G12/13 Signaling in Asthma

Authors

Elizabeth L. McDuffie, Thomas Jefferson UniversityFollow
Reynold A Panettieri
Charles P. Scott, Thomas Jefferson UniversityFollow

Document Type

Article

Publication Date

8-2-2024

Comments

Correction Issued and Article Updated on October 14th, 2024.

This article is the author's final published version in Respiratory Research, Volume 25, Issue 1, August 2024, Article number 295.

The published version is available at https://doi.org/10.1186/s12931-024-02920-0.

Copyright © 2024 The Authors.

Abstract

Shortening of airway smooth muscle and bronchoconstriction are pathognomonic for asthma. Airway shortening occurs through calcium-dependent activation of myosin light chain kinase, and RhoA-dependent calcium sensitization, which inhibits myosin light chain phosphatase. The mechanism through which pro-contractile stimuli activate calcium sensitization is poorly understood. Our review of the literature suggests that pro-contractile G protein coupled receptors likely signal through G12/13 to activate RhoA and mediate calcium sensitization. This hypothesis is consistent with the effects of pro-contractile agonists on RhoA and Rho kinase activation, actin polymerization and myosin light chain phosphorylation. Recognizing the likely role of G12/13 signaling in the pathophysiology of asthma rationalizes the effects of pro-contractile stimuli on airway hyperresponsiveness, immune activation and airway remodeling, and suggests new approaches for asthma treatment.

Recommended Citation

McDuffie, Elizabeth L.; Panettieri, Reynold A; and Scott, Charles P., "G12/13 Signaling in Asthma" (2024). Department of Biochemistry and Molecular Biology Faculty Papers. Paper 262.
https://jdc.jefferson.edu/bmpfp/262

Creative Commons License

This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.

PubMed ID

39095798

Language

English