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Contractile function of fibroblast fiber in activation with calf serum and thromboxane A2
Author(s) -
Hiromi Nobe,
Nobe Koji,
Paul Richard J,
Honda Kazuo,
Ishida Yukisato
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.816.7
Subject(s) - contraction (grammar) , fibroblast , chemistry , thromboxane a2 , calcium , calcium in biology , contractility , thromboxane , connective tissue , endocrinology , medicine , microbiology and biotechnology , biochemistry , biology , receptor , platelet , pathology , in vitro
Wound repair processes involve epithelialization, connective tissue deposition and contraction. Contraction is one of the important steps, inasmuch as it draws the margins of open wounds together. We used fibroblast fibers reconstituted in a three‐dimensional collagen matrix with NIH 3T3 fibroblast cells characterize nonmuscle contractility and calcium signaling. Calf serum (CS:3~30%) and thromboxane A 2 (TXA 2 :1~1000nM) elicited dose‐dependent increases in isometric force with the similar time courses. The maximal force to TXA 2 was 65% of that to CS. CS‐induced contraction was dependent on an intracellular calcium stores. While, the TXA 2 response depended on both calcium release from intracellular stores and calcium influx from the extracellular medium. The Rho kinase inhibitor suppressed TXA 2 ‐ and CS‐induced responses. In contrast, inhibition of protein kinase C only reduced the TXA 2 response. Moreover, addition of TXA 2 during the CS contracture further enhanced force and calcium signal. TXA 2 ‐induced responses are not differential mechanism in the CS‐induced contraction. We considering the healing process, TXA 2 functions not only as a blood coagulation factor at the initial stage of wound repair but also as a contractile factor for fibroblasts in the later repair processes.