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Sökning: WFRF:(Jiang Hai Long) > (2017) > Deletion Of XIAP re...

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FältnamnIndikatorerMetadata
00004979naa a2200469 4500
001oai:DiVA.org:liu-136628
003SwePub
008170421s2017 | |||||||||||000 ||eng|
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-1366282 URI
0247 a https://doi.org/10.1038/cddis.2017.702 DOI
040 a (SwePub)liu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Liu, Yongu Sichuan University, Peoples R China; Sichuan University, Peoples R China4 aut
2451 0a Deletion Of XIAP reduces the severity of acute pancreatitis via regulation of cell death and nuclear factor-kappa B activity
264 c 2017-03-16
264 1b NATURE PUBLISHING GROUP,c 2017
338 a electronic2 rdacarrier
500 a Funding Agencies|National Natural Science Fund of China (NSFC) [30830100, 81170439, 81470886, 81500486]; Scientific Research Foundation for the Returned Overseas Chinese Scholars, State Education Ministry (SRF for ROCS, SEM) [20101174-4-2]
520 a Severe acute pancreatitis (SAP) still remains a clinical challenge, not only for its high mortality but the uncontrolled inflammatory progression from acute pancreatitis (AP) to SAP. Cell death, including apoptosis and necrosis are critical pathology of AP, since the severity of pancreatitis correlates directly with necrosis and inversely with apoptosis Therefore, regulation of cell death from necrosis to apoptosis may have practicably therapeutic value. X-linked inhibitor of apoptosis protein (XIAP) is the best characterized member of the inhibitor of apoptosis proteins (IAP) family, but its function in AP remains unclear. In the present study, we investigated the potential role of XIAP in regulation of cell death and inflammation during acute pancreatitis. The in vivo pancreatitis model was induced by the administration of cerulein with or without lipopolysaccharide (LPS) or by the administration of L-arginine in wild-type or XIAP-deficient mice, and ex vivo model was induced by the administration of cerulein+LPS in AR42J cell line following XIAP inhibition. The severity of acute pancreatitis was determined by serum amylase activity and histological grading. XIAP deletion on cell apoptosis, necrosis and inflammatory response were examined. Caspases activities, nuclear factor kappa B (NF-kappa B) activation and receptor-interacting protein kinase1 (RIP1) degradation were assessed by western blot. Deletion of XIAP resulted in the reduction of amylase activity, decrease of NF-kappa B activation and less release of TNF-alpha and IL-6, together with increased caspases activities and RIP1 degradation, leading to enhanced apoptosis and reduced necrosis in pancreatic acinar cells and ameliorated the severity of acute pancreatitis. Our results indicate that deletion of XIAP switches cell death away from necrosis to apoptosis and decreases the inflammatory response, effectively attenuating the severity of AP/SAP. The critical role of XIAP in cell death and inflammation suggests that inhibition of XIAP represents a potential therapeutic strategy for the treatment of acute pancreatitis.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Cell- och molekylärbiologi0 (SwePub)301082 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Cell and Molecular Biology0 (SwePub)301082 hsv//eng
7001 a Chen, Xiao-Dongu Sichuan University, Peoples R China4 aut
7001 a Yu, Jiangu Sichuan University, Peoples R China4 aut
7001 a Chi, Jun-Linu Sichuan University, Peoples R China4 aut
7001 a Long, Fei-Wuu Sichuan University, Peoples R China4 aut
7001 a Yang, Hong-Weiu Sichuan University, Peoples R China4 aut
7001 a Chen, Ke-Lingu Sichuan University, Peoples R China4 aut
7001 a Lv, Zhao-Yingu Sichuan University, Peoples R China4 aut
7001 a Zhou, Binu Sichuan University, Peoples R China4 aut
7001 a Peng, Zhi-Haiu Shanghai Jiao Tong University, Peoples R China4 aut
7001 a Sun, Xiao-Fengu Linköpings universitet,Avdelningen för Kirurgi, Ortopedi och Onkologi,Medicinska fakulteten,Region Östergötland, Onkologiska kliniken US,Sichuan University, Peoples R China4 aut0 (Swepub:liu)xiasu45
7001 a Li, Yuanu Sichuan University, Peoples R China4 aut
7001 a Zhou, Zong-Guangu Sichuan University, Peoples R China4 aut
7102 a Sichuan University, Peoples R China; Sichuan University, Peoples R Chinab Sichuan University, Peoples R China4 org
7730 t Cell Death and Diseased : NATURE PUBLISHING GROUPg 8q 8x 2041-4889
8564 u https://liu.diva-portal.org/smash/get/diva2:1089865/FULLTEXT01.pdfx primaryx Raw objecty fulltext:print
8564 u https://doi.org/10.1038/cddis.2017.70
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-136628
8564 8u https://doi.org/10.1038/cddis.2017.70

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