12 research outputs found
Purinergic inhibition of Na+,K+,Cl− cotransport in C11-MDCK cells: Role of stress-activated protein kinases
Previously, we observed that sustained activation of P2Y1 leads to inhibition of Na+,K+,Cl− cotransport (NKCC) in C11 cells resembling intercalated cells from collecting ducts of the Madin-Darby canine kidney. This study examined the role of stress-activated protein kinases (SAPK) in NKCC inhibition triggered by purinergic receptors. Treatment of C11 cells with ATP led to sustained phosphorylation of SAPK such as JNK and p38. Activation of these kinases also occurred in anisomycin-treated cells. Surprisingly, we observed that compounds SP600125 and SB202190, known as potent inhibitors of JNK and p38 in cell-free systems, activated rather than inhibited phosphorylation of the kinases in C11 cells. Importantly, similarly to ATP, all the above-listed activators of JNK and p38 phosphorylation inhibited NKCC. Thus, our results suggest that activation of JNK and/or p38 contributes to NKCC suppression detected in intercalated-like cells from distal tubules after their exposure to P2Y1 agonists
Effect of Transforming Growth Factor-β1, Interleukin-6, and Interferon-γ on the Expression of Type I Collagen, Heat Shock Protein 47, Matrix Metalloproteinase (MMP)-1 and MMP-2 by Fibroblasts from Normal Gingiva and Hereditary Gingival Fibromatosis
Interleukin-1β-Induced Transdifferentiation of Renal Proximal Tubular Cells Is Mediated by Activation of JNK and p38 MAPK
Analysis of differentially expressed advanced glycation end product-modified proteins in diabetic rat kidney
Plant growth enhancement and associated physiological responses are coregulated by ethylene and gibberellin in response to harpin protein Hpa1
Angiotensin-Converting Enzyme Inhibition Decreases Growth Factor Expression in the Neonatal Rat Kidney
Tubular iron deposition and iron handling proteins in human healthy kidney and chronic kidney disease
Iron metabolism in the pathogenesis of iron-induced kidney injury
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118694.pdf (postprint version ) (Open Access)In the past 8 years, there has been renewed interest in the role of iron in both acute kidney injury (AKI) and chronic kidney disease (CKD). In patients with kidney diseases, renal tubules are exposed to a high concentration of iron owing to increased glomerular filtration of iron and iron-containing proteins, including haemoglobin, transferrin and neutrophil gelatinase-associated lipocalin (NGAL). Levels of intracellular catalytic iron may increase when glomerular and renal tubular cells are injured. Reducing the excessive luminal or intracellular levels of iron in the kidney could be a promising approach to treat AKI and CKD. Understanding the role of iron in kidney injury and as a therapeutic target requires insight into the mechanisms of iron metabolism in the kidney, the role of endogenous proteins involved in iron chelation and transport, including hepcidin, NGAL, the NGAL receptor and divalent metal transporter 1, and iron-induced toxic effects. This Review summarizes emerging knowledge, which suggests that complex mechanisms of iron metabolism exist in the kidney, modulated directly or indirectly by cellular iron content, inflammation, ischaemia and oxidative stress. The potential exists for prevention and treatment of iron-induced kidney injury by customized iron removal or relocation, aided by detailed insight into the underlying pathological mechanisms