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  • Sphingosylphosphorylcholine alleviates hypoxia-caused apoptosis in cardiac myofibroblasts via CaM/p38/STAT3 pathway.

Sphingosylphosphorylcholine alleviates hypoxia-caused apoptosis in cardiac myofibroblasts via CaM/p38/STAT3 pathway.

Apoptosis : an international journal on programmed cell death (2020-10-18)
Ying Li, Qi Qi, Wan-Cheng Yang, Tian-Liang Zhang, Chen-Chen Lu, Yu-Juan Yao, Wei-Hua Kong, Jing Zhao
ABSTRACT

Blockade of hypoxia-caused nonmyocytes apoptosis helps improve survival and mitigate ventricular remodeling and dysfunction during the chronic stage of myocardial infarction. But tools affecting nonmyocyte apoptosis are very rare. Sphingosylphosphorylcholine (SPC), a naturally occurring bioactive sphingolipid in plasma, was proved to protect cardiomyocyte against apoptosis in an ischemic model in our previous study. Here, we showed that SPC also inhibited hypoxia-induced apoptosis in myofibroblasts, an important type of nonmyocytes in the heart. Calmodulin (CaM) is an identified receptor of SPC. We clarified that SPC inhibited myofibroblast apoptosis through CaM as evidenced by decreased cleaved caspase 3, PARP1 and condensed nucleus. Furthermore, the employment of inhibitor and agonist of p38 and STAT3 suggests that SPC inhibits myofibroblast apoptosis by regulating the phosphorylation of p38 and STAT3, and they act as downstream of CaM. The present work may provide new evidence on the regulation of myofibroblasts apoptosis by SPC and a novel target for heart remodeling after hypoxia.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
3-Methyladenine, autophagy inhibitor
Sigma-Aldrich
Sphingosylphosphorylcholine, ≥98%, powder
Supelco
Stainless Steel HPLC Fittings, ferrule, 1/8 in. tubing
Sigma-Aldrich
Hoechst 33258 solution, 1 mg/mL in H2O, ≥98.0% (HPLC)