Thiazolidinedione attenuate proteinuria and glomerulosclerosis in Adriamycin-induced nephropathy rats via slit diaphragm protection
Aim: The slit diaphragm (SD) of podocyte impairment contributes to massive proteinuria and progressive glomerulosclerosis in many human glomerular diseases. The aim of the study was to determine if thiazolidinedione (TZD) reduce proteinuria and glomerulosclerosis in focal segmental glomeruloscleros...
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Published in | Nephrology (Carlton, Vic.) Vol. 15; no. 1; pp. 75 - 83 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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Melbourne, Australia
Blackwell Publishing Asia
01.02.2010
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Abstract | Aim: The slit diaphragm (SD) of podocyte impairment contributes to massive proteinuria and progressive glomerulosclerosis in many human glomerular diseases. The aim of the study was to determine if thiazolidinedione (TZD) reduce proteinuria and glomerulosclerosis in focal segmental glomerulosclerosis (FSGS) by preserving the structure and function of SD.
Methods: Adriamycin‐induced FSGS rat models were employed. Urinary protein content was measured dynamically during the experiment. Additional biochemical parameters in serum samples were measured after the animals were killed. Glomerular sclerosis index (SI) and podocyte foot processes fusion rate (PFR) were evaluated. The protein and mRNA expressing levels of nephrin, podocin and CD2‐associated protein (CD2AP) in glomeruli were assessed by immunohistochemistry and real‐time quantitative polymerase chain reaction, respectively. The density of podocytes was also evaluated after anti‐Wilms' tumour‐1 immunohistochemical staining.
Results: Rosiglitazone treatment partially reduced proteinuria, but did not significantly affect the serum levels of triglyceride, cholesterol, albumin, glucose, urea nitrogen and creatinine in Adriamycin‐induced FSGS rats. Glomerular SI and podocyte foot PFR were significantly attenuated by rosiglitazone treatment. Rosiglitazone prevented the reduction of nephrin, podocin and CD2AP protein expression induced by Adriamycin, however, the mRNA expression levels of these SD‐related markers did not change significantly. Rosiglitazone therapy did not reverse Adriamycin‐mediated reduction of the density of podocytes.
Conclusions: The study data suggest that TZD are promising therapeutic agents on FSGS, and the mechanism may be mediated in part by directly protecting the structure and function of SD.
This study provides direct evidence that the PPAR‐γ agonist, rosiglitazone, can protect against the loss of podocyte foot processes and down‐regulation of podocyte slit diaphragm proteins in experimental focal and segmental glomerulosclerosis. Interestingly, rosiglitazone reduced the degree of glomerulosclerosis and proteinuria, but did not prevent the loss of WT‐1+ podocytes. |
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AbstractList | The slit diaphragm (SD) of podocyte impairment contributes to massive proteinuria and progressive glomerulosclerosis in many human glomerular diseases. The aim of the study was to determine if thiazolidinedione (TZD) reduce proteinuria and glomerulosclerosis in focal segmental glomerulosclerosis (FSGS) by preserving the structure and function of SD.
Adriamycin-induced FSGS rat models were employed. Urinary protein content was measured dynamically during the experiment. Additional biochemical parameters in serum samples were measured after the animals were killed. Glomerular sclerosis index (SI) and podocyte foot processes fusion rate (PFR) were evaluated. The protein and mRNA expressing levels of nephrin, podocin and CD2-associated protein (CD2AP) in glomeruli were assessed by immunohistochemistry and real-time quantitative polymerase chain reaction, respectively. The density of podocytes was also evaluated after anti-Wilms' tumour-1 immunohistochemical staining.
Rosiglitazone treatment partially reduced proteinuria, but did not significantly affect the serum levels of triglyceride, cholesterol, albumin, glucose, urea nitrogen and creatinine in Adriamycin-induced FSGS rats. Glomerular SI and podocyte foot PFR were significantly attenuated by rosiglitazone treatment. Rosiglitazone prevented the reduction of nephrin, podocin and CD2AP protein expression induced by Adriamycin, however, the mRNA expression levels of these SD-related markers did not change significantly. Rosiglitazone therapy did not reverse Adriamycin-mediated reduction of the density of podocytes.
The study data suggest that TZD are promising therapeutic agents on FSGS, and the mechanism may be mediated in part by directly protecting the structure and function of SD. Aim: The slit diaphragm (SD) of podocyte impairment contributes to massive proteinuria and progressive glomerulosclerosis in many human glomerular diseases. The aim of the study was to determine if thiazolidinedione (TZD) reduce proteinuria and glomerulosclerosis in focal segmental glomerulosclerosis (FSGS) by preserving the structure and function of SD. Methods: Adriamycin‐induced FSGS rat models were employed. Urinary protein content was measured dynamically during the experiment. Additional biochemical parameters in serum samples were measured after the animals were killed. Glomerular sclerosis index (SI) and podocyte foot processes fusion rate (PFR) were evaluated. The protein and mRNA expressing levels of nephrin, podocin and CD2‐associated protein (CD2AP) in glomeruli were assessed by immunohistochemistry and real‐time quantitative polymerase chain reaction, respectively. The density of podocytes was also evaluated after anti‐Wilms' tumour‐1 immunohistochemical staining. Results: Rosiglitazone treatment partially reduced proteinuria, but did not significantly affect the serum levels of triglyceride, cholesterol, albumin, glucose, urea nitrogen and creatinine in Adriamycin‐induced FSGS rats. Glomerular SI and podocyte foot PFR were significantly attenuated by rosiglitazone treatment. Rosiglitazone prevented the reduction of nephrin, podocin and CD2AP protein expression induced by Adriamycin, however, the mRNA expression levels of these SD‐related markers did not change significantly. Rosiglitazone therapy did not reverse Adriamycin‐mediated reduction of the density of podocytes. Conclusions: The study data suggest that TZD are promising therapeutic agents on FSGS, and the mechanism may be mediated in part by directly protecting the structure and function of SD. This study provides direct evidence that the PPAR‐γ agonist, rosiglitazone, can protect against the loss of podocyte foot processes and down‐regulation of podocyte slit diaphragm proteins in experimental focal and segmental glomerulosclerosis. Interestingly, rosiglitazone reduced the degree of glomerulosclerosis and proteinuria, but did not prevent the loss of WT‐1+ podocytes. Aim: The slit diaphragm (SD) of podocyte impairment contributes to massive proteinuria and progressive glomerulosclerosis in many human glomerular diseases. The aim of the study was to determine if thiazolidinedione (TZD) reduce proteinuria and glomerulosclerosis in focal segmental glomerulosclerosis (FSGS) by preserving the structure and function of SD. Methods: Adriamycin‐induced FSGS rat models were employed. Urinary protein content was measured dynamically during the experiment. Additional biochemical parameters in serum samples were measured after the animals were killed. Glomerular sclerosis index (SI) and podocyte foot processes fusion rate (PFR) were evaluated. The protein and mRNA expressing levels of nephrin, podocin and CD2‐associated protein (CD2AP) in glomeruli were assessed by immunohistochemistry and real‐time quantitative polymerase chain reaction, respectively. The density of podocytes was also evaluated after anti‐Wilms' tumour‐1 immunohistochemical staining. Results: Rosiglitazone treatment partially reduced proteinuria, but did not significantly affect the serum levels of triglyceride, cholesterol, albumin, glucose, urea nitrogen and creatinine in Adriamycin‐induced FSGS rats. Glomerular SI and podocyte foot PFR were significantly attenuated by rosiglitazone treatment. Rosiglitazone prevented the reduction of nephrin, podocin and CD2AP protein expression induced by Adriamycin, however, the mRNA expression levels of these SD‐related markers did not change significantly. Rosiglitazone therapy did not reverse Adriamycin‐mediated reduction of the density of podocytes. Conclusions: The study data suggest that TZD are promising therapeutic agents on FSGS, and the mechanism may be mediated in part by directly protecting the structure and function of SD. This study provides direct evidence that the PPAR‐γ agonist, rosiglitazone, can protect against the loss of podocyte foot processes and down‐regulation of podocyte slit diaphragm proteins in experimental focal and segmental glomerulosclerosis. Interestingly, rosiglitazone reduced the degree of glomerulosclerosis and proteinuria, but did not prevent the loss of WT‐1+ podocytes. AIMThe slit diaphragm (SD) of podocyte impairment contributes to massive proteinuria and progressive glomerulosclerosis in many human glomerular diseases. The aim of the study was to determine if thiazolidinedione (TZD) reduce proteinuria and glomerulosclerosis in focal segmental glomerulosclerosis (FSGS) by preserving the structure and function of SD.METHODSAdriamycin-induced FSGS rat models were employed. Urinary protein content was measured dynamically during the experiment. Additional biochemical parameters in serum samples were measured after the animals were killed. Glomerular sclerosis index (SI) and podocyte foot processes fusion rate (PFR) were evaluated. The protein and mRNA expressing levels of nephrin, podocin and CD2-associated protein (CD2AP) in glomeruli were assessed by immunohistochemistry and real-time quantitative polymerase chain reaction, respectively. The density of podocytes was also evaluated after anti-Wilms' tumour-1 immunohistochemical staining.RESULTSRosiglitazone treatment partially reduced proteinuria, but did not significantly affect the serum levels of triglyceride, cholesterol, albumin, glucose, urea nitrogen and creatinine in Adriamycin-induced FSGS rats. Glomerular SI and podocyte foot PFR were significantly attenuated by rosiglitazone treatment. Rosiglitazone prevented the reduction of nephrin, podocin and CD2AP protein expression induced by Adriamycin, however, the mRNA expression levels of these SD-related markers did not change significantly. Rosiglitazone therapy did not reverse Adriamycin-mediated reduction of the density of podocytes.CONCLUSIONSThe study data suggest that TZD are promising therapeutic agents on FSGS, and the mechanism may be mediated in part by directly protecting the structure and function of SD. |
Author | LI, SHANG-MEI HUANG, YU-YING TAO, JING-LI LIU, HUA-FENG GUO, LI-QIN CHEN, KENG CHEN, XIAO-WEN |
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Snippet | Aim: The slit diaphragm (SD) of podocyte impairment contributes to massive proteinuria and progressive glomerulosclerosis in many human glomerular diseases.... The slit diaphragm (SD) of podocyte impairment contributes to massive proteinuria and progressive glomerulosclerosis in many human glomerular diseases. The aim... Aim: The slit diaphragm (SD) of podocyte impairment contributes to massive proteinuria and progressive glomerulosclerosis in many human glomerular diseases.... AIMThe slit diaphragm (SD) of podocyte impairment contributes to massive proteinuria and progressive glomerulosclerosis in many human glomerular diseases. The... |
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SubjectTerms | Animals Doxorubicin - administration & dosage Glomerulosclerosis, Focal Segmental - prevention & control Kidney Diseases - chemically induced Kidney Diseases - complications Male podocyte Podocytes - drug effects podocythopathy proteinuria Proteinuria - prevention & control Rats Rats, Sprague-Dawley slit diaphragm thiazolidinedione Thiazolidinediones - therapeutic use |
Title | Thiazolidinedione attenuate proteinuria and glomerulosclerosis in Adriamycin-induced nephropathy rats via slit diaphragm protection |
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