{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:09:25Z","timestamp":1787015365162,"version":"build-2736575974"},"reference-count":21,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2020,3,31]],"date-time":"2020-03-31T00:00:00Z","timestamp":1585612800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Cultivate Project of South Campus, Renji Hospital for National Natural Science Foundation","award":["2017PYM10"],"award-info":[{"award-number":["2017PYM10"]}]},{"name":"National Natural Science Foundation of Shanghai","award":["201640142"],"award-info":[{"award-number":["201640142"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2020,5]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    The mechanisms underlying coagulation abnormalities in sepsis and septic acute lung injury remain unclear. Tissue factor (TF) initiates coagulation; its production can be regulated by reactive oxygen species (ROS); and monocytes\/macrophages produce pathological TF during sepsis. The SUMO2\/3 protease SENP3 is redox\u2010sensitive, and SENP3 accumulation in lipopolysaccharide (LPS)\u2010activated macrophages is ROS\u2010dependent. To explore whether SENP3 contributes to LPS\u2010activated coagulation, we used mice with\n                    <jats:italic>Senp3<\/jats:italic>\n                    conditional knockout (cKO) in myeloid cells. In the model of LPS\u2010induced sepsis, SENP3 cKO mice exhibited less severe acute lung injury than SENP3\n                    <jats:sup>fl\/fl<\/jats:sup>\n                    mice. SENP3 cKO mice exhibited decreased TF expression in monocytes and alveolar macrophages, with consequently compromised coagulation in their blood and lungs. In vitro results showed that ROS\u2010induced SENP3 accumulation contributed to LPS\u2010induced TF expression, which was reduced by JNK inhibitor SP600125. Furthermore, mice injected with LPS following SP600125 (75\u00a0mg\/kg) treatment showed decreased monocytes\/macrophages TF production and alleviated coagulation activation, with less severe lung injury and higher survival rates. Collectively, the results suggest that SENP3 mediates LPS\u2010induced coagulation activation by up\u2010regulating monocyte\/macrophage TF production in a JNK\u2010dependent manner. This work provides new insights into ROS regulation of LPS\u2010activated coagulation and reveals a link between SUMOylation and coagulation.\n                  <\/jats:p>","DOI":"10.1111\/jcmm.15199","type":"journal-article","created":{"date-parts":[[2020,3,31]],"date-time":"2020-03-31T21:19:45Z","timestamp":1585689585000},"page":"5454-5462","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["SENP3 in monocytes\/macrophages up\u2010regulates tissue factor and mediates lipopolysaccharide\u2010induced acute lung injury by enhancing JNK phosphorylation"],"prefix":"10.1111","volume":"24","author":[{"given":"Xuelian","family":"Chen","sequence":"first","affiliation":[{"name":"Emergency Department South Campus, Renji Hospital Shanghai Jiaotong University School of Medicine Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yimin","family":"Lao","sequence":"additional","affiliation":[{"name":"Shanghai Key Laboratory of Tumor Microenvironment and Inflammation Department of Biochemistry and Molecular Cell Biology Institutes of Medical Sciences Shanghai Jiao Tong University School of Medicine Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Yi","sequence":"additional","affiliation":[{"name":"Shanghai Key Laboratory of Tumor Microenvironment and Inflammation Department of Biochemistry and Molecular Cell Biology Institutes of Medical Sciences Shanghai Jiao Tong University School of Medicine Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jie","family":"Yang","sequence":"additional","affiliation":[{"name":"Shanghai Key Laboratory of Tumor Microenvironment and Inflammation Department of Biochemistry and Molecular Cell Biology Institutes of Medical Sciences Shanghai Jiao Tong University School of Medicine Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuangjun","family":"He","sequence":"additional","affiliation":[{"name":"Emergency Department South Campus, Renji Hospital Shanghai Jiaotong University School of Medicine Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1970-9322","authenticated-orcid":false,"given":"Yi","family":"Chen","sequence":"additional","affiliation":[{"name":"Emergency Department South Campus, Renji Hospital Shanghai Jiaotong University School of Medicine Shanghai 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