Document Type

Article

Publication Date

1-6-2017

Comments

This article has been peer reviewed. It is the author’s final published version in Journal of Smooth Muscle Research

Volume 53, Issue 1, January 2017, Pages 1-19.

The published version is available at DOI: 10.1540/jsmr.53.1. Copyright © Eto & Kitazawa.

Abstract

A hallmark of smooth muscle cells is their ability to adapt their functions to meet temporal and chronic fluctuations in their demands. These functions include force development and growth. Understanding the mechanisms underlying the functional plasticity of smooth muscles, the major constituent of organ walls, is fundamental to elucidating pathophysiological rationales of failures of organ functions. Also, the knowledge is expected to facilitate devising innovative strategies that more precisely monitor and normalize organ functions by targeting individual smooth muscles. Evidence has established a current paradigm that the myosin light chain phosphatase (MLCP) is a master regulator of smooth muscle responsiveness to stimuli. Cellular MLCP activity is negatively and positively regulated in response to G-protein activation and cAMP/cGMP production, respectively, through the MYPT1 regulatory subunit and an endogenous inhibitor protein named CPI-17. In this article we review the outcomes from two decade of research on the CPI-17 signaling and discuss emerging paradoxes in the view of signaling pathways regulating smooth muscle functions through MLCP.

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Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial 4.0 License

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