No abstract available.
Iron* ; Mesangial Cells* ; Perfusion*

No abstract available.
Collagen* ; Heparin* ; Mesangial Cells*

No abstract available.
Extracellular Matrix* ; Glucose* ; Mesangial Cells*

No abstract available.
Animals ; Epidermal Growth Factor* ; Mesangial Cells* ; Rats*

No abstract available.
Collagen* ; Glucose* ; Insulin* ; Mesangial Cells* ; Somatostatin*

Mesangial cell proliferation contributes to the development of glomerulonephritis and is associated with glomerulosclerosis. It has been reported that IL-6 is a pluri-potent cytokine which is involved in the mesangial inflammation and the activation of IL-6 is related to the recruitment of transcriptional factors or cytokines such as IL-1beta. It has been known that bacterial infection sometimes precedes the exacerbation of glomerulonephritis and bacterial LPS, a potent activator of IL-6, is presumed to be one of the mediators of this inflammatory process. To understand the underlying mechanisms of how IL-6 is activated by LPS, we examined the serial changes of the expression of IL-1beta, IL-6 and NF IL-6(nuclear factor for IL-6) using the growth arrested human mesangial cells at 0, 2, 4, 8, and 18 hours after LPS stimulation. Exposure of serum-free mesangial cells to LPS resulted in the production and the expression of IL-1beta and IL-6. However, there was a steady increase of IL-1b expression throughout the 18 hours, while the peak expression of IL-6 was around 4 hours after LPS stimulation and this peak expression of IL-6 was preceded by NF IL-6. Interestingly, the NF IL-6 expression was not observed in the IL-6 stimulation by r-IL-1beta stimulation. Furthermore, the addition of anti-IL-1beta prior to the LPS stimulation reduced the IL-6 expression partially, but, it did not affect the NF IL-6 expression. These results demonstrated that the mesangial IL-6 expression by LPS is mediated by NF IL-6 as well as IL-1beta in a separate pathways. The capacity of LPS to express IL-6 by these mechanisms may play a role in the mesangial inflammatory process.
Bacterial Infections ; Cytokines ; Glomerulonephritis ; Humans* ; Inflammation ; Interleukin-6* ; Mesangial Cells

No abstract available.
Chemokine CCL2* ; Humans* ; Mesangial Cells* ; Monocytes* ; Reactive Oxygen Species*

No abstract available.
Animals ; Glucose* ; Mesangial Cells* ; Phospholipases A2* ; Phospholipases* ; Rats*

To depend body potassium balance during chronic hypokalemia, the kidney actively reabsorbs potassium. Previous work suggested that potassium reclamation occurred at the distal tubule and collecting duct. We used immunohistochemistry of normal and potassium-deprived(two weeks) rats to determine the intrarenal distribution and alteration of expression of Na/K-ATPase alpha1 and beta1 subunit protein and also whether the increased numbers of both subunits reside in the apical or basolateral membranes. In the normal rats, alpha1 and beta1 immunoreactivity was prominent in the medullary and cortical thick ascending limb, distal convoluted tubule, and connecting segment. Cortical collecting duct, glomerular epithelial cell, and intraglomerular mesangial cell exhibited moderate immunoreactivity, whereas proximal tubule and medullary collecting duct were weakly labeled in alpha1 subunit. In beta1 subunit, cortical collecting duct and proximal tubule exhibited moderate immunoreactivity, and medullary collecting duct was very weakly labeled. In the K-deprived rats, a pattern of cellular labeling of both subunits was identical to that of normal rats. Marked increases of immunoreactivity were evident in the inner stripe of the outer medullary collecting duct and proximal portion of the inner medullary collecting duct. In these segment, alpha1 and beta1 immunoreactivity was expressed at the basolateral pole, and no apical expression was detected. In contrast, immunoreactivity of the medullary and cortical thick ascending limb, distal convoluted tubule, connecting segment, and cortical collecting duct was decreased. These results suggest that Na/K-ATPase alpha1 and beta1 subunit are differentially expressed in different nephron segments and chronic hypokalemia must also upregulate K exit pathways in the basolateral membrane of inner stripe of the outer medullary collecting duct and proximal portion of the inner medullary collecting duct to promote recycling and limit secretion of K.
Animals ; Epithelial Cells ; Extremities ; Hypokalemia* ; Immunohistochemistry ; Kidney ; Membranes ; Mesangial Cells ; Nephrons ; Potassium ; Rats ; Recycling

This study was designed to investigate the mole- cular mechanism of chemokine induction by lipopoly-saccharide(LPS) of E. coli. Chemokine gene expression was evaluated by the reverse transcriptase-polymerase chain reaction(RT-PCR) assay using RNAs isolated either from kidneys of LPS-injected inice or from the mesangial cells stimulated with LPS, IFN-r or TNF-a. LPS was shown to induce interferon gamma(IFN- 7 ) inducible protein 10 (IP-10) and monokine induced by interferon gamma (MIG) in kidney. IP-10 gene expression was induced by LPS and IFN-r, but MIG gene expression was induced by IFN-r in mesangial cell. Chemokines induced by LPS increased splenocyte migration. Sodium salicylate, wortmanin and piperazine blocked LPS mediated chemokine induction suggesting the activation of nuclear factor-a B pathway. It is concluded from this study that mesangial cells are the target of LPS in the renal failure resulting from the systemic infections. LPS induces chemokines directly and/or indirectly in the mesan- gial cells, and these chemokines may associated with renal inflammation.
Chemokines ; Gene Expression* ; Inflammation ; Interferons ; Kidney ; Mesangial Cells* ; Renal Insufficiency ; RNA ; Sodium Salicylate