{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T13:50:51Z","timestamp":1791121851388,"version":"4.1.0"},"reference-count":50,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2004,1,23]],"date-time":"2004-01-23T00:00:00Z","timestamp":1074816000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100000024","name":"The Canadian Institutes of Health Research","doi-asserted-by":"crossref","award":["#MOP-42400"],"award-info":[{"award-number":["#MOP-42400"]}],"id":[{"id":"10.13039\/501100000024","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Fondation de l'H\u00f4pital du Saint-Sacrement"},{"name":"Centre de recherche du CHA"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2004,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>During wound healing, the transition from granulation to scar tissue shows a decrease in myofibroblast cellularity. Previous results have correlated the disappearance of these cells with the induction of apoptotic cell death by some unknown stimuli. In contrast, hypertrophic scar appearance after wound healing is thought to be linked to a disorder of apoptotic function which induces myofibroblast persistence in granulation tissue. Oxidative stress being an important mediator of apoptosis, we have evaluated the apoptotic response of normal and pathological wound myofibroblasts (WMyo and HMyo respectively) in their interaction with two oxidative stress inducers: hydrogen peroxide, using a high concentration as a single dose, and sodium ascorbate which induced a continuous release of H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> at a low concentration. Our results showed that, according to the H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> treatment type, HMyo were more sensitive (after ascorbate treatment) or less sensitive (after H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> treatment) when compared to WMyo and Fb. We next assessed the presence of several molecules known to be involved in the antioxidant network protecting cells against H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> injury and found HMyo to have a higher level of activity of glutathione peroxidase and a lower level of activity of catalase than WMyo. These results can help explain the contradictory responses of myofibroblasts according to the oxidative stress treatment. This is the first study linking refractory oxidative stress mediated cell death to cellular phenotype in hypertrophic myofibroblasts, and indicates a pivotal role for the antioxidant enzyme system in this type of resistance. \u00a9 2004 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcp.20003","type":"journal-article","created":{"date-parts":[[2004,5,27]],"date-time":"2004-05-27T20:02:50Z","timestamp":1085688170000},"page":"263-271","source":"Crossref","is-referenced-by-count":11,"title":["Sensitivity of myofibroblasts to H<sub>2<\/sub>O<sub>2<\/sub>\u2010mediated apoptosis and their antioxidant cell 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