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. 2014 May 1;20(13):1964–1976. doi: 10.1089/ars.2013.5286

FIG. 1.

FIG. 1.

Hypoxia differentially regulates β3-endonexin and HIF-1α expression. (A–C) Human microvascular endothelial cells-1 (HMEC-1) were exposed to hypoxia (1% oxygen, Hx) or normoxic conditions (0 h) for increasing time points. (A, B) Western blot analyses were performed with antibodies against HIF-1α and β3-endonexin isoforms. β-actin staining served as a loading control. Normoxic controls (0 h) were set equal to 100% (n=3, *p<0.05 vs. 0 h). (C) RT-qPCR was performed with primers amplifying human β3-endonexin and HIF-1α as well as 18S rRNA for normalization. Normoxic controls (0 h) were set equal to 1 (n=3, *p<0.05 vs. 0 h). (D) Total RNA was isolated from mice that were exposed to hypoxia (10% oxygen) for 2 weeks or from mice breathing room air (0 week). RT-qPCR was performed with primers amplifying murine β3-endonexin and 18S rRNA for normalization. Normoxic controls (0 week) were set equal to 1 (n=3, *p<0.05 vs. 0 week). HIF, hypoxia-inducible factor; PCR, polymerase chain reaction; RT-qPCR, real-time quantitative PCR.