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Conference Paper: Major Vault Protein Contributes to Increased Interstitial Fibrosis in a Murine Model of CKD

TitleMajor Vault Protein Contributes to Increased Interstitial Fibrosis in a Murine Model of CKD
Authors
Issue Date2020
PublisherAmerican Society of Nephrology. The Journal's web site is located at http://www.jasn.org
Citation
American Society of Nephrology (ASN) Kidney Week 2020: Reimagined, Digital Meeting, 22-25 October 2020. In Journal of the American Society of Nephrology, 2020, v. 31 n. Suppl., p. 537, abstract no. PO1710 How to Cite?
AbstractBACKGROUND: Chronic kidney disease (CKD) is a global health issue characterized by interstitial fibrosis and tubular atrophy, and progressive CKD results in kidney failure. There is currently no effective intervention for interstitial fibrosis. We previously showed that major vault protein (MVP), a key component of the vault complex, contributed to increased matrix protein deposition in murine unilateral ureteral obstruction (UUO) animal model. We extended our investigations to a murine model of CKD. METHODS: CKD was induced in MVP wild-type (WT) and knockout (KO) mice by feeding with standard chow containing 0.2% adenine for 8 weeks, after which time mice were sacrificed and kidneys were harvested and examined. Spot urine albumin-to-creatinine ratio was also measured. MVP WT and KO mice fed with standard chow served as controls. RESULTS: MVP WT mice with CKD showed increased MVP expression, predominantly in proximal tubular epithelial cells, compared to MVP WT control mice, and this was accompanied by development of proteinuria, tubular atrophy, tubulo-interstitial macrophage infiltration, and increased interstitial α-smooth muscle actin, fibronectin and collagen III expression. MVP KO mice with CKD showed less proteinuria (P<0.05) and less severe kidney histopathological features with reduced immune cell infiltration, and also reduced expression of fibrosis mediators compared to WT CKD mice. Exogenous TNF-α, IL-6, or MCP-1 increased MVP expression in cultured renal proximal tubular epithelial cells. CONCLUSION: The data suggest that progressive CKD in this murine model is accompanied by increased renal tubular epithelial MVP expression, and MVP may contribute to the pathogenesis of tubulo-interstitial injury and damage.
DescriptionSession 1201 Glomerular Diseases: Fibrosis and Extracellular Matrix - Abstract no. PO1710
Persistent Identifierhttp://hdl.handle.net/10722/300846
ISSN
2023 Impact Factor: 10.3
2023 SCImago Journal Rankings: 3.409

 

DC FieldValueLanguage
dc.contributor.authorWong, CY-
dc.contributor.authorYung, SSY-
dc.contributor.authorChan, CYC-
dc.contributor.authorChan, DTM-
dc.date.accessioned2021-07-06T03:11:01Z-
dc.date.available2021-07-06T03:11:01Z-
dc.date.issued2020-
dc.identifier.citationAmerican Society of Nephrology (ASN) Kidney Week 2020: Reimagined, Digital Meeting, 22-25 October 2020. In Journal of the American Society of Nephrology, 2020, v. 31 n. Suppl., p. 537, abstract no. PO1710-
dc.identifier.issn1046-6673-
dc.identifier.urihttp://hdl.handle.net/10722/300846-
dc.descriptionSession 1201 Glomerular Diseases: Fibrosis and Extracellular Matrix - Abstract no. PO1710-
dc.description.abstractBACKGROUND: Chronic kidney disease (CKD) is a global health issue characterized by interstitial fibrosis and tubular atrophy, and progressive CKD results in kidney failure. There is currently no effective intervention for interstitial fibrosis. We previously showed that major vault protein (MVP), a key component of the vault complex, contributed to increased matrix protein deposition in murine unilateral ureteral obstruction (UUO) animal model. We extended our investigations to a murine model of CKD. METHODS: CKD was induced in MVP wild-type (WT) and knockout (KO) mice by feeding with standard chow containing 0.2% adenine for 8 weeks, after which time mice were sacrificed and kidneys were harvested and examined. Spot urine albumin-to-creatinine ratio was also measured. MVP WT and KO mice fed with standard chow served as controls. RESULTS: MVP WT mice with CKD showed increased MVP expression, predominantly in proximal tubular epithelial cells, compared to MVP WT control mice, and this was accompanied by development of proteinuria, tubular atrophy, tubulo-interstitial macrophage infiltration, and increased interstitial α-smooth muscle actin, fibronectin and collagen III expression. MVP KO mice with CKD showed less proteinuria (P<0.05) and less severe kidney histopathological features with reduced immune cell infiltration, and also reduced expression of fibrosis mediators compared to WT CKD mice. Exogenous TNF-α, IL-6, or MCP-1 increased MVP expression in cultured renal proximal tubular epithelial cells. CONCLUSION: The data suggest that progressive CKD in this murine model is accompanied by increased renal tubular epithelial MVP expression, and MVP may contribute to the pathogenesis of tubulo-interstitial injury and damage.-
dc.languageeng-
dc.publisherAmerican Society of Nephrology. The Journal's web site is located at http://www.jasn.org-
dc.relation.ispartofJournal of the American Society of Nephrology-
dc.relation.ispartofAmerican Society of Nephrology (ASN) Kidney Week 2020-
dc.titleMajor Vault Protein Contributes to Increased Interstitial Fibrosis in a Murine Model of CKD-
dc.typeConference_Paper-
dc.identifier.emailYung, SSY: ssyyung@hku.hk-
dc.identifier.emailChan, DTM: dtmchan@hku.hk-
dc.identifier.authorityYung, SSY=rp00455-
dc.identifier.authorityChan, DTM=rp00394-
dc.description.natureabstract-
dc.identifier.hkuros323301-
dc.identifier.volume31-
dc.identifier.issueSuppl.-
dc.identifier.spage537, abstract no. PO1710-
dc.identifier.epage537, abstract no. PO1710-
dc.publisher.placeUnited States-

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