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Contraction band necrosis and dephosphorylated cardiac connexin 43 in rat myocardium after 14 days cocaine administration

ABSTRACT: Contraction band necrosis and dephosphorylated cardiac connexin 43 in rat myocardium after 14 days cocaine administration

PROVIDER: PRJNA823029 | ENA |

REPOSITORIES: ENA

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Contraction band necrosis and dephosphorylated cardiac connexin 43 in rat myocardium after 14 days cocaine administration

Project description:To obtain insight of the changes of myocardium after repeated cocaine administration, we performed transcriptiome analysis. Total RNAs from the control and cocaine groups (day 14) were subjected to DNA microarray analysis.

2022-04-07 | GSE200127 | GEO

Contraction Band Necrosis with Dephosphorylated Connexin 43 in Rat Myocardium after Daily Cocaine Administration.

Project description:Contraction band necrosis (CBN) is a common abnormality found in the myocardium of cocaine abusers, but is rarely reported in experimental models of cocaine abuse. Connexin 43 (Cx43) is essential for cardiac intercellular communication and the propagation of CBN. Under stress or injury, cardiac Cx43 is dephosphorylated, which is related to cardiomyocyte dysfunction and pathogenesis, whereas adiponectin exerts beneficial effects in the myocardium. In this study, we explore the effects of cocaine on cardiac Cx43 in vivo. Rats were administered cocaine via the tail vein at 20 mg/kg/day for 14 days, and showed widespread CBN, microfocal myocarditis and myocardial fibrosis, corresponding to a dysfunction of cardiac mitochondria under increased oxidative stress. The increase in dephosphorylated cardiac Cx43 and its negative correlation with the myocardial distribution of CBN after cocaine administration were determined. In addition, apoptosis and necroptosis, as well as increased adiponectin levels, were observed in the myocardium after cocaine exposure. Accordingly, we found altered profiles of cardiac Cx43, CBN and its negative correlation with dephosphorylated cardiac Cx43, and the possible involvement of adiponectin in the myocardium after 14 days of cocaine administration. The latter might play a protective role in the cardiotoxicity of cocaine. The current findings would be beneficial for establishing novel therapeutic strategies in cocaine-induced cardiac consequences.

| S-EPMC9570416 | biostudies-literature

Sustained splenic contraction after daily cocaine administration in rats

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Alpha kinase 3 signaling at the M-band maintains sarcomere integrity and proteostasis in striated muscle

Project description:Muscle contraction is driven by the molecular machinery of the sarcomere. While the constituent components of the sarcomere are well characterized, it is less clear how the activity and turnover of sarcomeric proteins is regulated. In particular, phosphorylation is critical regulator of muscle function. Thus, identification of regulatory kinases is key to understanding the sarcomere function. Pathogenic variants in alpha kinase 3 (ALPK3) cause cardiomyopathy and musculoskeletal disease, but little is known about this atypical kinase. Here we show that ALPK3 localizes to the M-Band of the sarcomere and define the ALPK3-dependent phosphoproteome. ALPK3 deficiency disrupted sarcomeric organization and calcium kinetics in hPSC-derived cardiomyocytes and reduced force generation in cardiac organoids. Phosphoproteomic profiling identified ALPK3-dependant phospho-peptides that were enriched for sarcomeric components of the M-band and the ubiquitin-binding protein SQSTM1. Analysis of the ALPK3 interactome confirmed binding to M-band proteins including SQSTM1. Importantly, in hPSC-derived cardiomyocytes modeling ALPK3 deficiency and cardiomyopathic ALPK3 mutations, sarcomeric organization and M-band localization of SQSTM1 were abnormal. These data suggest ALPK3 has an integral role in maintaining sarcomere integrity and proteostasis in striated muscle. We propose this mechanism may underly disease pathogenesis in patients with ALPK3 variants.

2023-01-10 | GSE215304 | GEO

Transcriptomic modulation by adenosine 2A receptors in normal and endotoxemic myocardium

Project description:Analysis of venticular myocardium from adenosine 2A receptors (A2AR) knockouts following LPS stimulation. Results provide insight into the molecular components of A2AR mediated protection, but also reveal pathogenetic components of endotoxemic myocarditis as a result of LPS exposure. These findings demonstrate that intrinsic A2AR activity exerts limited transcriptional effects in unstressed heart, modifying G-coupled cAMP/PKA signal paths. LPS-dependent injury and dysfunction is associated with profound up-regulation of inflammatory/immune processes, fibrotic and cell death paths, and NF-kB, Erk/MAPK and JAK/Stat signaling, with shifts in multiple determinants of cardiac contraction and survival. Intrinsic A2AR activity modulates key aspects of these inflammatory responses, involving MAPK, JAK/Stat and NF-kB signaling Total RNA obtained from adenosine 2A receptor knockout or wild-type murine ventricular myocardium that were treated for 24 hours with either saline or lipopolysaccharide (n=4/group).

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Transcription profiling of mouse with ablation of connexin 30 in the stria vascularis

Project description:Effect of the ablation of connexin 30 in the stria vascularis

2007-04-16 | E-MEXP-558 | biostudies-arrayexpress

Mapping the anti-cancer activity of α-connexin carboxyl-terminal (aCT1) peptide in resistant HER2+ breast cancer

Project description: This study aims to examine the mechanisms for the anti-cancer effects of a therapeutic peptide agent targeted to connexin 43 (Cx43) called alpha-connexin carboxyl-terminal peptide (aCT1). Findings from this study identify the effect of aCT1 on breast cancer signaling using a resistant HER2+ breast cancer cell line.

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Co-IP (AP-MS) of Connexin-43 - Gap junction protein Connexin-43 is a direct transcriptional regulator of N-cadherin in vivo

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25 kDa band from HSPA1A immunoprecipitation

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2022-08-25 | PXD036266 | Pride

Osteocyte Connexin 43 Hemichannels Influence Bone Marrow Mesenchymal Stromal Cell Fate through Prostagladin E2

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2024-12-16 | GSE252059 | GEO

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