The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Platelet-derived growth factor and transforming growth factor-beta enhance tissue repair activities by unique mechanisms.
Open accessAbstract
Platelet-derived growth factor (PDGF) and transforming growth factor-beta (TGF-beta) markedly potentiate tissue repair in vivo. In the present experiments, both in vitro and in vivo responses to PDGF and TGF-beta were tested to identify mechanisms whereby these growth factors might each enhance the wound-healing response. Recombinant human PDGF B-chain homodimers (PDGF-BB) and TGF-beta 1 had identical dose-response curves in chemotactic assays with monocytes and fibroblasts as the natural proteins from platelets. Single applications of PDGF-BB (2 micrograms, 80 pmol) and TGF-beta 1 (20 micrograms, 600 pmol) were next applied to linear incisions in rats and each enhanced the strength required to disrupt the wounds at 5 d up to 212% of paired control wounds. Histological analysis of treated wounds demonstrated an in vivo chemotactic response of macrophages and fibroblasts to both PDGF-BB and to TGF-beta 1 but the response to TGF-beta 1 was significantly less than that observed with PDGF-BB. Marked increases of procollagen type I were observed by immunohistochemical staining in fibroblasts in treated wounds during the first week. The augmented breaking strength of TGF-beta 1 was not observed 2 and 3 wk after wounding. However, the positive influence of PDGF-BB on wound breaking strength persisted through the 7 wk of testing. Furthermore, PDGF-BB-treated wounds had persistently increased numbers of fibroblasts and granulation tissue through day 21, whereas the enhanced cellular influx in TGF-beta 1-treated wounds was not detectable beyond day 7. Wound macrophages and fibroblasts from PDGF-BB-treated wounds contained sharply increased levels of immunohistochemically detectable intracellular TGF-beta. Furthermore, PDGF-BB in vitro induced a marked, time-dependent stimulation of TGF-beta mRNA levels in cultured normal rat kidney fibroblasts. The results suggest that TGF-beta transiently attracts fibroblasts into the wound and may stimulate collagen synthesis directly. In contrast, PDGF is a more potent chemoattractant for wound macrophages and fibroblasts and may stimulate these cells to express endogenous growth factors, including TGF-beta, which, in turn, directly stimulate new collagen synthesis and sustained enhancement of wound healing over a more prolonged period of time.
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Cites
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Cited by
Transforming Growth Factor‐β: Major Role in Regulation of Extracellular Matrix
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The molecular biology of chronic wounds and delayed healing in diabetes
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Estrogen accelerates cutaneous wound healing associated with an increase in TGF-β1 levels
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Self-citationBasics of Cutaneous Wound Repair
CLARK, R. A. F. (1993) · The Journal of Dermatologic Surgery and Oncology · doi:10.1111/j.1524-4725.1993.tb00413.x · Cited by 210
Delayed Wound Healing in the Absence of Intercellular Adhesion Molecule-1 or L-Selectin Expression
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Effect of Growth Factors on the Proliferation of Ligament Fibroblasts from Skeletally Mature Rabbits
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Growth factor and procollagen type I gene expression in human liver disease
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The Contrasting Role of Extracellular Vesicles in Vascular Inflammation and Tissue Repair
Oggero, S., Austin-Williams, S., & Norling, L. V. (2019) · Frontiers in Pharmacology · doi:10.3389/fphar.2019.01479 · Cited by 85
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Metadata
- Authors
- Pierce, G. F., Mustoe, T. A., Lingelbach, J., Masakowski, V. R., Griffin, G. L., Senior, R. M., & Deuel, T. F.
- Venue
- The Journal of cell biology
- Publisher
- Rockefeller University Press
- Published
- 1989-07-01
- Volume
- 109
- Issue
- 1
- Pages
- 429-440
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- OpenAlex
- W2154636701
- Cited by
- 598
- References
- 4
- FWCI
- 35.46
- Type
- journal article
- Language
- en
- Open access
- green
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