Journal article
Internal affairs: tenascin-C as a clinically relevant, endogenous driver of innate
- Abstract:
- To protect against danger, the innate immune system must promptly and accurately sense alarm signals, and mount an appropriate response to restore homeostasis. One endogenous trigger of immunity is tenascin-C, a large hexameric protein of the extracellular matrix. Upregulated upon tissue injury and cellular stress, tenascin-C is expressed during inflammation and tissue remodeling, where it influences cellular behavior by interacting with a multitude of molecular targets, including other matrix components, cell surface proteins, and growth factors. Here, we discuss how these interactions confer upon tenascin-C distinct immunomodulatory capabilities that make this matrix molecule necessary for efficient tissue repair. We also highlight in vivo studies that provide insight into the consequences of misregulated tenascin-C expression on inflammation and fibrosis during a wide range of inflammatory diseases. Finally, we examine how its unique expression pattern and inflammatory actions make tenascin-C a viable target for clinical exploitation in both diagnostic and therapeutic arenas.
- Publication status:
- Published
- Peer review status:
- Peer reviewed
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- Files:
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(Preview, Accepted manuscript, pdf, 546.7KB, Terms of use)
-
- Publisher copy:
- 10.1369/0022155418757443
Authors
- Publisher:
- SAGE Publications
- Journal:
- Journal of Histochemistry and Cytochemistry More from this journal
- Volume:
- 66
- Issue:
- 4
- Pages:
- 289-304
- Publication date:
- 2018-01-31
- Acceptance date:
- 2017-11-28
- DOI:
- EISSN:
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1551-5044
- ISSN:
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0022-1554
- Keywords:
- Pubs id:
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pubs:822134
- UUID:
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uuid:2297f04a-095b-494b-8c24-d4da62a209a7
- Local pid:
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pubs:822134
- Source identifiers:
-
822134
- Deposit date:
-
2018-01-31
Terms of use
- Copyright holder:
- © Marzeda and Midwwod, 2018
- Copyright date:
- 2018
- Notes:
- This is the author accepted manuscript following peer review version of the article. The final version is available online from SAGE Publications at: 10.1369/0022155418757443
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