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Taurine prevents high glucose-induced angiopoietin-2/tie-2 system alterations and apoptosis in retinal microvascular pericytes - PubMed

. 2014 Nov;396(1-2):239-48.

doi: 10.1007/s11010-014-2159-3. Epub 2014 Jul 25.

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Taurine prevents high glucose-induced angiopoietin-2/tie-2 system alterations and apoptosis in retinal microvascular pericytes

Kaihong Zeng et al. Mol Cell Biochem. 2014 Nov.

Abstract

Previously, we confirmed that taurine prevented diabetes-induced apoptosis in retinal glial cells via its anti-oxidation and anti-glutamate excitotoxicity mechanisms. The aim of this study is to investigate the effects of taurine on angiopoietin-2 (Ang-2)/Tie-2 system expressions and apoptosis in high glucose-treated retinal microvascular pericytes (RMPs). Also, the possible mechanism involved in the inhibition of taurine on RMPs apoptosis is investigated. The expressions of Ang-2, Tie-2 were detected by qRT-PCR and ELISA. The level of phosphorylated Tie-2 (P-Tie-2) was examined by ELISA. Hoechst 33342 and Annexin V/PI staining were used to detect RMPs apoptosis. The activity of caspase-3 was detected by assay kit. In 25 mM high glucose group, the expression of Ang-2 was increased significantly, taurine down-regulated Ang-2 in a dose (0.1, 1, and 10 mM)-dependent manner (P < 0.05). The Tie-2 expression and P-Tie-2 level were decreased in high glucose group (P < 0.05). Interestingly, taurine at 1 and 10 mM showed significant increase in Tie-2 expression and P-Tie-2 level (P < 0.05). The number of apoptotic RMPs and the activity of caspase-3 increased in the presence of high glucose (P < 0.05). Treatment with taurine at 1 mM decreased the number of apoptotic RMPs and the activity of caspase-3 (P < 0.05). Blocking antibody and small interfering RNA (siRNA) treatment showed that taurine required Tie-2 to perform its anti-apoptotic effect. Taken together, our data suggest that high glucose-induced Ang-2/Tie-2 system expressions alteration can be reversed by taurine, and that taurine can inhibit high glucose-induced RMPs apoptosis via Tie-2.

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