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*

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

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

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

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

Glomerular mesangial cells have receptors to various growth factors and vasoactive peptides such as platelet-derived growth factor(PDGF), and endothelin(ET), which are important mediators for the progression of glomerular diseases. Heparin has been reported to have anti-proliferative effects in vascular smooth muscle cells and mesangial cells. Furthermore, the treatment with heparin suppresses the progression of experimental mesangioproliferative glomerulonephritis. The present study was carried out to further ascertain inhibitory effects of heparin and possible mechanisms of its action, particularly in relation to the effect on ET production of mesangial cells. The effect of heparin on PDGF-stimulated proliferation was assessed by [3H]thymidine uptake as well as the increase of number of cells, and ET production was evaluated in cultured rat mesangial cells. The results were as follows: 1) PDGF at a concentration of 10 ng/ml stimulated [3H]thymidine uptake significantly(mean+/-S.D., 512.0+/-38.6 cpm/well vs. 3300.4+/-432.5, p<0.05), and also increased the number of cells significantly, compared to control(23.0+/-3.5X10(3)/well vs. 66.5+/-8.9, p<0.05). 2) Heparin inhibited the PDGF(10ng/ml)-stimulated proliferation of mesangial cells in a dose-dependent manner(100microgram/ml, 3300.4+/-432.5cpm/well vs. 1452.5+/-264.7, 66.5+/-8.9 cpm/well vs. 20.0+/-6.5, p<0.05). 3) While N-desulfated heparin did not show the inhibitory effect on [3H]thymidine uptake, the potency of intact heparin(100microgram/ml) was 56.2+/-8.0% inhibition, which was similar to chondroitin sulfate(48.9+/-5.4%). N-desulfated N-acetylated heparin showed 25.7+/-9.7% inhibition. 4) PDGF stimulated the production of ET in a dose-dependent manner(25ng/ml, 4.2+/-0.7pg/ml/mg of protein vs 15.7+/-1.4, p<0.05). 5) Heparin inhibited the PDGF(25ng/ml)-stimulated ET production in a dose-dependent pattern(100microgram/ml, 12.6+/-3.5 vs. 2.5+/-1.1, p<0.05). From the above results, it is concluded that heparin has a significant inhibitory effect on proliferation and ET production in mesangial cells, and this anti-proliferative effect of heparin appears to be related to the structure of heparin, especially N-sulfation. In conclusion, heparin may reduce glomerular injury through these inhibitory effects on mesangial cells, but the further studies such as in vivo experiments considering the anticoagulation effect are needed.
Animals ; Chondroitin ; Endothelins* ; Glomerulonephritis ; Heparin* ; Intercellular Signaling Peptides and Proteins ; Mesangial Cells* ; Muscle, Smooth, Vascular ; Peptides ; Rats