Deletion of Smad3 prevents renal fibrosis and inflammation in type 2 diabetic nephropathy
Transforming growth factor (TGF)-β/Smad3 signaling is highly activated in kidneys of patients with type 2 diabetic nephropathy (T2DN), however, the precise role of Smad3 in the pathogenesis of diabetic nephropathy remains unclear. Smad3 knockout (KO)-db/db mice were generated by intercrossing of mal...
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Published in | Metabolism, clinical and experimental Vol. 103; p. 154013 |
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Abstract | Transforming growth factor (TGF)-β/Smad3 signaling is highly activated in kidneys of patients with type 2 diabetic nephropathy (T2DN), however, the precise role of Smad3 in the pathogenesis of diabetic nephropathy remains unclear.
Smad3 knockout (KO)-db/db mice were generated by intercrossing of male and female double-heterozygous Smad3+/− db/m mice. Renal functions including urinary albumin excretion and serum creatinine were determined. Renal histological injury including renal fibrosis and inflammation were examined by periodic acid Schiff (PAS), periodic acid-silver methenamine (PASM), and immunohistochemistry (IHC) staining.
Smad3 knockout (KO)-db/db mice were protected from the development of diabetic kidney injury, characterized by the normal levels of urinary albumin excretion and serum creatinine without any evidence for renal fibrosis and inflammation. In contrast, Smad3 wild-type (WT) db/db and Smad3+/− db/db mice developed progressively decline in renal function over the 12 to 32-week time course, including increased microalbuminuria and elevated levels of serum creatinine. Pathologically, Smad3 WT db/db and Smad3+/− db/db mice exhibited a marked deposition of collagen-I (colI), collagen-IV(col-IV), and an increased infiltration of F4/80+ macrophages in kidney. Mechanistically, Smad3 deficiency decreased the lncRNA Erbb4-IR transcription, while increased miR-29b transcription and therefore protected the kidney from progressive renal injury in db/db mice.
Results from this study imply that Smad3 may represent as a novel and effective therapeutic target for T2DN.
•Smad3 deficiency prevents renal dysfunction in type 2 diabetic nephropathy.•Smad3 deficiency prevents renal fibrosis and inflammation in type 2 diabetic nephropathy.•Smad3 deficiency decreased the lncRNA Erbb4-IR transcription, while increased miR-29b transcription. |
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AbstractList | Transforming growth factor (TGF)-β/Smad3 signaling is highly activated in kidneys of patients with type 2 diabetic nephropathy (T2DN), however, the precise role of Smad3 in the pathogenesis of diabetic nephropathy remains unclear.
Smad3 knockout (KO)-db/db mice were generated by intercrossing of male and female double-heterozygous Smad3
db/m mice. Renal functions including urinary albumin excretion and serum creatinine were determined. Renal histological injury including renal fibrosis and inflammation were examined by periodic acid Schiff (PAS), periodic acid-silver methenamine (PASM), and immunohistochemistry (IHC) staining.
Smad3 knockout (KO)-db/db mice were protected from the development of diabetic kidney injury, characterized by the normal levels of urinary albumin excretion and serum creatinine without any evidence for renal fibrosis and inflammation. In contrast, Smad3 wild-type (WT) db/db and Smad3
db/db mice developed progressively decline in renal function over the 12 to 32-week time course, including increased microalbuminuria and elevated levels of serum creatinine. Pathologically, Smad3 WT db/db and Smad3
db/db mice exhibited a marked deposition of collagen-I (colI), collagen-IV(col-IV), and an increased infiltration of F4/80
macrophages in kidney. Mechanistically, Smad3 deficiency decreased the lncRNA Erbb4-IR transcription, while increased miR-29b transcription and therefore protected the kidney from progressive renal injury in db/db mice.
Results from this study imply that Smad3 may represent as a novel and effective therapeutic target for T2DN. BACKGROUNDTransforming growth factor (TGF)-β/Smad3 signaling is highly activated in kidneys of patients with type 2 diabetic nephropathy (T2DN), however, the precise role of Smad3 in the pathogenesis of diabetic nephropathy remains unclear. METHODSSmad3 knockout (KO)-db/db mice were generated by intercrossing of male and female double-heterozygous Smad3+/- db/m mice. Renal functions including urinary albumin excretion and serum creatinine were determined. Renal histological injury including renal fibrosis and inflammation were examined by periodic acid Schiff (PAS), periodic acid-silver methenamine (PASM), and immunohistochemistry (IHC) staining. RESULTSSmad3 knockout (KO)-db/db mice were protected from the development of diabetic kidney injury, characterized by the normal levels of urinary albumin excretion and serum creatinine without any evidence for renal fibrosis and inflammation. In contrast, Smad3 wild-type (WT) db/db and Smad3+/- db/db mice developed progressively decline in renal function over the 12 to 32-week time course, including increased microalbuminuria and elevated levels of serum creatinine. Pathologically, Smad3 WT db/db and Smad3+/- db/db mice exhibited a marked deposition of collagen-I (colI), collagen-IV(col-IV), and an increased infiltration of F4/80+ macrophages in kidney. Mechanistically, Smad3 deficiency decreased the lncRNA Erbb4-IR transcription, while increased miR-29b transcription and therefore protected the kidney from progressive renal injury in db/db mice. CONCLUSIONResults from this study imply that Smad3 may represent as a novel and effective therapeutic target for T2DN. Transforming growth factor (TGF)-β/Smad3 signaling is highly activated in kidneys of patients with type 2 diabetic nephropathy (T2DN), however, the precise role of Smad3 in the pathogenesis of diabetic nephropathy remains unclear. Smad3 knockout (KO)-db/db mice were generated by intercrossing of male and female double-heterozygous Smad3+/− db/m mice. Renal functions including urinary albumin excretion and serum creatinine were determined. Renal histological injury including renal fibrosis and inflammation were examined by periodic acid Schiff (PAS), periodic acid-silver methenamine (PASM), and immunohistochemistry (IHC) staining. Smad3 knockout (KO)-db/db mice were protected from the development of diabetic kidney injury, characterized by the normal levels of urinary albumin excretion and serum creatinine without any evidence for renal fibrosis and inflammation. In contrast, Smad3 wild-type (WT) db/db and Smad3+/− db/db mice developed progressively decline in renal function over the 12 to 32-week time course, including increased microalbuminuria and elevated levels of serum creatinine. Pathologically, Smad3 WT db/db and Smad3+/− db/db mice exhibited a marked deposition of collagen-I (colI), collagen-IV(col-IV), and an increased infiltration of F4/80+ macrophages in kidney. Mechanistically, Smad3 deficiency decreased the lncRNA Erbb4-IR transcription, while increased miR-29b transcription and therefore protected the kidney from progressive renal injury in db/db mice. Results from this study imply that Smad3 may represent as a novel and effective therapeutic target for T2DN. •Smad3 deficiency prevents renal dysfunction in type 2 diabetic nephropathy.•Smad3 deficiency prevents renal fibrosis and inflammation in type 2 diabetic nephropathy.•Smad3 deficiency decreased the lncRNA Erbb4-IR transcription, while increased miR-29b transcription. |
ArticleNumber | 154013 |
Author | Sheng, Jingyi Xu, Bi-Hua You, Yong-Ke Huang, Xiao-Ru Lan, Hui-Yao Wang, Qingwen Ma, Ronald C.W. |
Author_xml | – sequence: 1 givenname: Bi-Hua surname: Xu fullname: Xu, Bi-Hua organization: Department of Rheumatism and Immunology, Peking University Shenzhen Hospital, Shenzhen, China – sequence: 2 givenname: Jingyi surname: Sheng fullname: Sheng, Jingyi organization: Department of Rheumatism and Immunology, Peking University Shenzhen Hospital, Shenzhen, China – sequence: 3 givenname: Yong-Ke surname: You fullname: You, Yong-Ke organization: Department of Rheumatism and Immunology, Peking University Shenzhen Hospital, Shenzhen, China – sequence: 4 givenname: Xiao-Ru surname: Huang fullname: Huang, Xiao-Ru organization: Department of Rheumatism and Immunology, Peking University Shenzhen Hospital, Shenzhen, China – sequence: 5 givenname: Ronald C.W. surname: Ma fullname: Ma, Ronald C.W. organization: Department of Rheumatism and Immunology, Peking University Shenzhen Hospital, Shenzhen, China – sequence: 6 givenname: Qingwen surname: Wang fullname: Wang, Qingwen email: wqw_sw@163.com organization: Department of Medicine & Therapeutics, Li Ka Shing Institute of Health Sciences, Lui Chi Woo Institute of Innovative Medicine, The Chinese University of Hong Kong, Hong Kong, China – sequence: 7 givenname: Hui-Yao surname: Lan fullname: Lan, Hui-Yao email: hylan@cuhk.edu.hk organization: Department of Rheumatism and Immunology, Peking University Shenzhen Hospital, Shenzhen, China |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31734275$$D View this record in MEDLINE/PubMed |
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Keywords | EndoMT T1DN MCP-1 PAS IHC JNK LncRNA DN ICAM-1 T2DN CTGF SE GBM ANOVA Col-IV STZ P-NF-κB/65 TGF-β Diabetic nephropathy AngII WT AGE DAB KO VEGF Inflammation IL-8 MAPK EMT IL-6 PASM UUO ACR P-IκBα SIS3 Smad3 and TGF-β TNF-α Fibrosis Col-I P-Smad3 PCR Erk |
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article-title: Targeted disruption of TGF-beta1/Smad3 signaling protects against renal tubulointerstitial fibrosis induced by unilateral ureteral obstruction publication-title: J Clin Invest doi: 10.1172/JCI200319270 contributor: fullname: Sato |
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Snippet | Transforming growth factor (TGF)-β/Smad3 signaling is highly activated in kidneys of patients with type 2 diabetic nephropathy (T2DN), however, the precise... BACKGROUNDTransforming growth factor (TGF)-β/Smad3 signaling is highly activated in kidneys of patients with type 2 diabetic nephropathy (T2DN), however, the... |
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SubjectTerms | Albuminuria - complications Albuminuria - genetics Animals Diabetes Mellitus, Experimental - complications Diabetes Mellitus, Experimental - genetics Diabetes Mellitus, Type 2 - complications Diabetes Mellitus, Type 2 - genetics Diabetic Nephropathies - genetics Diabetic Nephropathies - prevention & control Diabetic nephropathy Female Fibrosis Fibrosis - genetics Fibrosis - prevention & control Gene Deletion Inflammation Kidney - pathology Male Mice Mice, Inbred C57BL Mice, Knockout Smad3 and TGF-β Smad3 Protein - genetics |
Title | Deletion of Smad3 prevents renal fibrosis and inflammation in type 2 diabetic nephropathy |
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