The DOI matches its Crossref record; 29 of the 29 references it cites were found in a registry or an index.
Molecular mechanisms linking wound inflammation and fibrosis: knockdown of osteopontin leads to rapid repair and reduced scarring
Open accessAbstract
Previous studies of tissue repair have revealed osteopontin (OPN) to be up-regulated in association with the wound inflammatory response. We hypothesize that OPN may contribute to inflammation-associated fibrosis. In a series of in vitro and in vivo studies, we analyze the effects of blocking OPN expression at the wound, and determine which inflammatory cells, and which paracrine factors from these cells, may be responsible for triggering OPN expression in wound fibroblasts. Delivery of OPN antisense oligodeoxynucleotides into mouse skin wounds by release from Pluronic gel decreases OPN protein levels at the wound and results in accelerated healing and reduced granulation tissue formation and scarring. To identify which leukocytic lineages may be responsible for OPN expression, we cultured fibroblasts in macrophage-, neutrophil-, or mast cell–conditioned media (CM), and found that macrophage- and mast cell–secreted factors, specifically platelet-derived growth factor (PDGF), induced fibroblast OPN expression. Correspondingly, Gleevec, which blocks PDGF receptor signaling, and PDGF-Rβ–neutralizing antibodies, inhibited OPN induction by macrophage-CM. These studies indicate that inflammation-triggered expression of OPN both hinders the rate of repair and contributes to wound fibrosis. Thus, OPN and PDGF are potential targets for therapeutic modulation of skin repair to improve healing rate and quality.
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Selective depletion of macrophages reveals distinct, opposing roles during liver injury and repair
Duffield, J. S., Forbes, S. J., Constandinou, C. M., Clay, S., Partolina, M., Vuthoori, S., Wu, S., Lang, R., & Iredale, J. P. (2005) · Journal of Clinical Investigation · doi:10.1172/jci200522675 · Cited by 1,649
Inflammatory cells during wound repair: the good, the bad and the ugly
Martin, P., & Leibovich, S. J. (2005) · Trends in Cell Biology · doi:10.1016/j.tcb.2005.09.002 · Cited by 1,340
Self-citationShah, M., Foreman, D. M., & Ferguson, M. W. J. (1995) · Journal of Cell Science · doi:10.1242/jcs.108.3.985 · Cited by 1,169
Wound Macrophages Express TGF-α and Other Growth Factors in Vivo: Analysis by mRNA Phenotyping
Rappolee, D. A., Mark, D., Banda, M. J., & Werb, Z. (1988) · Science · doi:10.1126/science.3041594 · Cited by 1,104
Denhardt, D. T., Noda, M., O’Regan, A. W., Pavlin, D., & Berman, J. S. (2001) · Journal of Clinical Investigation · doi:10.1172/jci12980 · Cited by 1,059
Procollagen trafficking, processing and fibrillogenesis
Canty, E. G., & Kadler, K. E. (2005) · Journal of Cell Science · doi:10.1242/jcs.01731 · Cited by 764
Altered wound healing in mice lacking a functional osteopontin gene (spp1).
Liaw, L., Birk, D. E., Ballas, C. B., Whitsitt, J. S., Davidson, J. M., & Hogan, B. L. (1998) · Journal of Clinical Investigation · doi:10.1172/jci2131 · Cited by 663
Wound Healing in the PU.1 Null Mouse—Tissue Repair Is Not Dependent on Inflammatory Cells
Martin, P., D'Souza, D., Martin, J., Grose, R., Cooper, L., Maki, R., & McKercher, S. R. (2003) · Current Biology · doi:10.1016/s0960-9822(03)00396-8 · Cited by 491
Self-citationUp-Regulation and Profibrotic Role of Osteopontin in Human Idiopathic Pulmonary Fibrosis
Pardo, A., Gibson, K., Cisneros, J., Richards, T. J., Yang, Y., Becerril, C., Yousem, S., Herrera, I., Ruiz, V., Selman, M., et al. (2005) · PLoS Medicine · doi:10.1371/journal.pmed.0020251 · Cited by 489
Lynch, S. E., Nixon, J. C., Colvin, R. B., & Antoniades, H. N. (1987) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.84.21.7696 · Cited by 440
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Wound repair and regeneration: Mechanisms, signaling, and translation
Eming, S. A., Martin, P., & Tomic-Canic, M. (2014) · Science Translational Medicine · doi:10.1126/scitranslmed.3009337 · Cited by 3,562
Self-citationInflammation and wound healing: the role of the macrophage
Koh, T. J., & DiPietro, L. A. (2011) · Expert Reviews in Molecular Medicine · doi:10.1017/s1462399411001943 · Cited by 1,667
Inflammation and metabolism in tissue repair and regeneration
Eming, S. A., Wynn, T. A., & Martin, P. (2017) · Science · doi:10.1126/science.aam7928 · Cited by 1,369
Self-citationExtracellular Matrix and Dermal Fibroblast Function in the Healing Wound
Tracy, L. E., Minasian, R. A., & Caterson, E. J. (2016) · Advances in Wound Care · doi:10.1089/wound.2014.0561 · Cited by 1,008
Metadata
- Authors
- Mori, R., Shaw, T. J., & Martin, P.
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2008-01-07
- Volume
- 205
- Issue
- 1
- Pages
- 43-51
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2142480558
- Cited by
- 294
- References
- 29
- FWCI
- 24.01
- Type
- journal article
- Language
- en
- Open access
- green
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