{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,31]],"date-time":"2026-07-31T19:53:39Z","timestamp":1785527619808,"version":"3.56.0"},"reference-count":26,"publisher":"Wiley","issue":"19","license":[{"start":{"date-parts":[[2020,8,26]],"date-time":"2020-08-26T00:00:00Z","timestamp":1598400000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2020,8,26]],"date-time":"2020-08-26T00:00:00Z","timestamp":1598400000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2020,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Acute lung injury (ALI) induced by sepsis is characterized by an inflammatory process related to the up\u2010regulation of inflammatory cytokines and chemokines. In the present study, we explored the role of circC3P1 in sepsis\u2010induced ALI in vitro and in vivo. The caecal ligation and puncture (CLP)\u2010induced sepsis model was established through CLP surgery. Forty adult male C57BL\/6 mice were randomly assigned into sham, CLP, CLP + vector and CLP + circC3P1 (each n\u00a0=\u00a010). Primary murine pulmonary microvascular endothelial cells (MPVECs) were transfected with circC3P1 or empty vector 24\u00a0hours prior to LPS treatment via Lipofectamine 2000. The expressions of circC3P1, tumour necrosis factor\u2010\u03b1 (TNF\u2010\u03b1), interleukin\u20106 (IL\u20106) and IL\u20101\u03b2 were evaluated after 6\u2010h LPS treatment. Cell apoptosis was evaluated via flow cytometry. The CLP group demonstrated pulmonary morphological abnormalities, increased concentrations of TNF\u2010\u03b1, IL\u20106 and IL\u20101\u03b2 in the lung tissue, compared with the sham group. MPVECs treated with LPS significantly elevated TNF\u2010\u03b1, IL\u20106 and IL\u20101\u03b2 levels and increased cell apoptosis than that in the control group. The circC3P1 overexpression in sepsis\u2010induced ALI mice attenuated pulmonary injury, inflammation and apoptosis. Besides, circC3P1 revealed anti\u2010inflammatory and anti\u2010apoptotic effect in MPVEC\u2010treated LPS. CircC3P1 overexpression reduced cell apoptosis and pro\u2010inflammatory cytokines levels via down\u2010regulating miR\u201021. CircC3P1 attenuated pro\u2010inflammatory cytokine production and cell apoptosis in ALI induced by sepsis through modulating miR\u201021, indicating that circC3P1 is a promising therapeutic biomarker for sepsis\u2010induced ALI.<\/jats:p>","DOI":"10.1111\/jcmm.15685","type":"journal-article","created":{"date-parts":[[2020,9,2]],"date-time":"2020-09-02T15:31:35Z","timestamp":1599060695000},"page":"11221-11229","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":58,"title":["CircC3P1 attenuated pro\u2010inflammatory cytokine production and cell apoptosis in acute lung injury induced by sepsis through modulating miR\u201021"],"prefix":"10.1111","volume":"24","author":[{"given":"Wen\u2010Yang","family":"Jiang","sequence":"first","affiliation":[{"name":"Department of Thoracic Surgery Renmin Hospital of Wuhan University Wuhan 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