Proliferation and Na+/H+ antiport activity in human fibroblasts from type I diabetic patients with nephropathy.
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.
Soussan
K
K
Département de Néphrologie, Hôpital Necker, Paris, France.
Dausse
E
E
Hannedouche
T
T
Timsit
J
J
Lemoult
F
F
Boitard
C
C
Grünfeld
J P
JP
Guicheney
P
P
D000328:Adult; D002352:Carrier Proteins / Q000502:physiology*; D002455:Cell Division / Q000502:physiology; D002478:Cells, Cultured; D004247:DNA / Q000096:biosynthesis; D003922:Diabetes Mellitus, Type 1 / Q000150:complications / Q000473:pathology* / Q000503:physiopathology*; D003928:Diabetic Nephropathies / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D005260:Female; D005347:Fibroblasts / Q000378:metabolism / Q000473:pathology* / Q000502:physiology*; D005453:Fluorescence; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008297:Male; D017923:Sodium-Hydrogen Exchangers; D013936:Thymidine / Q000378:metabolism; D014316:Tritium
D002352:Carrier Proteins; D017923:Sodium-Hydrogen Exchangers; D014316:Tritium; D004247:DNA; D013936:Thymidine