Characterization of the activation of latent TGF-beta by co-cultures of endothelial cells and pericytes or smooth muscle cells: a self-regulating system.
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The conversion of latent transforming growth factor beta (LTGF-beta) to the active species, transforming growth factor beta (TGF-beta), has been characterized in heterotypic cultures of bovine aortic endothelial (BAE) cells and bovine smooth muscle cells (SMCs). The formation of TGF-beta in co-cultures of BAE cells and SMCs was documented by a specific radioreceptor competition assay, while medium from homotypic cultures of BAE cells or SMCs contained no active TGF-beta as determined by this assay. The concentration of TGF-beta in the conditioned medium of heterotypic co-cultures was estimated to be 400-1,200 pg/ml using the inhibition of BAE cell migration as an assay. Northern blotting of poly A+ RNA extracted from both homotypic and heterotypic cultures of BAE cells and SMCs revealed that BAE cells produced both TGF-beta 1 and TGF-beta 2, while SMCs produced primarily TGF-beta 1. No change in the expression of these two forms of TGF-beta was apparent after 24 h in heterotypic cultures. Time course studies on the appearance of TGF-beta indicated that most of the active TGF-beta was generated within the first 12 h after the establishment of co-cultures. The generation of TGF-beta in co-cultures stimulated the production of the protease inhibitor plasminogen activator inhibitor-1 (PAI-1). The inclusion of neutralizing antibodies to TGF-beta in the co-culture medium blocked the observed increase in PAI-1 levels. The increased expression of PAI-1 subsequent to TGF-beta formation blocked the activation of the protease required for conversion of LTGF-beta to TGF-beta as the inclusion of neutralizing antibodies to PAI-1 in the co-culture medium resulted in prolonged production of TGF-beta. This effect was lost upon removal of the PAI-1 antibodies. Thus, the activation of LTGF-beta appears to be a self-regulating system.
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Endothelial cell-specific inactivation or repression of TGF-β signaling can suppress atherosclerosis-associated vascular inflammation by enhancing vascular integrity through reversal of EndMT.
“Conversely, endothelial cell-specific inactivation or repression of TGF-β signaling can suppress atherosclerosis-associated vascular inflammation by enhancing vascular integrity through reversal of EndMT277.”
From TGFβ biology in cancer progression and immunotherapy (2021) · cites this paper as [277]
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References 39 · Cited by 444
- Authors
- Sato, Y., Tsuboi, R., Lyons, R., Moses, H., & Rifkin, D. B.
- Affiliations
- NYU Langone Health (US)
- Venue
- The Journal of cell biology
- Publisher
- Rockefeller University Press
- Published
- 1990-08-01
- Volume
- 111
- Issue
- 2
- Pages
- 757-763
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- PMC
- PMC2116212
- OpenAlex
- W2115598567
- Cited by
- 444
- References
- 39
- Citations by year
- 2026: 1 · 2023: 7 · 2022: 3 · 2021: 6 · 2020: 3 · 2019: 1 · 2018: 1 · 2017: 3 · 2016: 6 · 2015: 9 · 2014: 2 · 2013: 5 · 2012: 6
- FWCI
- 12.00
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- cc-by-nc-sa
- Locations
- The Journal of Cell Biology (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Protease and Inhibitor Mechanisms
- Keywords
- latent TGF-beta activation, TGF-beta, endothelial cells, smooth muscle cells, pericytes, plasminogen activator inhibitor-1, protease inhibition, TGF-β1, TGF-beta2, cell migration inhibition, self-regulation
- MeSH terms
- Animals, Cattle, Cell Communication, Cell Movement, Cells, Cultured, Endothelium, Vascular, Kinetics, Muscle, Smooth, Muscle, Smooth, Vascular, Poly A, Protein Processing, Post-Translational, Receptors, Cell Surface, RNA, RNA, Messenger, Transforming Growth Factors, Receptors, Transforming Growth Factor beta, Macromolecular Substances
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