Stimulation of the chemotactic migration of human fibroblasts by transforming growth factor beta.
Open accessAbstract
Transforming growth factor beta (TGF-beta) is a potent chemoattractant in vitro for human dermal fibroblasts. Intact disulfide and perhaps the dimeric structure of TGF-beta is essential for its ability to stimulate chemotactic migration of fibroblasts, since reduction with 2-ME results in a marked loss of its potency as a chemoattractant. Although epidermal growth factor (EGF) appears to be capable of modulating some effects of TGF-beta, it does not alter the chemotactic response of fibroblasts to TGF-beta. Specific polyvalent rabbit antibodies to homogeneously pure TGF-beta block its chemotactic activity but has no effect on the other chemoattractants tested (platelet-derived growth factor, fibronectin, and denatured type I collagen). Since TGF-beta is secreted by a variety of neoplastic and normal cells including platelets, monocytes/macrophages, and lymphocytes, it may play a critical role in vivo in embryogenesis, host response to tumors, and the repair response that follows damage to tissues by immune and nonimmune reactions.
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TGF-β/Smad signaling, in cooperation with Erk MAPK and Akt-mTOR signaling, promotes activation and myofibroblast differentiation of CAFs, similar to fibroblast differentiation upon wounding and inflammation.
“TGF-β/Smad signaling, in cooperation with Erk MAPK and Akt-mTOR signaling, promotes activation and myofibroblast differentiation of CAFs, similar to fibroblast differentiation upon wounding and inflammation228,251,252.”
From TGFβ biology in cancer progression and immunotherapy (2021) · cites this paper as [252]
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- Authors
- Postlethwaite, A. E., Keski-Oja, J., Moses, H. L., & Kang, A. H.
- Affiliations
- University of Tennessee Health Science Center (US)
- Vanderbilt University (US)
- Venue
- The Journal of experimental medicine
- Publisher
- Rockefeller University Press
- Published
- 1987-01-01
- Volume
- 165
- Issue
- 1
- Pages
- 251-256
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC2188256
- OpenAlex
- W2164094961
- Cited by
- 777
- References
- 17
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 6 · 2023: 8 · 2022: 8 · 2021: 17 · 2020: 10 · 2019: 9 · 2018: 15 · 2017: 11 · 2016: 15 · 2015: 13 · 2014: 13 · 2013: 10 · 2012: 11
- FWCI
- 15.84
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Experimental Medicine (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01am016506-13, 5r01am026034-07)
- National Cancer Institute (CA42572)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
- Keywords
- TGF-beta, chemotactic migration, dermal fibroblasts, chemoattractants, disulfide bonds, dimeric structure, 2-mercaptoethanol reduction, epidermal growth factor, antibody blocking, platelet-derived growth factor, fibronectin, type I collagen, tissue repair, host response to tumor, embryonic development
- MeSH terms
- Blood Platelets, Chemotaxis, Epidermal Growth Factor, Fibroblasts, Humans, Peptides, Transforming Growth Factors
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