Increased expression of desmin and vimentin reduces bladder smooth muscle contractility via JNK2.
Publication/Presentation Date
2-1-2020
Abstract
Bladder dysfunction is associated with the overexpression of the intermediate filament (IF) proteins desmin and vimentin in obstructed bladder smooth muscle (BSM). However, the mechanisms by which these proteins contribute to BSM dysfunction are not known. Previous studies have shown that desmin and vimentin directly participate in signal transduction. In this study, we hypothesized that BSM dysfunction associated with overexpression of desmin or vimentin is mediated via c-Jun N-terminal kinase (JNK). We employed a model of murine BSM tissue in which increased expression of desmin or vimentin was induced by adenoviral transduction to examine the sufficiency of increased IF protein expression to reduce BSM contraction. Murine BSM strips overexpressing desmin or vimentin generated less force in response to KCl and carbachol relative to the levels in control murine BSM strips, an effect associated with increased JNK2 phosphorylation and reduced myosin light chain (MLC
Volume
34
Issue
2
First Page
2126
Last Page
2146
ISSN
1530-6860
Published In/Presented At
Javed, E., Thangavel, C., Frara, N., Singh, J., Mohanty, I., Hypolite, J., Birbe, R., Braverman, A. S., Den, R. B., Rattan, S., Zderic, S. A., Deshpande, D. A., Penn, R. B., Ruggieri, M. R., Sr, Chacko, S., & Boopathi, E. (2020). Increased expression of desmin and vimentin reduces bladder smooth muscle contractility via JNK2. FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 34(2), 2126–2146. https://doi.org/10.1096/fj.201901301R
Disciplines
Business Administration, Management, and Operations | Health and Medical Administration | Management Sciences and Quantitative Methods
PubMedID
31909533
Department(s)
Administration and Leadership
Document Type
Article