{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T13:34:50Z","timestamp":1790775290764,"version":"4.1.0"},"reference-count":42,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2016,6,30]],"date-time":"2016-06-30T00:00:00Z","timestamp":1467244800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Natural Science Foundation of China (NSFC)","award":["81272153"],"award-info":[{"award-number":["81272153"]}]},{"name":"Natural Science Foundation of China (NSFC)","award":["81471883"],"award-info":[{"award-number":["81471883"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Dermatology"],"published-print":{"date-parts":[[2016,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Hypertrophic scarring is a common dermal fibroproliferative disorder characterized by excessive collagen deposition. Prostaglandin E\n                    <jats:sub>2<\/jats:sub>\n                    (\n                    <jats:styled-content style=\"fixed-case\">PGE<\/jats:styled-content>\n                    <jats:sub>2<\/jats:sub>\n                    ), an important inflammatory product synthesized via the arachidonic acid cascade, has been shown to act as a fibroblast modulator and to possess antifibroblastic activity. However, the mechanism underlying the antifibrotic effect of\n                    <jats:styled-content style=\"fixed-case\">PGE<\/jats:styled-content>\n                    <jats:sub>2<\/jats:sub>\n                    remains unclear. In this study, we explored the effects of\n                    <jats:styled-content style=\"fixed-case\">PGE<\/jats:styled-content>\n                    <jats:sub>2<\/jats:sub>\n                    on\n                    <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\n                    \u2010\n                    <jats:italic>\u03b2<\/jats:italic>\n                    1\u2010treated dermal fibroblasts in terms of collagen production and to determine the regulatory pathways involved, as well as understand the antiscarring function of\n                    <jats:styled-content style=\"fixed-case\">PGE<\/jats:styled-content>\n                    <jats:sub>2<\/jats:sub>\n                    <jats:italic>in vivo<\/jats:italic>\n                    . We found that\n                    <jats:styled-content style=\"fixed-case\">PGE<\/jats:styled-content>\n                    <jats:sub>2<\/jats:sub>\n                    inhibited\n                    <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\n                    \u2010\n                    <jats:italic>\u03b2<\/jats:italic>\n                    1\u2010induced collagen synthesis by regulating the balance of matrix metalloproteinases (\n                    <jats:styled-content style=\"fixed-case\">MMP<\/jats:styled-content>\n                    s) and tissue inhibitor of metalloproteinase (\n                    <jats:styled-content style=\"fixed-case\">TIMP<\/jats:styled-content>\n                    ). It did so by upregulating\n                    <jats:styled-content style=\"fixed-case\">cAMP<\/jats:styled-content>\n                    through the E prostanoid (\n                    <jats:styled-content style=\"fixed-case\">EP<\/jats:styled-content>\n                    )2 receptor. We determined that inhibition of the\n                    <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\n                    \u2010\n                    <jats:italic>\u03b2<\/jats:italic>\n                    1\/Smad pathway by\n                    <jats:styled-content style=\"fixed-case\">PGE<\/jats:styled-content>\n                    <jats:sub>2<\/jats:sub>\n                    is associated with its ability to inhibit collagen synthesis. An\n                    <jats:italic>in vivo<\/jats:italic>\n                    study further confirmed that\n                    <jats:styled-content style=\"fixed-case\">PGE<\/jats:styled-content>\n                    <jats:sub>2<\/jats:sub>\n                    inhibits hypertrophic scar formation by decreasing collagen production. Our results demonstrate that the novel anti\u2010scarring function of\n                    <jats:styled-content style=\"fixed-case\">PGE<\/jats:styled-content>\n                    <jats:sub>2<\/jats:sub>\n                    is achieved by balancing MMPs\/TIMP expression and decreasing collagen production.\n                  <\/jats:p>","DOI":"10.1111\/exd.13014","type":"journal-article","created":{"date-parts":[[2016,3,21]],"date-time":"2016-03-21T13:49:51Z","timestamp":1458568191000},"page":"604-610","source":"Crossref","is-referenced-by-count":49,"title":["Prostaglandin E\n                    <sub>2<\/sub>\n                    inhibits collagen synthesis in dermal fibroblasts and prevents hypertrophic scar formation\n                    <i>in vivo<\/i>"],"prefix":"10.1111","volume":"25","author":[{"given":"Jingling","family":"Zhao","sequence":"first","affiliation":[{"name":"Department of Burns The First Affiliated Hospital of Sun Yat\u2010sen University Guangzhou 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