Proliferative and Synthetic Responses of Airway Smooth Muscle in Asthma.
- Author:
Jung Yeon SHIM
1
Author Information
1. Department of Pediatrics, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea. jy7.shim@samsung.com
- Publication Type:Review
- Keywords:
Airway smooth muscle;
Asthma;
Extracellular matrix;
Proliferation;
Remodeling
- MeSH:
Apoptosis;
Asthma*;
Cell Adhesion;
Cell Movement;
Cell Proliferation;
Chemokines;
Cytokines;
Extracellular Matrix;
Extracellular Matrix Proteins;
Intercellular Signaling Peptides and Proteins;
Mitogens;
Muscle, Smooth*;
p21-Activated Kinases;
Phosphotransferases;
Protein Kinases;
Receptors, Adrenergic;
Receptors, Glucocorticoid
- From:Korean Journal of Pediatrics
2005;48(6):580-587
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
New evidence is emerging that airway smooth muscle (ASM) may act as an immunomodulatory cell by providing pro-inflammatory cytokines and chemokines, polypeptide growth factors, extracellular matrix proteins, cell adhesion receptors and co-stimulatory molecules. ASM can promote the formation of the interstitial extracellular matrix, and potentially contribute to the alterations within the extracellular matrix in asthma. In addition, extracellular matrix components can alter the proliferative, survival, and cytoskeletal synthetic function of ASM cells through integrin-directed signaling. Increased ASM mass is one of the most important features of the airway wall remodeling process in asthma. Three different mechanisms may contribute to the increased ASM mass: cell proliferation, increased migration and decreased rate of apoptosis. The major signaling pathways of cell proliferation activated by ASM mitogens are those dependent on extracellular signal-regulated kinase and phosphoinositide 3'-kinase. The key signaling mechanisms of cell migration have been identified as the p38 mitogen-activated protein kinase and the p21-activated kinase 1 pathways. ASM cells contain beta2-adrenergic receptors and glucocorticoid receptors. They may represent a key target for beta2- adrenergic receptor agonist/corticosteroid interactions which have antiproliferative activity against a broad spectrum of mitogens.
