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Hypoxia‐inducible factor‐1α regulates matrix metalloproteinase‐1 activity in human bone marrow‐derived mesenchymal stem cells
Author(s) -
Lin Jiunn-Liang,
Wang Ming Jen,
Lee Donching,
Liang Chun-Chin,
Lin Shankung
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.06.033
Subject(s) - mmp3 , mmp1 , matrix metalloproteinase , mesenchymal stem cell , biology , bone marrow , stem cell , hypoxia (environmental) , messenger rna , in vitro , hypoxia inducible factors , metalloproteinase , microbiology and biotechnology , endocrinology , cancer research , andrology , medicine , immunology , gene expression , chemistry , gene , biochemistry , organic chemistry , oxygen
We examined the mRNA levels of hypoxia‐inducible factor‐1α (HIF‐1α) in bone marrow mesenchymal stem cells (bmMSCs) of eight osteoarthritis patients. BmMSC‐1, expressing higher HIF‐1α mRNA and protein than bmMSC‐5, elicited higher matrix metalloproteinase‐1 (MMP1) activity and stronger invasive capacity. In vitro invasion assays and quantitative PCR analyses showed that targeted inhibition of HIF‐1α in bmMSC‐1 decreased its invasion and expressions of MMP1 and MMP3, whereas overexpression of HIF‐1α in bmMSC‐5 increased its invasion and expressions of MMP1 and MMP3. Therefore, HIF‐1α can regulate MMP1 and MMP3 expressions in human bmMSCs, which might suggest a pathophysiological role of bmMSC expressing high HIF‐1α in bone diseases.