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Proteolysis of mitochondrial calpain-13 in cerebral ischemia-reperfusion injury. | LitMetric

Proteolysis of mitochondrial calpain-13 in cerebral ischemia-reperfusion injury.

Biochem Biophys Rep

Laboratory of Cell Biochemistry, Department of Biological Science, Graduate School of Science and Engineering, Iwate University, Morioka, Iwate, Japan.

Published: September 2024

AI Article Synopsis

Article Abstract

Calpains are calcium-dependent cysteine proteases activated by intracellular Ca. Although calpains mainly exist in the cytosol, calpain-13 is present in the mitochondria in mouse brains; however, the enzymatic properties and physiological functions of calpain-13 remain unknown. Hence, in this study, we predicted and evaluated the enzymatic properties of calpain-13. Based on our bioinformatic approaches, calpain-13 possessed a catalytic triad and EF-hand domain, similar to calpain-1, a well-studied calpain. Therefore, we hypothesized that calpain-13 had calpain-1-like enzymatic properties; however, calpain-13 was not proteolyzed in C57BL/6J mouse brains. Subsequently, cerebral ischemia/reperfusion (I/R) injury caused proteolysis of mitochondrial calpain-13. Thus, our study showed that mitochondrial calpain-13 was proteolyzed in the mitochondria of the I/R injured mouse brain. This finding could be valuable in further research elucidating the involvement of calpain-13 in cell survival or death in brain diseases, such as cerebral infarction.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11267081PMC
http://dx.doi.org/10.1016/j.bbrep.2024.101768DOI Listing

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