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L-Cystathionine Protects Against Homocysteine-Induced Mitochondria-Dependent Apoptosis of Vascular Endothelial Cells

Xiuli Wang, Yi Wang, Lulu Zhang, Da Zhang, Lu Bai, Wei Kong, Yaqian Huang, Chaoshu Tang, Junbao Du, Hongfang Jin

Oxid Med Cell Longev. 2019 Nov 25;2019:1253289.

PMID: 31885769

Abstract:

The study was aimed at investigating the effects of L-cystathionine on vascular endothelial cell apoptosis and its mechanisms. Cultured human umbilical vein endothelial cells (HUVECs) were used in the study. Apoptosis of vascular endothelial cells was induced by homocysteine. Apoptosis, mitochondrial superoxide anion, mitochondrial membrane potential, mitochondrial permeability transition pore (MPTP) opening, and caspase-9 and caspase-3 activities were examined. Expression of Bax, Bcl-2, and cleaved caspase-3 was tested and BTSA1, a Bax agonist, and HUVEC Bax overexpression was used in the study. Results showed that homocysteine obviously induced the apoptosis of HUVECs, and this effect was significantly attenuated by the pretreatment with L-cystathionine. Furthermore, L-cystathionine decreased the production of mitochondrial superoxide anion and the expression of Bax and restrained its translocation to mitochondria, increased mitochondrial membrane potential, inhibited mitochondrial permeability transition pore (MPTP) opening, suppressed the leakage of cytochrome c from mitochondria into the cytoplasm, and downregulated activities of caspase-9 and caspase-3. However, BTSA1, a Bax agonist, or Bax overexpression successfully abolished the inhibitory effect of L-cystathionine on Hcy-induced MPTP opening, caspase-9 and caspase-3 activation, and HUVEC apoptosis. Taken together, our results indicated that L-cystathionine could protect against homocysteine-induced mitochondria-dependent apoptosis of HUVECs.

Chemicals Related in the Paper:

Catalog Number Product Name Structure CAS Number Price
AP314761143 BTSA1 BTSA1 314761-14-3 Price
AP56882 L-Cystathionine L-Cystathionine 56-88-2 Price
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