Under inflammatory conditions after burn/trauma injuries, circulating neutrophils are frequently hyperactive, contributing to excessive superoxide production and related tissue damage. Although normal neutrophil activation is cooperatively controlled by Ca(2+)-independent and Ca(2+)-linked signaling pathways, exuberant Ca(2+)-linked signaling appears to cause neutrophil hyperactivation in the injury conditions.
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Constitutive deletion of the obscurin-Ig58/59 domains induces atrial remodeling and Ca2+-based arrhythmogenesis.
JCI Insight
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Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, United States of America.
Obscurin is a giant protein that coordinates diverse aspects of striated muscle physiology. Obscurin immunoglobulin domains 58/59 (Ig58/59) associate with essential sarcomeric and Ca2+ cycling proteins. To explore the pathophysiological significance of Ig58/59, we generated the Obscn-ΔIg58/59 mouse model, expressing obscurin constitutively lacking Ig58/59.
View Article and Find Full Text PDFUbiquitination-deficit of Cnot4 impairs the capacity of proliferation and differentiation in mouse embryonic stem cells.
Biochem Biophys Res Commun
February 2025
Department of Histology and Embryology, School of Basic Medical Sciences, Harbin Medical University, Harbin, 150081, China. Electronic address:
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View Article and Find Full Text PDFPiezo1 aggravates ischemia/reperfusion-induced acute kidney injury by Ca-dependent calpain/HIF-1α/Notch signaling.
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Macrophages play a vital role in the inflammation and repair processes of ischemia/reperfusion-induced acute kidney injury (IR-AKI). The mechanosensitive ion channel Piezo1 is significant in these inflammatory processes. However, the exact role of macrophage in IR-AKI is unknown.
View Article and Find Full Text PDFMechanoreceptor Piezo1 channel-mediated interleukin expression in conjunctival epithelial cells: Linking mechanical stress to ocular inflammation.
Ocul Surf
January 2025
Department of Physiology, Showa University Graduate School of Medicine, 1-5-8 Hatanodai, Shinagawa, Tokyo, 142-8555, Japan.
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