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Thymosin β4 stabilizes hypoxia‐inducible factor‐1α protein in an oxygen‐independent manner
Author(s) -
Ock Mee Sun,
Song Kyoung Seob,
Kleinman Hynda,
Cha HeeJae
Publication year - 2012
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2012.06657.x
Subject(s) - angiogenesis , vascular endothelial growth factor , thymosin , chemistry , hypoxia (environmental) , microbiology and biotechnology , hypoxia inducible factors , messenger rna , hypoxia inducible factor 1 , vascular endothelial growth factor a , vegf receptors , biology , transcription factor , cancer research , oxygen , biochemistry , gene , organic chemistry
The small actin‐binding protein thymosin β4 (Tβ4) is understood to stimulate angiogenesis. Previously, we reported that Tβ4 induces angiogenesis by increasing vascular endothelial growth factor (VEGF) expression, but the mechanism underlying how Tβ4 upregulates VEGF expression remain unknown. To identify the mechanism of VEGF induction by Tβ4, we measured VEGF promoter activity and analyzed the effect of Tβ4 on VEGF RNA stability. The Tβ4 peptide had no effect on either VEGF promoter activity or VEGF RNA stability. We focused on the possibility that Tβ4 may indirectly induce VEGF expression via hypoxia‐inducible factor (HIF)‐1α. We determined that Tβ4 increased the stability of HIF‐1α protein under normoxic conditions. These data suggest that Tβ4 indirectly induces VEGF expression by increasing the protein stability of HIF‐1α in an oxygen‐independent manner.