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17-AAG, a Hsp90 inhibitor, attenuates the hypoxia-induced expression of SDF-1α and ILK in mouse RPE cells

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Abstract

The aim of this study was to investigate the changes of SDF-1α and ILK expression in mouse retinal pigment epithelium (RPE) cells in response to hypoxia, and the effect of 17-Allylamino-17-demethoxygeldanamycin (17-AAG), a heat shock protein 90 (Hsp90) inhibitor, on the hypoxia-induced expression of SDF-1α and ILK. RPE cells were cultured with 200 μmol/L cobalt chloride (CoCl2) for different times (1, 3, 6, 12, 24, 72 h) to imitate chemical hypoxia. Pretreatment of 17-AAG was 1 h prior to hypoxic insult. Cellular viability after 17-AAG treatment was assessed by MTT assay, and the changes of SDF-1α and ILK expression were examined by RT-PCR and Western blot. Up-regulation of SDF-1α and ILK expression in response to hypoxia was observed. One hour pretreatment of 17-AAG could remarkably decreased the hypoxia-induced SDF-1α and ILK expression in vitro. Our results indicated that SDF-1α and ILK involved in the hypoxic response of RPE cells, and 1 h pretreatment of 17-AAG had an inhibitive effect on the hypoxia-induced SDF-1α and ILK expression.

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Abbreviations

Hsp90:

Heat shock protein 90

RPE:

Retinal pigment epithelium

EPCs:

Endothelium progenitor cells

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Acknowledgments

The authors wish to thank all the participants and researchers who took participation in the study. This work was supported by department of Biopharmaceutical Sciences, College of Pharmacy, Harbin Medical University and Harbin Engineering University.

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Correspondence to Xiao Mei Zhang.

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Wang, Y.Q., Zhang, X.M., Wang, X.D. et al. 17-AAG, a Hsp90 inhibitor, attenuates the hypoxia-induced expression of SDF-1α and ILK in mouse RPE cells. Mol Biol Rep 37, 1203–1209 (2010). https://doi.org/10.1007/s11033-009-9490-x

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  • DOI: https://doi.org/10.1007/s11033-009-9490-x

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