{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,22]],"date-time":"2026-03-22T12:02:17Z","timestamp":1774180937279,"version":"3.50.1"},"reference-count":18,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2005,7,22]],"date-time":"2005-07-22T00:00:00Z","timestamp":1121990400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["pathsocjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Pathology"],"published-print":{"date-parts":[[2005,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Heat shock protein 27 (HSP27) mediates cytoprotective effects through its function as a molecular chaperone and through the phosphorylation\u2010dependent stabilization of actin filaments. The role of HSP27 in gastric ulcer formation and healing is, however, unknown. The expression of HSP27 was studied in human gastric tissue specimens obtained from patients with gastric ulcers and from healthy <jats:italic>Helicobacter pylori<\/jats:italic>\u2010negative individuals, who received low\u2010dose aspirin, rofecoxib, and the combination in a prospective study. The susceptibility of the gastric mucosa to indomethacin\u2010induced lesions was further studied in transgenic mice overexpressing human HSP27 (Tg<jats:sup>huHSP27<\/jats:sup>) and compared with wild\u2010type mice (Wt). The expression of HSP27, COX\u20101, and COX\u20102 was investigated in Tg<jats:sup>huHSP27<\/jats:sup> mice and Wt mice by immunohistochemistry and western blot analysis. While no specific changes in HSP27 expression were found following exposure of healthy human gastric mucosa to oral administration of aspirin or refocoxib, chronic gastric ulcers showed strong HSP27 expression at the ulcer base and margins. Here it was expressed by granulation tissue and regenerating surface epithelium. In Tg<jats:sup>huHSP27<\/jats:sup> mice, overexpression of HSP27 led to a significant decrease of indomethacin\u2010induced erosions and ulcers compared with Wt mice. COX\u20101 and COX\u20102 levels did not change. HSP27 is involved in chronic gastric ulcer repair mechanisms in humans, while overexpression of human HSP27 in gastric epithelial cells in mice reduces the susceptibility to non\u2010steroidal anti\u2010inflammatory drug (NSAID)\u2010induced gastric ulceration. This indicates that HSP27 expression is critical for mucosal protection in the stomach. Copyright \u00a9 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley &amp; Sons, Ltd.<\/jats:p>","DOI":"10.1002\/path.1815","type":"journal-article","created":{"date-parts":[[2005,7,22]],"date-time":"2005-07-22T11:38:50Z","timestamp":1122032330000},"page":"177-184","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":32,"title":["Protective role of heat shock protein 27 in gastric mucosal injury"],"prefix":"10.1002","volume":"207","author":[{"given":"Matthias 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