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Title:
Rapamycin promotes podocyte autophagy and ameliorates renal injury in diabetic mice | Molecular and Cellular Biochemistry
Description:
The aim was to explore the effects of rapamycin on autophagy and injury of podocytes in streptozocin (STZ)-induced type 1 diabetic mice, and its role in delaying progression of diabetic nephropathy. In this study, male Balb/c mice were divided into three groups: control (n = 12), STZ-induced diabetic (n = 12), and rapamycin-treated diabetic (DM + Rapa) (n = 12), which received intraperitoneal injection of rapamycin (2 mg/kg/48 h) after induction of DM. Levels of urinary albumin (UA), blood urea nitrogen, serum creatinine, and kidney weight/body weight were measured at week 12. Renal pathologic changes, number of podocytes autophagy, and organelles injury were investigated by PAS staining, transmission electron microscopy, and immunofluorescence staining, respectively. Western blot was performed to determine the expression of LC3 (a podocyte autophagy marker), phosphorylated mammalian target of rapamycin, p-p70S6K, bax, and caspase-3 protein. Podocytes count was evaluated by immunofluorescence staining and Wilms tumor 1 immunohistochemistry, and Western blot of nephrin and podocin. The results indicated that rapamycin could reduce the kidney weight/body weight and UA secretion. It could alleviate podocyte foot process fusion, glomerular basement membrane thickening, and matrix accumulation, and increase the number of autophagosomes, and LC3-expressing podocytes. Down-regulation of bax and caspase-3 protein, and up-regulation of nephrin and podocin protein were observed in the glomeruli of diabetic mice after administration of rapamycin. In conclusion, rapamycin can ameliorate renal injury in diabetic mice by increasing the autophagy activity and inhibition of apoptosis of podocytes.
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Keywords {š}
article, google, scholar, pubmed, diabetic, cas, rapamycin, nephropathy, autophagy, podocyte, injury, kidney, mice, wang, zhao, cell, podocytes, renal, diabetes, central, guan, access, disease, mol, biochem, mtor, privacy, cookies, content, type, glomerular, liu, development, nephrol, publish, research, search, ameliorates, huang, yang, progression, cells, int, rats, clin, chen, china, function, data, information,
Topics {āļø}
month download article/chapter hyperglycemia-induced podocyte injury ampkα-regulated autophagy induction kidney weight/body weight related subjects cellular biochemistry aims full article pdf growth signal integration podocyte autophagy marker privacy choices/manage cookies pi3k-induced stat1/3 stz-induced diabetic experimental diabetic nephropathy glomerular epithelial cells oxidative stress parameters chronic allograft nephropathy diabetic renal injury rapamycin-treated diabetic ameliorates renal injury diabetic kidney disease ghrl gene prevents maintains podocyte homeostasis hepg2 hepatocyte cells mtor pathway article xiao check access instant access article molecular ameliorate renal injury european economic area ke yang received intraperitoneal injection transmission electron microscopy single intravenous injection asians versus whites phosphatidylinositol kinase homologue usf1 transcription factor shu-chien ac strong therapeutic potential wiggins rc proteinuric experimental nephropathies military medical university conditions privacy policy de cavaglieri cassia diabetic mice published article log de azevedo mj accepting optional cookies diabetic rats treated blood urea nitrogen
Questions {ā}
- Baehrecke EH (2005) Autophagy: dual roles in life and death?
- Lasaridis AN, Sarafidis PA (2003) Diabetic nephropathy and antihypertensive treatment: what are the lessons from clinical trials?
- Lu MK, Gong XG, Guan KL (2011) mTOR in podocyte function: is rapamycin good for diabetic nephropathy?
- Skoberne A, Konieczny A, Schiffer M (2009) Glomerular epithelial cells in the urine: what has to be done to make them worthwhile?
- Torras J, Herrero-Fresneda I, Gulias O, Flaguer M, Vidal A, Cruzado JM, Lioberas N, Franguesa MI, Grinyo JM (2009) Rapamycin has dual opposing effects on proteinuric experimental nephropathies: is it a matter of podocyte damage?
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headline:Rapamycin promotes podocyte autophagy and ameliorates renal injury in diabetic mice
description:The aim was to explore the effects of rapamycin on autophagy and injury of podocytes in streptozocin (STZ)-induced type 1 diabetic mice, and its role in delaying progression of diabetic nephropathy. In this study, male Balb/c mice were divided into three groups: control (nĀ =Ā 12), STZ-induced diabetic (nĀ =Ā 12), and rapamycin-treated diabetic (DMĀ +Ā Rapa) (nĀ =Ā 12), which received intraperitoneal injection of rapamycin (2Ā mg/kg/48Ā h) after induction of DM. Levels of urinary albumin (UA), blood urea nitrogen, serum creatinine, and kidney weight/body weight were measured at week 12. Renal pathologic changes, number of podocytes autophagy, and organelles injury were investigated by PAS staining, transmission electron microscopy, and immunofluorescence staining, respectively. Western blot was performed to determine the expression of LC3 (a podocyte autophagy marker), phosphorylated mammalian target of rapamycin, p-p70S6K, bax, and caspase-3 protein. Podocytes count was evaluated by immunofluorescence staining and Wilms tumor 1 immunohistochemistry, and Western blot of nephrin and podocin. The results indicated that rapamycin could reduce the kidney weight/body weight and UA secretion. It could alleviate podocyte foot process fusion, glomerular basement membrane thickening, and matrix accumulation, and increase the number of autophagosomes, and LC3-expressing podocytes. Down-regulation of bax and caspase-3 protein, and up-regulation of nephrin and podocin protein were observed in the glomeruli of diabetic mice after administration of rapamycin. In conclusion, rapamycin can ameliorate renal injury in diabetic mice by increasing the autophagy activity and inhibition of apoptosis of podocytes.
datePublished:2014-05-22T00:00:00Z
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Rapamycin
Podocyte injury
Autophagy
mTOR signal pathway
Diabetic nephropathy
Biochemistry
general
Cardiology
Cancer Research
Medical Biochemistry
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headline:Rapamycin promotes podocyte autophagy and ameliorates renal injury in diabetic mice
description:The aim was to explore the effects of rapamycin on autophagy and injury of podocytes in streptozocin (STZ)-induced type 1 diabetic mice, and its role in delaying progression of diabetic nephropathy. In this study, male Balb/c mice were divided into three groups: control (nĀ =Ā 12), STZ-induced diabetic (nĀ =Ā 12), and rapamycin-treated diabetic (DMĀ +Ā Rapa) (nĀ =Ā 12), which received intraperitoneal injection of rapamycin (2Ā mg/kg/48Ā h) after induction of DM. Levels of urinary albumin (UA), blood urea nitrogen, serum creatinine, and kidney weight/body weight were measured at week 12. Renal pathologic changes, number of podocytes autophagy, and organelles injury were investigated by PAS staining, transmission electron microscopy, and immunofluorescence staining, respectively. Western blot was performed to determine the expression of LC3 (a podocyte autophagy marker), phosphorylated mammalian target of rapamycin, p-p70S6K, bax, and caspase-3 protein. Podocytes count was evaluated by immunofluorescence staining and Wilms tumor 1 immunohistochemistry, and Western blot of nephrin and podocin. The results indicated that rapamycin could reduce the kidney weight/body weight and UA secretion. It could alleviate podocyte foot process fusion, glomerular basement membrane thickening, and matrix accumulation, and increase the number of autophagosomes, and LC3-expressing podocytes. Down-regulation of bax and caspase-3 protein, and up-regulation of nephrin and podocin protein were observed in the glomeruli of diabetic mice after administration of rapamycin. In conclusion, rapamycin can ameliorate renal injury in diabetic mice by increasing the autophagy activity and inhibition of apoptosis of podocytes.
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Rapamycin
Podocyte injury
Autophagy
mTOR signal pathway
Diabetic nephropathy
Biochemistry
general
Cardiology
Cancer Research
Medical Biochemistry
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