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

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

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

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

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

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

BACKGROUND: Modified lipoproteins may be involved in nephro- and glomerulosclerosis. Diabetic nephropathy-like lesions have also been induced in a rat model by glycated and glycoxidized albumin. In cultured rat or human mesangial cells, enhanced cell proliferation and production of mesangial matrix in response to lipoproteins and their modified forms have been demonstrated by [3H]-thymidine incorporation and cell counting assays. But these methods are relatively complex and most of them have used only one or two of the lipoprotein, albumin and their modified forms. METHODS: We investigated the effects of native and modifed lipoproteins, and albumin on cultured human mesangial cell proliferation using non-radioactive colorimetric method by MTS/PMS assay. Lipoproteins added were low density lipoprotein(LDL), high density lipoprotein(HDL), very low density lipoprotein(VLDL), oxidized LDL(oxidation with copper sulfate in vitro) and glycated LDL and we also used albumin, glycated albumin, and interleukin-1beta as a positive control. RESULTS: Interleukin-1beta promoted the proliferation of cultured human mesangial cells up to concentration 20 ng/mL. LDL induced the proliferation of mesangial cells in a concentration-dependent manner up to concentration 100 microgram/mL. HDL and VLDL had no significant proliferative effect. Oxidized LDL caused the proliferation of mesangial cells at low concentration up to concentration 25 microgram/mL. Addition of glycated LDL resulted in a concentration- dependent inhibition of mesangial cells. Albumin and glycated albumin inhibited the proliferation of mesangial cells at low concentration of 100 microgram/mL, but cell growth was increased at higher concentrations. CONCLUSION: We demonstrated the effects of the single and modified proteins on the proliferation of cultured human mesangial cell by relatively simple colorimetric method. Results were almostly identical to those of previous studies obtained by radioactive method or cell counting assay.
Animals ; Cell Count ; Cell Proliferation ; Copper Sulfate ; Humans* ; Interleukin-1beta ; Lipoproteins* ; Mesangial Cells* ; Models, Animal ; Rats