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Regulation of Gap Junction Proteins by Alveolar Epithelial Cells in Response to Injury*

V. Abraham, PhD; K. DeBolt, MS; R. Savani, MD; Michael Koval, PhD
Author and Funding Information

*From the Institute for Environmental Medicine (Drs. Abraham, DeBolt, and Koval), Departments of Pediatrics (Dr. Savani) and Physiology (Dr. Koval), University of Pennsylvania School of Medicine, Philadelphia, PA.

Correspondence to: Michael Koval, PhD, University of Pennsylvania Medical Center, 1 John Morgan Bldg/6068, 3620 Hamilton Walk, Philadelphia, PA 19104



Chest. 1999;116(suppl_1):35S. doi:10.1378/chest.116.suppl_1.35S
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Extract

Gap junction proteins (connexins) form channels that allow flow of aqueous cytoplasmic small molecules between neighboring cells. To examine phenotypic differences in gap junction expression, primary rat type II alveolar epithelial cells were cultured either in minimum essential medium (MEM) + 10% fetal bovine serum or on Madin-Darby canine kidney-derived extracellular matrix in MEM + 2% fetal bovine serum + 5 ng/mL keratinocyte growth factor (KGF). Type II cells grown in KGF retained surfactant protein C (SP-C) expression, while cells cultured in MEM showed little, if any, SP-C production. By reverse transcriptase-polymerase chain reaction analysis, type II cells cultured in MEM showed increasing expression of Cx43 and Cx46 messenger RNA and decreasing expression of Cx26, Cx32, and Cx37. In contrast, cells cultured in KGF retained expression of Cx26 and Cx32. By immunofluorescence microscopy, type II cells cultured for 4 days in MEM had Cx43 and Cx46 present at the cell surface. Cx32 and Cx43 were present in the plasma membrane of type II cells cultured in KGF; however, Cx46 was retained in an intracellular compartment, most likely corresponding to the trans Golgi network.


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