High glucose stimulate collagen Ⅰ synthesis in renal tubular epithelial cells via activated TGF-β/Smad signaling pathway
- VernacularTitle:高糖通过TGF-β1/Smad信号通路介导肾小管上皮细胞1型胶原合成的机制探讨
- Author:
Liao SUN
- Publication Type:Journal Article
- Keywords:
Glucose/PD;
Transforming growth factor beta;
DNA-binding proteins;
Kidney tubules;
Epithelial cells;
Collagentype Ⅰ
- From:
Journal of Chinese Physician
2008;10(11):1453-1456
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the molecular mechanisms that high glucose stimulate collagen Ⅰ synthesis in renal tubular epi-thelial cells. Methods Normal rat pwximal tubular epithelial (NRK52E) cells were cultured grown in RPMI-1640 medium and were divid-ed four groups: mannitol group, high glucose group, high glucose + neutralizing TGF-β1 antibody group, high glucose + IgG1 group. TGF-β1 in the supematant of cultured cells were measured by enzyme-linked immunosorbent assay (ELISA). Nuclear expression of p-Smad2/3 were examined by immunocytochemistry. Expression of collagen Ⅰ mRNA was detected by RT-PCR. Expression of collagen Ⅰ pro-tein was detected by Western blot. Results High glucose up-regulated the expression of collagen Ⅰ mRNA by time-dependent manor. Com-pared with mannitol group, high glucose markedly increased the level of TGF-β1 in supernatant of cultured cell after 24h and 48h and upreg-ulated p-Smad2/3 nuclear expression(t =4. 2, t = 3.25, P <0.01). Neutralizing TGF-β1 antibody inhibited high glucose- induced p-Smad2/3 nuclear expression, downregulated high glucose-induced collagen Ⅰ mRNA and protein expression(t = 3.12, t =3.02, P < 0.01). Conclusion High glucose stimulated collagen Ⅰ synthesis in renal tubular epithelial cells via activated TGF-β/Smad signaling path-way.