Tissue Expression of Atrial and Ventricular Myosin Light Chains in the Mechanism of Adaptation to Oxidative Stress.

Publisher: MDPI Country of Publication: Switzerland NLM ID: 101092791 Publication Model: Electronic Cited Medium: Internet ISSN: 1422-0067 (Electronic) Linking ISSN: 14220067 NLM ISO Abbreviation: Int J Mol Sci Subsets: MEDLINE

Original Publication: Basel, Switzerland : MDPI, [2000-

Adaptation, Physiological/*physiology ; Heart Atria/*metabolism ; Heart Ventricles/*metabolism ; Myosin Light Chains/*metabolism ; Oxidative Stress/*physiology; Animals ; DNA Helicases/metabolism ; Gene Expression/physiology ; Heart Ventricles/pathology ; L-Lactate Dehydrogenase/metabolism ; Male ; Matrix Metalloproteinase 2/metabolism ; Myocardial Reperfusion Injury/metabolism ; Myocardial Reperfusion Injury/pathology ; Myocardium/metabolism ; Oxygen/metabolism ; Rats ; Rats, Wistar ; Reactive Nitrogen Species/metabolism ; Reactive Oxygen Species/metabolism

Ischemia/reperfusion (I/R) injury induces post-translational modifications of myosin light chains (MLCs), increasing their susceptibility to degradation by matrix metalloproteinase 2 (MMP-2). This results in the degradation of ventricular light chains (VLC1) in heart ventricles. The aim of the study was to investigate changes in MLCs content in the mechanism of adaptation to oxidative stress during I/R. Rat hearts, perfused using the Langendorff method, were subjected to I/R. The control group was maintained in oxygen conditions. Lactate dehydrogenase (LDH) activity and reactive oxygen/nitrogen species (ROS/RNS) content were measured in coronary effluents. Atrial light chains (ALC1) and ventricular light chains (VLC1) gene expression were examined using RQ-PCR. ALC1 and VLC1 protein content were measured using ELISA tests. MMP-2 activity was assessed by zymography. LDH activity as well as ROS/RNS content in coronary effluents was higher in the I/R group ( p = 0.01, p = 0.04, respectively), confirming heart injury due to increased oxidative stress. MMP-2 activity in heart homogenates was also higher in the I/R group ( p = 0.04). ALC1 gene expression and protein synthesis were significantly increased in I/R ventricles ( p < 0.01, 0.04, respectively). VLC1 content in coronary effluents was increased in the I/R group ( p = 0.02), confirming the increased degradation of VLC1 by MMP-2 and probably an adaptive production of ALC1 during I/R. This mechanism of adaptation to oxidative stress led to improved heart mechanical function.

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UMO-2016/23/B/NZ3/03151 National Science Centre

Keywords: ALC1; VLC1; adaptation; heart mechanical function; injury; ischemia; reperfusion

0 (Myosin Light Chains)
0 (Reactive Nitrogen Species)
0 (Reactive Oxygen Species)
EC 1.1.1.27 (L-Lactate Dehydrogenase)
EC 3.4.24.24 (Matrix Metalloproteinase 2)
EC 3.6.4.- (DNA Helicases)
S88TT14065 (Oxygen)

Date Created: 20201113 Date Completed: 20210302 Latest Revision: 20210302

20240829

PMC7664899

10.3390/ijms21218384

33182231