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Updated: Aug 6, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
Published on: June 3, 2018
Specific receptor subtype mediation of LPA-induced dual effects in cardiac fibroblasts
Jinghai Chen1, Yu Han, Weiquan Zhu
1Research Center for Cardiovascular Regenerative Medicine, Cardiovascular Institute and Fu Wai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China.
Abstract:
Lysophosphatidic acid (LPA) is a phospholipid messenger with diverse effects mediated via receptors LPA1, LPA2 and LPA3. Our previous study revealed that serum LPA level is elevated after myocardial infarction (MI). However, very little is known about the effects of LPA on cardiac fibroblasts (CFs) that play a crucial role in left ventricular remodeling after MI. Here we demonstrated that LPA dose-dependently induced proliferation and collagen synthesis with the maximum stimulation at 10 microM that was preferentially mediated by LPA3. LPA also dose-dependently induced apoptotic cell death, as estimated by MTT assay, hoechst staining, TUNEL and flow cytometric analysis, with an IC(50) of 50 microM. Moreover, apoptotic cell death may involve mitochondrial dysfunction and activation of caspase-3. Apoptosis induced by LPA might be mediated by LPA1. These data suggest that LPA exerts dual proliferative and proapoptotic actions mediated by specific LPA receptor subtypes.
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