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Alpha‐smooth muscle actin expression in rat and mouse mesenteric wounds after transforming growth factor‐β1 treatment
Author(s) -
Reza Ghassemifar M.,
Schultz Gregory S.,
Tarnuzzer Roy W.,
Salerud Göran,
Franzén Lennart E.
Publication year - 1997
Publication title -
wound repair and regeneration
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.847
H-Index - 109
eISSN - 1524-475X
pISSN - 1067-1927
DOI - 10.1046/j.1524-475x.1997.50408.x
Subject(s) - actin , transforming growth factor , growth factor , biology , microbiology and biotechnology , endocrinology , medicine , anatomy , chemistry , receptor
Rat mesenteric perforations heal by contraction within 5 to 7 days, whereas mouse mesenteric perforations seldom close within 3 weeks unless stimulated by transforming growth factor‐β1. In this article, we quantified the expression of alpha‐smooth muscle actin by quantitative‐reverse transcription‐polymerase chain reaction and the orientation of actin filaments at the wound margin by Fourier transformation image analysis after treatment with transforming growth factor‐β1. The expression of transforming growth factor‐β1 and its type II receptor was also assessed. Actin filaments were shown to increase with time at the wound margin in both species and the expression of alpha‐smooth muscle actin mRNA increased simultaneously. Transforming growth factor‐β1 enhanced the alpha‐smooth muscle actin expression four to five times in rats and three to four times in mice on day 5, but the number of copies expressed per cell was 15‐fold higher in rats than in mice. Transforming growth factor‐β1 was down‐regulated after wounding in free peritoneal cells of rats, but maintained until day 5 in transforming growth factor‐β1‐treated mice. The main finding of this study was that untreated, normal rats expressed substantially more alpha‐smooth muscle actin than mice. After treatment with transforming growth factor‐β1, this expression increased similarly in both species. It can be hypothesized that normal closure of mesenteric perforations requires a minimum level of actin expression. This level is not reached in normal mice, but is exceeded after stimulation. Perforations in the rat always close, because the alpha‐smooth muscle actin expression is always above this level.