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Cell-type-specific activation of mitogen-activated protein kinases in PAN-induced progressive renal disease in rats
Sang-Joon Park1, Kyu-Shik Jeong
1College of Veterinary Medicine, Kyungpook National University, Daegu 702-701, Republic of Korea.
Abstract:
We examined the time-course activation and the cell-type specific role of MAP kinases in puromycin aminonucleoside (PAN)-induced renal disease. The maximal activation of c-Jun-NH2-terminal kinase (JNK), extracellular signal regulated kinase (ERK), and p38 MAP kinase was detected on Days 52, 38, and 38 after PAN-treatment, respectively. p-JNK was localized in mesangial and proximal tubular cells at the early renal injury. It was expressed, therefore, in the inflammatory cells of tubulointerstitial lesions. While, p-ERK was markedly increased in the glomerular regions and macrophages p-p38 was observed in glomerular endothelial cells, tubular cells, and some inflammatory cells. The results show that the activation of MAP kinases in the early renal injury by PAN-treatment involves cellular changes such as cell proliferation or apoptosis in renal native cells. The activation of MAP kinases in infiltrated inflammatory cells and fibrotic cells plays an important role in destructive events such as glomerulosclerosis and tubulointerstitial fibrosis.
Insights
Mitogen-activated protein (MAP) kinases, including JNK, ERK, and p38, are activated during puromycin aminonucleoside (PAN)-induced kidney disease. Their activation in renal and inflammatory cells contributes to glomerulosclerosis and fibrosis.
Area of Science:
- Nephrology
- Molecular Biology
- Cell Biology
Background:
- Puromycin aminonucleoside (PAN) induces renal disease, characterized by glomerular and tubulointerstitial damage.
- Mitogen-activated protein (MAP) kinases are crucial signaling molecules involved in cellular responses to injury.
Purpose of the Study:
- To investigate the time-course activation and cell-type specific roles of JNK, ERK, and p38 MAP kinases in PAN-induced renal disease.
- To elucidate the involvement of MAP kinases in the pathogenesis of glomerulosclerosis and tubulointerstitial fibrosis.
Main Methods:
- PAN was administered to induce renal disease in a rodent model.
- Immunohistochemistry was used to detect the activation and localization of phosphorylated JNK, ERK, and p38.
- Time-course analysis of MAP kinase activation was performed.
Main Results:
- Maximal activation of JNK, ERK, and p38 occurred at specific time points post-PAN treatment (Days 5, 3, and 3, respectively).
- Activated JNK was found in mesangial, proximal tubular, and inflammatory cells.
- Activated ERK was prominent in glomerular regions and macrophages, while activated p38 was observed in glomerular endothelial cells, tubular cells, and inflammatory cells.
Conclusions:
- MAP kinase activation in renal native cells during early injury is linked to cellular proliferation and apoptosis.
- MAP kinase activation in inflammatory and fibrotic cells plays a significant role in the development of glomerulosclerosis and tubulointerstitial fibrosis.
- Targeting MAP kinase pathways may offer therapeutic potential for mitigating kidney damage in related diseases.
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