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Cited by 282

The DOI matches its Crossref record; 142 of the 142 references it cites were found in a registry or an index.

Type-1 pericytes accumulate after tissue injury and produce collagen in an organ-dependent manner

Open access
Birbrair, Alexander, Zhang, Tan, Files, Daniel Clark, Mannava, Sandeep, Smith, Thomas, Wang, Zhong-Min, Messi, Maria Laura, Mintz, Akiva, Delbono, Osvaldo·2014·Stem Cell Research & Therapy

Abstract

Introduction: Fibrosis, or scar formation, is a pathological condition characterized by excessive production and accumulation of collagen, loss of tissue architecture, and organ failure in response to uncontrolled wound healing. Several cellular populations have been implicated, including bone marrow-derived circulating fibrocytes, endothelial cells, resident fibroblasts, epithelial cells, and recently, perivascular cells called pericytes. We previously demonstrated pericyte functional heterogeneity in skeletal muscle. Whether pericyte subtypes are present in other tissues and whether a specific pericyte subset contributes to organ fibrosis are unknown. Methods: Here, we report the presence of two pericyte subtypes, type-1 (Nestin-GFP-/NG2-DsRed+) and type-2 (Nestin-GFP+/NG2-DsRed+), surrounding blood vessels in lungs, kidneys, heart, spinal cord, and brain. Using Nestin-GFP/NG2-DsRed transgenic mice, we induced pulmonary, renal, cardiac, spinal cord, and cortical injuries to investigate the contributions of pericyte subtypes to fibrous tissue formation in vivo. Results: A fraction of the lung’s collagen-producing cells corresponds to type-1 pericytes and kidney and heart pericytes do not produce collagen in pathological fibrosis. Note that type-1, but not type-2, pericytes increase and accumulate near the fibrotic tissue in all organs analyzed. Surprisingly, after CNS injury, type-1 pericytes differ from scar-forming PDGFRβ + cells. Conclusions: Pericyte subpopulations respond differentially to tissue injury, and the production of collagen by type-1 pericytes is organ-dependent. Characterization of the mechanisms underlying scar formation generates cellular targets for future anti-fibrotic therapeutics.

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Metadata

Authors
Birbrair, A., Zhang, T., Files, D. C., Mannava, S., Smith, T., Wang, Z.-M., Messi, M. L., Mintz, A., & Delbono, O.
Venue
Stem Cell Research & Therapy
Published
2014-11-06
Volume
5
Issue
6
Pages
122-122
ISSN
1757-6512 (ISSN-L)
OpenAlex
W1981750198
Cited by
282
References
142
FWCI
9.13
Type
journal article
Language
en
Open access
gold

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