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Kwon, Hyug Moo
Immunometabolism and Cancer Lab
Research Interests
  • TonEBP, Obesity, Cancer, Chronic inflammatory diseases, Brain disorder, Kidney disorder, Genomic instability

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Increased NFAT5 expression stimulates transcription of Hsp70 in preeclamptic placentas

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dc.contributor.author Park, J. K. ko
dc.contributor.author Kang, T. G. ko
dc.contributor.author Kang, M. Y. ko
dc.contributor.author Park, J. E. ko
dc.contributor.author Cho, I. A. ko
dc.contributor.author Shin, J. K. ko
dc.contributor.author Choi, W. J. ko
dc.contributor.author Lee, S. A. ko
dc.contributor.author Choi, W. S. ko
dc.contributor.author Kwon, H. Moo ko
dc.contributor.author Lee, J. H. ko
dc.contributor.author Paik, W. Y. ko
dc.date.available 2014-04-24T06:53:06Z -
dc.date.created 2014-04-24 ko
dc.date.issued 2014-02 ko
dc.identifier.citation PLACENTA, v.35, no.2, pp.109 - 116 ko
dc.identifier.issn 0143-4004 ko
dc.identifier.uri https://scholarworks.unist.ac.kr/handle/201301/4422 -
dc.description.abstract Objective We investigated the expression of heat shock protein 70 (Hsp70), nuclear factor of activated T cells 5 (NFAT5), and hypoxia-induced factor-1α (HIF-1α) in the placentas of normal and preeclamptic pregnancies and in human placental hypoxia models in vitro to examine the regulatory mechanisms of placental Hsp70 expression. Methods The expression levels of HIF-1α, NFAT5, and Hsp70 were examined in placental samples from 10 females with preeclampsia and 10 normotensive control patients and in human choriocarcinoma trophoblast cells treated with 1 mM CoCl2 by western blotting. Using models of placental hypoxia, pharmacological inhibition of HIF-1α with chetomin and shRNA knockdown and overexpression of NFAT5 were performed to investigate the roles of HIF-1α and NFAT5 in induction of Hsp70 by placental hypoxia. Results The levels of HIF-1α, NFAT5, and Hsp70 expression were significantly higher in the preeclamptic compared to normal placentas. In the placental hypoxia models, the expression of HIF-1α, NFAT5, and Hsp70 were significantly higher after 3, 6, and 12 h of 1 mM CoCl2 treatment, respectively. Pharmacological inhibition of HIF-1α suppressed the induction of NFAT5 and Hsp70 at the protein level. shRNA knockdown of NFAT5 suppressed the induction of Hsp70 protein and overexpression of NFAT5 stimulated the induction of Hsp70 mRNA and protein in models of human placental hypoxia in vitro. Conclusion HIF-1α positively regulates the induction of NFAT5 and Hsp70 by placental hypoxia and NFAT5 stimulates transcription of Hsp70 in response to placental hypoxia in models of human placental hypoxia in vitro. ko
dc.description.statementofresponsibility close -
dc.language 영어 ko
dc.publisher W B SAUNDERS CO LTD ko
dc.title Increased NFAT5 expression stimulates transcription of Hsp70 in preeclamptic placentas ko
dc.type ARTICLE ko
dc.identifier.scopusid 2-s2.0-84893798110 ko
dc.identifier.wosid 000333495700006 ko
dc.type.rims ART ko
dc.description.wostc 0 *
dc.description.scopustc 0 *
dc.date.tcdate 2014-10-18 *
dc.date.scptcdate 2014-07-12 *
dc.identifier.doi 10.1016/j.placenta.2013.12.005 ko
dc.identifier.url http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84893798110 ko
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