IMR Press / FBL / Volume 5 / Issue 3 / DOI: 10.2741/page

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Mitogen-activated signaling and cell cycle regulation in airway smooth muscle
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1 Department of Pediatrics, University of Chicago Children's Hospital, 5841 S. Maryland Avenue, MC 4064, Chicago, IL 60637-1470, USA
Academic Editor:Richard Pestell
Front. Biosci. (Landmark Ed) 2000, 5(3), 258–267;
Published: 1 February 2000
(This article belongs to the Special Issue Cell cycle dysregulation in disease)

Increased airway smooth muscle mass has been demonstrated in patients with bronchopulmonary dysplasia and asthma. These data highlight the need for a precise understanding of the events involved in airway smooth muscle mitogenesis. To that end, investigators have developed cell culture systems adopting tracheal and bronchial myocytes from different species. A growing body of literature suggests that common signal transduction pathways regulate airway smooth muscle cell cycle entry across species lines. This review summarizes what is known about mitogen-activated signal transduction in airway smooth muscle cells. The extracellular signal regulated kinase (ERK) and phosphatidylinositol 3-kinase (PI 3-kinase) pathways appear to be major positive regulators of airway smooth muscle proliferation. It is also conceivable that growth factor stimulation of airway smooth muscle simultaneously elicits signaling through negative regulatory pathways such as the p38 mitogen-activated protein (MAP) kinase pathway, perhaps as a safeguard against excessive growth.

Cyclin D1
Extracellular Signal Regulated Kinase
P38 Mitogen-Activated Protein Kinase
Phosphatidylinositol 3-Kinase
Platelet-Derived Growth Factor
Signal Transduction
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