Home General Physiology and Biophysics 2022 General Physiology and Biophysics Vol.41, No.4, p. 287–297, 2022

Journal info


Quarterly, 80 pp. per issue
Founded: 1982
ISSN  1338-4325 (online)

Published in English

Aims and Scope
Editorial Info
Abstracting and Indexing
Submission Guidelines

Select Journal







Webshop Cart

Your Cart is currently empty.

General Physiology and Biophysics Vol.41, No.4, p. 287–297, 2022

Title: S100 calcium-binding protein A12 knockdown ameliorates hypoxia-reoxygenation-induced inflammation and apoptosis in human cardiomyocytes by regulating caspase-4-mediated non-classical pyroptosis
Author: Qiming Li, Gang Deng, Yuzhang Gao
Abstract: Ischemic heart disease, especially myocardial infarction, poses a serious risk to human health. S100 calcium-binding protein A12 (S100A12) expression was previously reported to be upregulated in ST-segment elevation myocardial infarction. Therefore, the present study investigated the role of S100A12 in hypoxia/reoxygenation (H/R)-induced cardiomyocytes injury and the associated mechanism. An in vitro H/R-induced cardiomyocyte injury model was first established using AC16 cells. The expression level was found to be hugely upregulated in H/R-induced AC16 cells. Subsequently, cell transfection was conducted to knock down the expression level of S100A12, and the following cellular biological assays revealed that S100A12 knockdown could not only inhibit H/R-induced AC16 cell injury by improving cell viability and decreasing the release of lactate dehydrogenase, as well as reducing apoptotic cells, but also reduce the production of inflammatory cytokines (TNF-α, IL-1β and IL-6), restore the balance of oxidation-antioxidant factors (malondialdehyde, superoxide dismutase and glutathione), and inhibit the activated pyroptosis upon H/R induction. Then, co-immunoprecipitation was used to verify the interaction between S100A12 and caspase-4 (CASP4). CASP4 overexpression reversed the inhibitory effects of S100A12 downregulation on H/R-induced cardiomyocyte injury. In conclusion, these results suggest that S100A12 knockdown can ameliorate H/R-induced cardiomyocyte injury by regulating CASP4 expression. Therefore, S100A12 serves as a potential therapeutic target for the treatment of myocardial ischemia/reperfusion injury.
Keywords: S100 calcium-binding protein A12 — Caspase-4 — Cardiomyocyte — Inflammatory — Pyroptosis
Published online: 28-Jul-2022
Year: 2022, Volume: 41, Issue: 4 Page From: 287, Page To: 297
doi:10.4149/gpb_2022018


download file


© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.