期刊
CNS NEUROSCIENCE & THERAPEUTICS
卷 19, 期 3, 页码 145-153出版社
WILEY-BLACKWELL
DOI: 10.1111/cns.12049
关键词
Hypoxic inducible factor 1; Hypoxia; Migration; Neural progenitor cell; nuclear factor-B; Stromal cell-derived factor-1
资金
- National Natural Science Foundation of China [81101457, 81070063]
- Scientific Research Foundation for the Returned Overseas Chinese Scholars [HG3402]
Aims Stromal cell-derived factor 1 (SDF-1) is critical for neural progenitor cell (NPC) migration after ischemia for nerve repair, but how hypoxic induction of SDF-1 is regulated has not been fully addressed. Here, we examined the regulation of SDF-1 hypoxic induction by the transcription factors nuclear factor-B (NF-B) and hypoxic inducible factor 1 (HIF-1) in astrocytes. Methods and Results Stromal cell-derived factor-1 in astrocyte-conditioned medium (ACM) collected from hypoxic astrocytes induced a time- and dose-dependent increase in NPC migration using chemotaxis assay. The increase in NPC migration correlated with increased SDF-1 production in astrocytes by real-time PCR and ELISA assays. Astrocytes produced SDF-1 time-dependently upon 3% O2 treatment, which was associated with increased levels of NF-B and HIF-1 using Western blot analysis. Anti-HIF-1 compound, 3-(5-hydroxymethyl-2-furyl)-1-benzylindazole (YC-1) and NF-B inhibitor pyrrolidine dithiocarbamate (PDTC), decreased hypoxic induction of SDF-1, and PDTC pretreatment cancelled HIF-1 expression as well, thus NPC migration induced by ACM was decreased accordingly. Moreover, lentiviurs siRNA for NF-B p65 abrogated induction of HIF-1 and SDF-1 under hypoxia in astrocytes. Conclusions Hypoxic induction of SDF-1 is reliant upon NF-B and HIF-1. There is a cross-talk between HIF-1 and NF-B, both HIF-1 and SDF-1 are downstream targets of NF-B in hypoxia condition.
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