Researchers at Iwate University Zero in on Neurodegenerative Diseases and Conditions (Calpain-1 C2L domain peptide protects mouse hippocampus-derived neuronal HT22 cells against glutamate-induced oxytosis)

摘要

2021 SEP 07 (NewsRx) - By a News Reporter-Staff News Editor at Disease Prevention Daily - Research findings on neurodegenerative diseases and conditions are discussed in a new report. According to news reporting from Iwate, Japan, by NewsRx journalists, research stated, "Calpains are Ca2+-dependent cysteine proteases; their aberrant activation is associated with several neurodegenerative diseases. The m-calpain catalytic subunit, calpain-1, is located in the cytoplasm as well as in the mitochondria." Our news correspondents obtained a quote from the research from Iwate University: "Mitochondrial calpain-1 cleaves apoptosis-inducing factor (AIF), leading to apoptotic cell death. We have previously reported that short peptides of calpain-1 C2-like domain conjugated with cell penetrating peptide HIV-Tat (Tat-mCL) selectively inhibit mitochondrial calpain-1 and effectively prevent neurodegenerative diseases of the eye. In this study, we determined whether mitochondrial calpain-1 mediates oxytosis (oxidative glu-tamate toxicity) in hippocampal HT22 cells using Tat-mCL and newly generated polyhistidine-conjugated mCL peptide and compared their efficacies in preventing oxytosis. TUNEL assay and single strand DNA staining revealed that both mCL peptides inhibited glutamate-induced oxytosis. Additionally, both the peptides suppressed the mitochondrial AIF translocation into the nucleus. All polyhistidine-mCL peptides (containing 4-16 histidine residues) showed higher cell permeability than Tat-mCL."