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Cardiac Fibroblast Migration During In Vitro Wound Healing: The Role Of Specific Collagen Substrates
Author(s) -
Shamhart Patricia E.,
Naugle Jennifer E.,
Olson Erik R.,
Hruska Melaine A.,
Doane Kathleen J.,
Meszaros J. Gary
Publication year - 2007
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.21.6.a1428-c
Subject(s) - wound healing , fibroblast , extracellular matrix , myofibroblast , type i collagen , in vitro , chemistry , wound closure , microbiology and biotechnology , pathology , medicine , immunology , fibrosis , biochemistry , biology
Cardiac fibroblasts (CFs) control wound healing in the heart, producing extracellular matrix (ECM) proteins that include collagens I, III, and VI. In addition to ECM production, migration, proliferation, and differentiation of CFs are critical aspects of wound healing. We have previously examined CF function using in vitro collagen substrates, finding that CFs plated on collagen I and III increase in proliferation while those plated on type VI differentiate into hypersecretory myofibroblasts. The purpose of this study was to determine whether CF migration and in vitro wound healing are affected by specific collagen matrices. We performed in vitro wound healing assays (scratch assays) using CFs plated on types I, III, and VI collagen and tissue culture (TC) plastic as controls. At 6h post‐injury, wound closure was 10–20% on TC, 40–50% on I, 75–85% on III, and 5–15% on VI. At 12h, wound closure was 40–50% on TC, 80–90% on I, 95–100% on III, and 20–30% on VI. The wounds fully closed by 12h on type III collagen, by 24h on type I, after 24h on TC, however 48h were required on type VI. Overall, the preliminary data indicate that cardiac fibroblast migration and wound closure on the examined collagen matrices proceeds at different rates: type III > type I >> type VI, lending further evidence that the collagen‐specific composition of the ECM critically influences cardiac fibroblast function during wound healing.