+ Site Statistics
+ Search Articles
+ PDF Full Text Service
How our service works
Request PDF Full Text
+ Follow Us
Follow on Facebook
Follow on Twitter
Follow on LinkedIn
+ Subscribe to Site Feeds
Most Shared
PDF Full Text
+ Translate
+ Recently Requested

Proliferation and Na+/H+ antiport activity in human fibroblasts from type I diabetic patients with nephropathy



Proliferation and Na+/H+ antiport activity in human fibroblasts from type I diabetic patients with nephropathy



American Journal of Hypertension 6(2): 170-173



To investigate whether constitutive alterations of the Na+/H+ antiport or of cell proliferation control mechanisms are implicated in development of nephropathy in insulin-dependent diabetics (IDD), skin fibroblasts from controls, recent-onset IDD with normal or high glomerular filtration rates, and IDD with proteinuria were cultured by explant technique. The Na+/H+ antiport activity was studied using the pH sensitive fluorescent dye BCECF. The cell growth capacity was investigated by determination of cell DNA doubling time and by nuclear [3H]thymidine incorporation in response to serum. The Na+/H+ antiport activity and fibroblast growth capacity did not differ between fibroblasts from controls and IDD patients, suggesting the absence of a genetic alteration of the Na+/H+ antiport in the development of diabetic nephropathy.

Please choose payment method:






(PDF emailed within 0-6 h: $19.90)

Accession: 047098006

Download citation: RISBibTeXText

PMID: 8385959

DOI: 10.1093/ajh/6.2.170


Related references

Overactivity of sodium proton antiport and enhanced cell growth in fibroblasts of type 1 insulin dependent diabetic patients with nephropathy. Diabetologia 32(7): 549A, 1989

Enhanced growth and sodium-proton antiport activity response to serum in cultured fibroblasts of diabetic patients with nephropathy. Acta Diabetologica 29(3-4): 178-181, 1992

Leucocyte Na+/H+ antiport activity in type 1 (insulin-dependent) diabetic patients with nephropathy. Diabetologia 33(6): 371-377, 1990

Cyclin dependent kinase inhibitor p16 is decreased in cultured skin fibroblasts from type 1 diabetic patients with nephropathy A marker of diabetic nephropathy ?. Journal of the American Society of Nephrology 11(Program and Abstract Issue): 638A, 2000

Na+/H+ antiport activity and cell growth in cultured skin fibroblasts of IDDM patients with nephropathy. Diabetes 41(10): 1239-1246, 1992

Cyclin dependent kinase inhibitor p16 is decreased in cultured skin fibroblasts from type 1 diabetic patients with nephropathy An early marker of diabetic nephropathy. Journal of Investigative Medicine 48(5): 265A, 2000

In situ protein kinase C activity in cultured fibroblasts from type 1 diabetic patients with nephropathy. Diabetologia 41(Suppl. 1): A75, 1998

In situ protein Kinase C activity is increased in cultured fibroblasts from Type 1 diabetic patients with nephropathy. Diabetologia 46(4): 524-530, 2003

Platelet Na+/H+ antiport activity in patients with insulin-dependent diabetes mellitus with and without diabetic nephropathy. Clinical Investigator 71(2): 119-125, 1993

Platelet Na+/H+antiport activity in patients with insulin-dependent diabetes mellitus with and without diabetic nephropathy. Journal of Molecular Medicine 71(2): 119-125, 1993

Glycolytic enzyme expression and pyruvate kinase activity in cultured fibroblasts from type 1 diabetic patients with and without nephropathy. Biochimica et Biophysica Acta 1782(11): 627-633, 2008

Platelet sodium proton antiport activity in patients with insulin dependent diabetes mellitus with and without diabetic nephropathy. Journal of the American Society of Nephrology 2(3): 288, 1991

Glucose-induced TGF-beta1 in skin fibroblasts from type 1 diabetic patients with diabetic nephropathy. Diabetologia 41(Suppl. 1): A38, 1998

Differential gene expressions in skin fibroblasts of type 1 diabetic patients with diabetic nephropathy using GeneChipTM microarray. Journal of the American Society of Nephrology 12(Program and Abstract Issue): 832A, 2001

Lipids and cellular Na+/H+ antiport activity in diabetic nephropathy. Kidney International 41(4): 872-876, 1992