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Erratum Free access | 10.1172/JCI84508

CTGF directs fibroblast differentiation from human mesenchymal stem/stromal cells and defines connective tissue healing in a rodent injury model

Chang H. Lee, Bhranti Shah, Eduardo K. Moioli, and Jeremy J. Mao

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Published October 1, 2015 - More info

Published in Volume 125, Issue 10 on October 1, 2015
J Clin Invest. 2015;125(10):3992–3992. https://doi.org/10.1172/JCI84508.
Copyright © 2015, American Society for Clinical Investigation
Published October 1, 2015 - Version history
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CTGF directs fibroblast differentiation from human mesenchymal stem/stromal cells and defines connective tissue healing in a rodent injury model
Chang H. Lee, … , Eduardo K. Moioli, Jeremy J. Mao
Chang H. Lee, … , Eduardo K. Moioli, Jeremy J. Mao
Research Article

CTGF directs fibroblast differentiation from human mesenchymal stem/stromal cells and defines connective tissue healing in a rodent injury model

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Abstract

Fibroblasts are ubiquitous cells that demonstrate remarkable diversity. However, their origin and pathways of differentiation remain poorly defined. Here, we show that connective tissue growth factor (CTGF; also known as CCN2) is sufficient to induce human bone marrow mesenchymal stem/stromal cells (MSCs) to differentiate into fibroblasts. CTGF-stimulated MSCs lost their surface mesenchymal epitopes, expressed broad fibroblastic hallmarks, and increasingly synthesized collagen type I and tenacin-C. After fibroblastic commitment, the ability of MSCs to differentiate into nonfibroblastic lineages — including osteoblasts, chondrocytes, and adipocytes — was diminished. To address inherent heterogeneity in MSC culture, we established 18 single MSC–derived clones by limiting dilution. CTGF-treated MSCs were α-SMA–, differentiating into α-SMA+ myofibroblasts only when stimulated subsequently with TGF-β1, suggestive of stepwise processes of fibroblast commitment, fibrogenesis, and pathological fibrosis. In rats, in vivo microencapsulated delivery of CTGF prompted postnatal connective tissue to undergo fibrogenesis rather than ectopic mineralization. The knowledge that fibroblasts have a mesenchymal origin may enrich our understanding of organ fibrosis, cancer stroma, ectopic mineralization, scarring, and regeneration.

Authors

Chang H. Lee, Bhranti Shah, Eduardo K. Moioli, Jeremy J. Mao

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Original citation: J Clin Invest. 2010;120(9):3340–3349. doi:10.1172/JCI43230.

Citation for this erratum: J Clin Invest. 2015;125(10):3992. doi:10.1172/JCI84508.

During the preparation of the manuscript, Figure 1G was inadvertently mislabeled. The correct figure is below.

The JCI regrets the error.

Footnotes

See the related article beginning on page 3340.

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  • Version 2 (October 1, 2015): No description

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