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Changes in the expression of smooth muscle contractile proteins in TNBS- and DSS-induced colitis in mice
Reem Alkahtani1, Sunila Mahavadi, Othman Al-Shboul
1Department of Physiology, VCU Program in Enteric Neuromuscular Sciences, Virginia Commonwealth University, Richmond, VA, 23298-0551, USA.
Abstract:
Thin filament-associated proteins such as calponin, caldesmon, tropomyosin, and smoothelin are thought to regulate acto-myosin interaction and thus, muscle contraction. However, the effect of inflammation on the expression of thin filament-associated proteins is not known. The aim of the present study is to determine the changes in the expression of calponin, caldesmon, tropomyosin, and smoothelin in colonic smooth muscle from trinitrobenzene sulphonic acid (TNBS)- and dextran sodium sulphate (DSS)-induced colitis in mice. Expression of h-caldesmon, h2-calponin, α-tropomyosin, and smoothelin-A was measured by qRT-PCR and Western blot. Contraction in response to acetylcholine in dispersed muscle cells was measured by scanning micrometry. mRNA and protein expression of α-actin, h2-calponin, h-caldesmon, smoothelin, and α-tropomyosin in colonic muscle strips from mice with TNBS- or DSS-induced colitis was significantly increased compared to control animals. Contraction in response to acetylcholine was significantly decreased in muscle cells isolated from inflamed regions of TNBS- or DSS-treated mice compared to control mice. Our results show that increase in the expression of thin filament-associated contractile proteins, which inhibit acto-myosin interaction, could contribute to decrease in smooth muscle contraction in inflammation.
Insights
Inflammation increases thin filament proteins in the colon, which may inhibit muscle contraction. This study investigated these changes in mouse models of colitis.
Area of Science:
- Gastroenterology
- Muscle Physiology
- Inflammation Research
Background:
- Thin filament-associated proteins regulate muscle contraction by modulating acto-myosin interactions.
- The impact of inflammation on these proteins in colonic smooth muscle remains unclear.
Purpose of the Study:
- To investigate the expression of calponin, caldesmon, tropomyosin, and smoothelin in colonic smooth muscle during inflammation.
- To determine the functional consequences of these changes on muscle contraction.
Main Methods:
- Induction of colitis in mice using trinitrobenzene sulphonic acid (TNBS) and dextran sodium sulphate (DSS).
- Quantification of gene and protein expression using qRT-PCR and Western blot.
- Measurement of muscle cell contraction via scanning micrometry.
Main Results:
- Significant upregulation of mRNA and protein for α-actin, h2-calponin, h-caldesmon, smoothelin, and α-tropomyosin in inflamed colonic muscle.
- Reduced contractile response to acetylcholine in muscle cells from inflamed colonic regions.
Conclusions:
- Increased expression of inhibitory thin filament proteins in colonic smooth muscle during inflammation.
- This upregulation may contribute to the observed decrease in smooth muscle contractility during colitis.
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