Expression of hypoxia-inducible factor-1 by trophectoderm cells in response to hypoxia and epidermal growth factor
DC Field | Value | Language |
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dc.contributor.author | Jeong, Wooyoung | - |
dc.contributor.author | Bazer, Fuller W. | - |
dc.contributor.author | Song, Gwonhwa | - |
dc.contributor.author | Kim, Jinyoung | - |
dc.date.accessioned | 2021-09-04T04:06:34Z | - |
dc.date.available | 2021-09-04T04:06:34Z | - |
dc.date.created | 2021-06-18 | - |
dc.date.issued | 2016-01-08 | - |
dc.identifier.issn | 0006-291X | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/89817 | - |
dc.description.abstract | The low oxygen environment in the uterine environment requires pre-implantation embryos to adapt to oxygen deficiency. Hypoxia-inducible actor(HIF)-1 is a master regulator whereby cells adapt to changes in oxygen concentrations. In addition to hypoxic conditions, non-hypoxic stimuli such as growth factors also activate expression of HIF-1. In this study, the mechanisms underlying low oxygen-dependent and epidermal growth factor (EGF)-dependent expression of HIF-1 alpha were explored using porcine trophectoderm (pTr) cells. The results indicated that expression of HIF-1 alpha and HIF-1 beta mRNAs was not affected by low concentrations of oxygen; however, hypoxic conditions markedly increased the abundance of HIF-1 alpha protein, especially in nuclei of pTr cells. Even under normoxic conditions, the abundance of HIF-1 alpha protein increased in response to EGF. This EGF-mediated increase in HIF-1 alpha protein was blocked through inhibition of translation by cycloheximide. The inhibitors LY294002 (PI3K-AKT inhibitor), U0126 (inhibitor of ERK1/2) and rapamycin (mTOR inhibitor) also blocked the ability of EGF to increase HIF-1 alpha protein and to phosphorylate AKT, ERK1/2 and mTOR proteins. Both hypoxia and EGF induced proliferation of pTr cells. This ability of EGF to stimulate proliferation of pTr cells was suppressed by EGFR siRNA, but not HIF-1 alpha siRNA, but a significant decrease in EGF-induced HIF-1 alpha protein occurred when pTr cells were transfected with HIF-1 alpha siRNA. The results of the present study suggest that pTr cells adapt to oxygen deficiency and proliferate in response to an oxygen-dependent HIF-1 system, and that EGF at maternal conceptus interface can increase the abundance of HIF-1 alpha protein via translational regulation through AKT, ERK1/2 and mTOR signaling cascades. (C) 2015 Elsevier Inc. All rights reserved. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | ACADEMIC PRESS INC ELSEVIER SCIENCE | - |
dc.subject | SMOOTH-MUSCLE-CELLS | - |
dc.subject | FACTOR 1-ALPHA | - |
dc.subject | EARLY-PREGNANCY | - |
dc.subject | HIF-1 | - |
dc.subject | FACTOR-1-ALPHA | - |
dc.subject | PATHWAY | - |
dc.subject | ANGIOGENESIS | - |
dc.subject | HIF-1-ALPHA | - |
dc.subject | ACTIVATION | - |
dc.subject | MECHANISMS | - |
dc.title | Expression of hypoxia-inducible factor-1 by trophectoderm cells in response to hypoxia and epidermal growth factor | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Song, Gwonhwa | - |
dc.identifier.doi | 10.1016/j.bbrc.2015.11.091 | - |
dc.identifier.scopusid | 2-s2.0-84952638277 | - |
dc.identifier.wosid | 000368652300006 | - |
dc.identifier.bibliographicCitation | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.469, no.2, pp.176 - 182 | - |
dc.relation.isPartOf | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.citation.title | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.citation.volume | 469 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 176 | - |
dc.citation.endPage | 182 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Biophysics | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biophysics | - |
dc.subject.keywordPlus | SMOOTH-MUSCLE-CELLS | - |
dc.subject.keywordPlus | FACTOR 1-ALPHA | - |
dc.subject.keywordPlus | EARLY-PREGNANCY | - |
dc.subject.keywordPlus | HIF-1 | - |
dc.subject.keywordPlus | FACTOR-1-ALPHA | - |
dc.subject.keywordPlus | PATHWAY | - |
dc.subject.keywordPlus | ANGIOGENESIS | - |
dc.subject.keywordPlus | HIF-1-ALPHA | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | MECHANISMS | - |
dc.subject.keywordAuthor | HIF-1 | - |
dc.subject.keywordAuthor | Hypoxia | - |
dc.subject.keywordAuthor | EGF | - |
dc.subject.keywordAuthor | Trophectoderm | - |
dc.subject.keywordAuthor | Cell signaling | - |
dc.subject.keywordAuthor | Proliferation | - |
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