signals, which had been shown to form the heterotrimeric complex among activin, ActR type I and ActR type II were detected after cross linking. These upper signals were apparently increased by rh-Activin and decreased by rh-Follistatin. Therefore, it was suggested that they were resultant from activin and Act-R complex. OVCAR3 was exposed to the stress (42C, 1 hour heat shock), the protein level of ActR IIa increased and ActR IIb decreased from about 3 h to 24 h after the exposure to the heat stress (HS). On the other hand, the complex between activin and ActR IIa and IIb increased from 3 h after the exposure to HS. To investigate the effect of activin and follistatin on OVCAR3 proliferation after the exposure to HS, we counted the cell number at 96 h after the treatment with activin or follistatin in the condition either with or without HS. Proliferation of the cell in the presence of HS was stimulated by rh-Activin and inhibited by rh-Follistatin. These data suggest that activin might have the function to survive and to proliferate OVCAR3, due to, at least in part the increase in its binding capacity to ActRs through either autocrine or paracrine manner.

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