Glomerular disease has a tendency to progress to chronic renal failure after initial injury. There is no method to prevent or improve the progression of renal disease except minimal change nephrotic syndrome which can be improved by steroid
therapy. The
progression of renal disease can be identified as a glomerulosclerosis by histological examination, and it is known that mesangial cells have a significant pathogenic role in the progression of glomerulosclerdosis. The basic mechanism or
glomerulosclerosis is the proliferation and the collagen synthesis of mesangial cells.
In this study, after in vitro culture of rat mesangial cells the proliferation and the collagen synthesis of mesangial cells were measured. As factors which can effect on cultured rat mesangial cells, epidermal growth factor (EGF), and
transforming
growth factor-β(TGF-β) were chosen because EGF and TGF-βcan change the proliferation and the collagen synthesis of these cells.
Sprague-Dawley rats (age of 4-6 weeks) were sacrificed to culoture mesangial cells in vitro. TGF-βwas purified by FPLC (fast performance liquid chromatography) after extracting platelet concentrates by acidic ethanol. The activity of TGF-β was
confirmed by experiment that it could proliferate NRK 49F fibroblast from ATCC.
The results were as follows; The EGF increased H-thymidine uptake to 139±9%, 147±6%, 147±7%, 158±16% of the control value at a concentration of 1 ng/ml, 10ng/ml, 50ng/ml but there was no increase in 3H-proline uptake. At a concentration of
0.05
ng/ml, 0.35ng/ml of TGF-β, the [3H] thymidine uptake was increased to 150±50%, 185±38% but at a concentration of 2ng/ml the 3H-proline uptake was decreased to 74±17%, of the control. The 3H-proline uptake was increased to 119±4%, 113±3% at
a
concentration of 0.35ng/ml, 1ng/ml of TGFβbut at other concentration the 3H-proline uptake was not increased when compared to the control value.
In conclusion, EGF and TGF-βinfluence the proliferation and the collagen synthesis of measangial cells.
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