{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,20]],"date-time":"2026-10-20T00:43:05Z","timestamp":1792456985330,"version":"4.5.0"},"reference-count":72,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2011,9,12]],"date-time":"2011-09-12T00:00:00Z","timestamp":1315785600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2011,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Mechanical force significantly modulates both inflammation and fibrosis, yet the fundamental mechanisms that regulate these interactions remain poorly understood. Here we performed microarray analysis to compare gene expression in mechanically loaded wounds\n                    <jats:italic>vs<\/jats:italic>\n                    . unloaded control wounds in an established murine hypertrophic scar (HTS) model. We identified 853 mechanically regulated genes (false discovery rate &lt;2) at d 14 postinjury, a subset of which were enriched for T\u2010cell\u2010regulated pathways. To substantiate the role of T cells in scar mechanotransduction, we applied the HTS model to T\u2010cell\u2010deficient mice and wild\u2010type mice. We found that scar formation in T\u2010cell\u2010deficient mice was reduced by almost 9\u2010fold (\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.001) with attenuated epidermal (by 2.6\u2010fold,\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.01) and dermal (3.9\u2010fold,\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.05) proliferation. Mechanical stimulation was highly associated with sustained T\u2010cell\u2010dependent Th2 cytokine (IL\u20104 and IL\u201013) and chemokine (MCP\u20101) signaling. Further, T\u2010cell\u2010deficient mice failed to recruit systemic inflammatory cells such as macrophages or monocytic fibroblast precursors in response to mechanical loading. These findings indicate that T\u2010cell\u2010regulated fibrogenic pathways are highly mechanoresponsive and suggest that mechanical forces induce a chronic\u2010like inflammatory state through immune\u2010dependent activation of both local and systemic cell populations.\u2014Wong, V. W., Paterno, J., Sorkin, M., Glotzbach, J. P., Levi, K., Januszyk, M., Rustad, K. C., Longaker, M. T., Gurtner, G. C. Mechanical force prolongs acute inflammation\n                    <jats:italic>via<\/jats:italic>\n                    T\u2010cell\u2010dependent pathways during scar formation.\n                    <jats:italic>FASEB J.<\/jats:italic>\n                    25, 4498\u20134510 (2011).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.10-178087","type":"journal-article","created":{"date-parts":[[2011,9,13]],"date-time":"2011-09-13T02:42:27Z","timestamp":1315881747000},"page":"4498-4510","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":125,"title":["Mechanical force prolongs acute inflammation\n                    <i>via<\/i>\n                    T\u2010cell\u2010dependent pathways during scar formation"],"prefix":"10.1096","volume":"25","author":[{"given":"Victor 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