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Conference Paper: Tissue kallikrein mediates pro-inflammatory pathways in proximal tubular epithelial cells

TitleTissue kallikrein mediates pro-inflammatory pathways in proximal tubular epithelial cells
Authors
Issue Date2013
PublisherAmerican Society of Nephrology. The Journal's web site is located at https://www.asn-online.org/abstracts/
Citation
Kidney Week 2013, Atlanta, GA., 5-10 November 2013. In Journal of the American Society of Nephrology, 2013, v. 24, p. 315A, abstract no. TH-PO950 How to Cite?
AbstractBACKGROUND: Tissue kallikrein (KLK1) expression is up-regulated in human diabetic kidney tissue. Since the kallikrein-kininsystem (KKS) has been linked to cellular inflammatory process in many diseases, we explore the role of KLK1 in tubular pro-inflammatory responses under the diabetic milieu. METHODS: Human proximal tubular epithelial cells (PTEC) were incubated with recombinant KLK1 protein to examine the expression of pro-inflammatory cytokines and the activation of signaling pathways. Cells were then transfected with KLK1-specific or control siRNA to investigate the effect of KLK1 on advanced glycation end products (AGE)-induced pro-inflammatory responses. RESULTS: Recombinant KLK1 stimulated the production of inflammatory cytokines including IL-8, ICAM-1 and CCL-2, and activated the phosphorylation of p42/44 and p38 MAPK in PTEC. Increased expression of KLK1 was detected in PTEC stimulated with AGE (0.5 mg/ml), and molecular knockdown of endogenous KLK1 expression attenuated AGE-induced tubular IL-8 and ICAM-1 productions. CONCLUSIONS: Our data suggest for the first time that KLK1 mediates pro-inflammatory responses in renal tubule cells under a diabetic milieu, and pave the way for further investigation that targets KLK1 in ameliorating diabetic tubular injury.
DescriptionThursday Poster Presentation - Pathobiology: Clinical/Diagnostic Renal Pathology and Lab Medicine - I: no. TH-PO950
Persistent Identifierhttp://hdl.handle.net/10722/204261
ISSN
2015 Impact Factor: 8.491
2015 SCImago Journal Rankings: 4.699

 

DC FieldValueLanguage
dc.contributor.authorYiu, WHen_US
dc.contributor.authorWong, DWLen_US
dc.contributor.authorLeung, JCKen_US
dc.contributor.authorChan, LYYen_US
dc.contributor.authorLan, HYen_US
dc.contributor.authorLai, KNen_US
dc.contributor.authorTang, SCWen_US
dc.date.accessioned2014-09-19T21:43:10Z-
dc.date.available2014-09-19T21:43:10Z-
dc.date.issued2013en_US
dc.identifier.citationKidney Week 2013, Atlanta, GA., 5-10 November 2013. In Journal of the American Society of Nephrology, 2013, v. 24, p. 315A, abstract no. TH-PO950en_US
dc.identifier.issn1046-6673-
dc.identifier.urihttp://hdl.handle.net/10722/204261-
dc.descriptionThursday Poster Presentation - Pathobiology: Clinical/Diagnostic Renal Pathology and Lab Medicine - I: no. TH-PO950-
dc.description.abstractBACKGROUND: Tissue kallikrein (KLK1) expression is up-regulated in human diabetic kidney tissue. Since the kallikrein-kininsystem (KKS) has been linked to cellular inflammatory process in many diseases, we explore the role of KLK1 in tubular pro-inflammatory responses under the diabetic milieu. METHODS: Human proximal tubular epithelial cells (PTEC) were incubated with recombinant KLK1 protein to examine the expression of pro-inflammatory cytokines and the activation of signaling pathways. Cells were then transfected with KLK1-specific or control siRNA to investigate the effect of KLK1 on advanced glycation end products (AGE)-induced pro-inflammatory responses. RESULTS: Recombinant KLK1 stimulated the production of inflammatory cytokines including IL-8, ICAM-1 and CCL-2, and activated the phosphorylation of p42/44 and p38 MAPK in PTEC. Increased expression of KLK1 was detected in PTEC stimulated with AGE (0.5 mg/ml), and molecular knockdown of endogenous KLK1 expression attenuated AGE-induced tubular IL-8 and ICAM-1 productions. CONCLUSIONS: Our data suggest for the first time that KLK1 mediates pro-inflammatory responses in renal tubule cells under a diabetic milieu, and pave the way for further investigation that targets KLK1 in ameliorating diabetic tubular injury.-
dc.languageengen_US
dc.publisherAmerican Society of Nephrology. The Journal's web site is located at https://www.asn-online.org/abstracts/-
dc.relation.ispartofJASN Abstract Supplementen_US
dc.titleTissue kallikrein mediates pro-inflammatory pathways in proximal tubular epithelial cellsen_US
dc.typeConference_Paperen_US
dc.identifier.emailYiu, WH: whyiu@hku.hken_US
dc.identifier.emailLeung, JCK: jckleung@hku.hken_US
dc.identifier.emailChan, LYY: yychanb@hku.hken_US
dc.identifier.emailLai, KN: knlai@hku.hken_US
dc.identifier.emailTang, SCW: scwtang@hku.hken_US
dc.identifier.authorityLeung, JCK=rp00448en_US
dc.identifier.authorityLai, KN=rp00324en_US
dc.identifier.authorityTang, SCW=rp00480en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros235361en_US
dc.identifier.volume24-
dc.identifier.spage315A, abstract no. TH-PO950-
dc.identifier.epage315A, abstract no. TH-PO950-
dc.publisher.placeUnited States-

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