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Conference Paper: Complement C5a Moderates Renal Lipid Metabolism and Fibrosis in Diabetic Nephropathy

TitleComplement C5a Moderates Renal Lipid Metabolism and Fibrosis in Diabetic Nephropathy
Authors
Issue Date2017
PublisherAmerican Society of Nephrology. The Abstract's web site is located at https://www.asn-online.org/education/kidneyweek/archives/
Citation
American Society of Nephrology Kidney Week, New Orleans, USA, 31 October - 5 November 2017, In Journal of the American Society of Nephrology, 2017, v. 28 n. Abstract Suppl., p. 108 How to Cite?
AbstractBackground: Complement C5 activation has been implicated in tubulointerstitial injury with increased levels of tubular C5a in renal biopsies from patients with diabetic nephropathy. We investigated whether administration of a C5a inhibitor would confer protection against the progression of diabetic nephropathy in an animal model of type 2 diabetes. Methods: Uninephrectomized diabetic db/db mice were administrated with novel C5a inhibitor, NOX-D21 (10 mg/kg, a kind gift from NOXXON) or an equal volume of saline for a total of 12 weeks. Non-diabetic db/m mice were used as control. Results: In db/db mice, treatment with NOX-D21 for 12 weeks did not affect hyperglycemia, but significantly prevented the increase in serum creatinine and BUN levels. These NOX-D21 treated mice had reduced glomerulosclerosis and tubular damage compared to the vehicle-treated diabetic mice. In addition, blockade of C5 signaling reduced the overexpression of TGF-β1, activation of Akt signaling and interstitial expression of fibronectin and collagen type I in the diabetic kidney. NOX-D21 also ameliorated lipid abnormalities in db/db mice and resulted in significant decrease in serum triglycerides and expression of lipid metabolism-related genes (DAGT1 and SREBP-1) in the diabetic kidney. Conclusion: Our findings suggest a pathogenic role of C5a in diabetic nephropathy, especially in regulating TGF-β-driven renal fibrosis. Inhibition of C5a signaling partially improves renal function and ameliorates dyslipidemia in diabetic animals.
DescriptionPoster presentation - Complement Your Knowledge of Kidney Disease - no. TH-PO015
Persistent Identifierhttp://hdl.handle.net/10722/259725
ISSN
2015 Impact Factor: 8.491
2015 SCImago Journal Rankings: 4.699

 

DC FieldValueLanguage
dc.contributor.authorYiu, WH-
dc.contributor.authorLi, RX-
dc.contributor.authorWong, WLD-
dc.contributor.authorWu, H-
dc.contributor.authorChan, KW-
dc.contributor.authorChan, LYY-
dc.contributor.authorLeung, JCK-
dc.contributor.authorLai, KN-
dc.contributor.authorSacks, SH-
dc.contributor.authorZhou, W-
dc.contributor.authorTang, SCW-
dc.date.accessioned2018-09-03T04:12:54Z-
dc.date.available2018-09-03T04:12:54Z-
dc.date.issued2017-
dc.identifier.citationAmerican Society of Nephrology Kidney Week, New Orleans, USA, 31 October - 5 November 2017, In Journal of the American Society of Nephrology, 2017, v. 28 n. Abstract Suppl., p. 108-
dc.identifier.issn1046-6673-
dc.identifier.urihttp://hdl.handle.net/10722/259725-
dc.descriptionPoster presentation - Complement Your Knowledge of Kidney Disease - no. TH-PO015-
dc.description.abstractBackground: Complement C5 activation has been implicated in tubulointerstitial injury with increased levels of tubular C5a in renal biopsies from patients with diabetic nephropathy. We investigated whether administration of a C5a inhibitor would confer protection against the progression of diabetic nephropathy in an animal model of type 2 diabetes. Methods: Uninephrectomized diabetic db/db mice were administrated with novel C5a inhibitor, NOX-D21 (10 mg/kg, a kind gift from NOXXON) or an equal volume of saline for a total of 12 weeks. Non-diabetic db/m mice were used as control. Results: In db/db mice, treatment with NOX-D21 for 12 weeks did not affect hyperglycemia, but significantly prevented the increase in serum creatinine and BUN levels. These NOX-D21 treated mice had reduced glomerulosclerosis and tubular damage compared to the vehicle-treated diabetic mice. In addition, blockade of C5 signaling reduced the overexpression of TGF-β1, activation of Akt signaling and interstitial expression of fibronectin and collagen type I in the diabetic kidney. NOX-D21 also ameliorated lipid abnormalities in db/db mice and resulted in significant decrease in serum triglycerides and expression of lipid metabolism-related genes (DAGT1 and SREBP-1) in the diabetic kidney. Conclusion: Our findings suggest a pathogenic role of C5a in diabetic nephropathy, especially in regulating TGF-β-driven renal fibrosis. Inhibition of C5a signaling partially improves renal function and ameliorates dyslipidemia in diabetic animals.-
dc.languageeng-
dc.publisherAmerican Society of Nephrology. The Abstract's web site is located at https://www.asn-online.org/education/kidneyweek/archives/-
dc.relation.ispartofJournal of the American Society of Nephrology-
dc.relation.ispartofAmerican Society of Nephrology Kidney Week, 2017-
dc.titleComplement C5a Moderates Renal Lipid Metabolism and Fibrosis in Diabetic Nephropathy-
dc.typeConference_Paper-
dc.identifier.emailYiu, WH: whyiu@hku.hk-
dc.identifier.emailChan, LYY: yychanb@hku.hk-
dc.identifier.emailLeung, JCK: jckleung@hku.hk-
dc.identifier.emailLai, KN: knlai@hku.hk-
dc.identifier.emailTang, SCW: scwtang@hku.hk-
dc.identifier.authorityLeung, JCK=rp00448-
dc.identifier.authorityLai, KN=rp00324-
dc.identifier.authorityTang, SCW=rp00480-
dc.identifier.hkuros288275-
dc.identifier.volume28-
dc.identifier.issueAbstract Suppl.-
dc.identifier.spage108-
dc.identifier.epage108-
dc.publisher.placeUnited States-

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