CPNE3 interaction with RACK1 protects against myocardial ischemia/reperfusion injury

Abstract

Copine 3 (CPNE3) and receptor for activated C kinase 1 (RACK1) have been determined to be risk factors for patients with acute myocardial ischemia/reperfusion (I/R). The present study aimed to evaluate the role of CPNE3 and its interaction with RACK1 in myocardial (I/R) injury. Reverse transcription-quantitative PCR (RT-qPCR) and western blotting were performed to detect CPNE3 and RACK1 expression levels in H9c2 cells before and after the transfection of CPNE3 overexpression plasmid or small interfering RNA-RACK1. Cell viability was detected using a Cell Counting Kit-8 assay, and immunoprecipitation assays were performed to determine the interaction between CPNE3 and RACK1. A commercial kit was used to examine lactate dehydrogenase (LDH) levels. The expression levels of inflammatory cytokines were detected via RT-qPCR and western blotting. Cell apoptosis was assessed via TUNEL staining and western blotting. The results demonstrated that the expression levels of CPNE3 and RACK1 were decreased in hypoxia/reoxygenation (H/R)-induced H9c2 cardiomyocytes, which was consistent with the expression levels observed in the myocardial I/R injury rat model. It was found that CPNE3 overexpression upregulated RACK1 expression, increased cell viability and suppressed the release of LDH in H/R-induced H9c2 cells. Furthermore, CPNE3 overexpression inhibited the release of inflammatory cytokines and decreased cell apoptosis in H/R-induced cardiomyocytes by activating RACK1 expression. The present study suggested that CPNE3 served an important role in preventing I/R injury by interacting with RACK1, providing novel insight into the prevention of myocardial I/R injury, as well as the treatment and care of patients with myocardial I/R.

YAP1-CPNE3 positive feedback pathway promotes gastric cancer cell progression

“…Understanding the physiological functions of CPNE3 would be beneficial for identifying adverse reactions. CPNE3 has been reported to have the following physiological functions: it protects the heart against ischemia/reperfusion injury [ 31 ], modifies the relationship between anxiety and working memory [ 32 ], regulates insulin secretion and glucose uptake in pancreatic cells [ 33 ]; and low CPNE3 expression is associated with an increased risk of acute myocardial infarction [ 34 ]. We performed cellular assays to determine the function of CPNE3 in gastric epithelial cells after downregulation of CPNE3 expression in GES-1 cells.…”

Bioinformatics Analysis of next generation sequencing data for Risk Prediction in Patients with Type 1 diabetes mellitus

“…A previous study reported that LXN (latexin) [84], LMNA (lamin A/C) [85], PFKFB3 [86], NEU1 [87], TBK1 [88], GRN (granulin precursor) [89], CTSD (cathepsin D) [90], ACADS (acyl-CoA dehydrogenase short chain) [91], IRF7 [92], S1PR1 [93], ZAP70 [94], IDH1 [95], IL15 [96], PIK3R1 [97], OSM (oncostatin M) [98], SOCS3 [99], USP21 [100], CEP19 [101], KDM2A [102], TP53 [103], BRD2 [104], ATP6 [105], BRD4 [106], COX2 [107], RPS6 [108], ND2 [109], CYTB (cytochrome b) [110] and COX1 [111] are altered expressed in obesity. Altered expression of BCL3 [112], TRAF2 [113], NEU1 [114], SNAP29 [115], AGPAT2 [116], LPCAT3 [117], ADORA2B [118], CTSD (cathepsin D) [119], ACADS (acyl-CoA dehydrogenase short chain) [120], ACAD9 [121], E4F1 [122], IRF7 [123], TAF1 [124], S1PR1 [125], RASSF1 [126], ELAC2 [127], RNF146 [128], COX15 [129], SMYD2 [130], IDH1 [131], MTO1 [132], IL15 [133], PIK3R1 [134], ASB1 [135], OSM (oncostatin M) [136], ZNF791 [137], GBA (glucosylceramidase beta) [138], SOCS3 [139], SLC39A7 [140], AKIP1 [141], AMIGO2 [142], GLUL (glutamate-ammonia ligase) [143], SEMA4D [144], KDM2A [145], TP53 [146], JARID2 [147], CTBP1 [148], ATP6 [149], RPL7 [150], HSP90AA1 [151], BRD4 [152], PSMB4 [153], COX2 [154], JUND (JunD proto-oncogene, AP-1 transcription factor subunit) [155], RPS5 [156], RACK1 […”