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Conference Paper: Role of bone morphogenetic protein-7 (BMP7) in diabetic tubulopathy

TitleRole of bone morphogenetic protein-7 (BMP7) in diabetic tubulopathy
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. 697A-698A, abstract no. SA-PO308 How to Cite?
AbstractBACKGROUND: The potential renoprotective role of BMP7 in diabetic nephropathy remains unknown. METHODS: Nine-week-old db/db mice and their db/m littermates underwent uninephrectomy (Unx) or sham operation, and received rh-BMP7 (300ug/kg body weight) or vehicle intraperitoneally every other day for 8 weeks before sacrifice. Primary human proximal tubular epithelial cells (PTECs) were growth-arrested and exposed to glycated human serum albumin (AGE-HSA) with or without rh-BMP7. RESULTS: Compared with vehicle control, Unx db/db mice treated with rh-BMP7 for 8 weeks had significantly lower urinary albumin-to-creatinine ratio (4,566±2,767 ug/mg vs. 7,338±5,748 ug/mg, p<0.05), serum BUN (33.3±3.46 mg/dL vs. 37.5±2.95 mg/dL, p<0.05), and renal cortical gene expression of IL-6, ICAM-1, CCL-2 and CCL-5. PAS staining of kidney tissue showed significantly less severe tubular damage and interstitial inflammatory cell infiltration in the BMP7-treated group. In cultured human PTECs, exposure to AGEHSA induced overexpression of sICAM-1, CCL-2, IL-8 and IL-6, involving activation of p44/42 and p38 MAPK signaling. BMP7 dose-dependently attenuated AGE-induced upregulation of sICAM-1, CCL-2, IL-8 and IL-6 at both mRNA and protein levels. Moreover, BMP7 suppressed AGE-induced p38 and p44/42 MAPK phosphorylation and reactive oxygen species production in PTECs. CONCLUSIONS: Our results demonstrated for the first time that BMP7 attenuates tubular pro-inflammatory responses in diabetic kidney disease by suppressing oxidative stress and multiple signaling pathways including p38 and p44/42 MAPK. Its potential application as a therapeutic molecule in diabetic nephropathy warrants further investigation.
DescriptionSaturday Poster Presentation - Diabetes Mellitus and Obesity: Basic - Experimental - II: no. SA-PO308
Persistent Identifierhttp://hdl.handle.net/10722/204262
ISSN
2015 Impact Factor: 8.491
2015 SCImago Journal Rankings: 4.699

 

DC FieldValueLanguage
dc.contributor.authorLi, Ren_US
dc.contributor.authorYiu, WHen_US
dc.contributor.authorWu, Hen_US
dc.contributor.authorLin, Men_US
dc.contributor.authorWong, DWLen_US
dc.contributor.authorChan, LYYen_US
dc.contributor.authorLeung, JCKen_US
dc.contributor.authorLai, KNen_US
dc.contributor.authorTang, SCWen_US
dc.date.accessioned2014-09-19T21:43:11Z-
dc.date.available2014-09-19T21:43:11Z-
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. 697A-698A, abstract no. SA-PO308en_US
dc.identifier.issn1046-6673-
dc.identifier.urihttp://hdl.handle.net/10722/204262-
dc.descriptionSaturday Poster Presentation - Diabetes Mellitus and Obesity: Basic - Experimental - II: no. SA-PO308-
dc.description.abstractBACKGROUND: The potential renoprotective role of BMP7 in diabetic nephropathy remains unknown. METHODS: Nine-week-old db/db mice and their db/m littermates underwent uninephrectomy (Unx) or sham operation, and received rh-BMP7 (300ug/kg body weight) or vehicle intraperitoneally every other day for 8 weeks before sacrifice. Primary human proximal tubular epithelial cells (PTECs) were growth-arrested and exposed to glycated human serum albumin (AGE-HSA) with or without rh-BMP7. RESULTS: Compared with vehicle control, Unx db/db mice treated with rh-BMP7 for 8 weeks had significantly lower urinary albumin-to-creatinine ratio (4,566±2,767 ug/mg vs. 7,338±5,748 ug/mg, p<0.05), serum BUN (33.3±3.46 mg/dL vs. 37.5±2.95 mg/dL, p<0.05), and renal cortical gene expression of IL-6, ICAM-1, CCL-2 and CCL-5. PAS staining of kidney tissue showed significantly less severe tubular damage and interstitial inflammatory cell infiltration in the BMP7-treated group. In cultured human PTECs, exposure to AGEHSA induced overexpression of sICAM-1, CCL-2, IL-8 and IL-6, involving activation of p44/42 and p38 MAPK signaling. BMP7 dose-dependently attenuated AGE-induced upregulation of sICAM-1, CCL-2, IL-8 and IL-6 at both mRNA and protein levels. Moreover, BMP7 suppressed AGE-induced p38 and p44/42 MAPK phosphorylation and reactive oxygen species production in PTECs. CONCLUSIONS: Our results demonstrated for the first time that BMP7 attenuates tubular pro-inflammatory responses in diabetic kidney disease by suppressing oxidative stress and multiple signaling pathways including p38 and p44/42 MAPK. Its potential application as a therapeutic molecule in diabetic nephropathy warrants further investigation.-
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.titleRole of bone morphogenetic protein-7 (BMP7) in diabetic tubulopathyen_US
dc.typeConference_Paperen_US
dc.identifier.emailYiu, WH: whyiu@hku.hken_US
dc.identifier.emailWu, H: hjwu@hku.hken_US
dc.identifier.emailChan, LYY: yychanb@hku.hken_US
dc.identifier.emailLeung, JCK: jckleung@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.hkuros235362en_US
dc.identifier.volume24-
dc.identifier.spage697A, SA-PO308-
dc.identifier.epage698A-
dc.publisher.placeUnited States-

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