Influence of Mechanical Forces on Lung Cells

The pulmonary alveolar epithelium is comprised of two morphologically distinct cells, type I and type II cells. Type I cells are extremely large, squamous cells that make up 95% of the alveolar surface. Type II cells are smaller cuboidal cells that secrete and recycle surfactant and cover the remaining 5% of the alveolar surface. Mechanical distention of fetal lung tissue has been shown to stimulate expression of the type I cell phenotype and inhibit expression of the type II phenotype. Lumenal mechanical stim- 

Boitano et al. (1994) reported that Ca+2-conducting channels in airway epithelial cells were opened when mechanical stimulation was applied, causing a rapid depolarization of the stimulated cell. A mechanical strain-induced increase in cAMP content has been reported in fetal rabbit type II epithelial cells after continuous high amplitude strain for 24 h. An intermittent strain of 18% resulted in an increase in cAMP production in cultured rat fetal lung cells. Strain-induced fetal lung cell growth occurs via activation of PTK and PLC. 

Airway smooth muscle cells isolated from canine tracheae and bronchi subjected to cyclic strain exhibit increased cell number and DNA synthesis in cell culture. The content of total cellular protein, especially contractile proteins including myosin, myosin light chain kinase, and desmin, was increased compared to cells cultured under static conditions. 

Stretch-induced mechanical loading also appears to effect secondary messenger activation in airway smooth muscle cells. A 20% single static stretch of rat pulmonary smooth muscle cells increases both Ca+2 influx and efflux. Mechanical strain rapidly increases tyrosine phosphorylation of ppl25FAK and paxillin in airway smooth muscle cells cultured in type I collagen matrices. Tyrosine kinase inhibitors hindered strain-induced reorientation and elongation of airway smooth muscle cells. 

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