Expression of Alpha-Smooth Muscle Actin, TGF-β1 and TGF-β Type II Receptor during Connective Tissue Contraction
Closure of rat mesenteric perforation is considered to occur by connective tissue contraction, a process that has been shown to be stimulated by transforming growth factor-β1. In the present study, we assessed the expression of alpha-smooth muscle actin during closure by quantitative-reverse transcr...
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Published in | In vitro cellular & developmental biology. Animal Vol. 33; no. 8; pp. 622 - 627 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Society for In Vitro Biology
01.09.1997
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Subjects | |
Online Access | Get full text |
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Summary: | Closure of rat mesenteric perforation is considered to occur by connective tissue contraction, a process that has been shown to be stimulated by transforming growth factor-β1. In the present study, we assessed the expression of alpha-smooth muscle actin during closure by quantitative-reverse transcription-polymerase chain reaction and in situ hybridization. The expression of transforming growth factor-β1 and transforming growth factor-β type II receptor was also estimated in mesenteric membranes and free peritoneal cells after wounding. A larger expression of alpha-smooth muscle actin was seen around the wound edges compared to unwounded tissue. Both alpha-smooth muscle actin and transforming growth factor-β type II receptor were expressed during Days 0, 3, 5, 7, and 10. The expression of alpha-smooth muscle actin on Day 5 was >100 times higher than on Day 0. Transforming growth factor-β1 was expressed in both membranes and free peritoneal cells of unoperated control animals but down-regulated after wounding, a finding that has not been reported previously. It reappeared on Days 7 and 10 in free peritoneal cells but not in perforated membranes. The enhanced expression of alpha-smooth muscle actin and down-regulation of transforming growth factor-β1 expression after wounding appears to be important phenomena in tissue contraction and repair. |
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ISSN: | 1071-2690 1543-706X |
DOI: | 10.1007/s11626-997-0112-4 |