Growth factor and extracellular matrix in glomerulosclerosis

足细胞主要存在于细胞周期的G1期晚期，即使处于增殖状态，且细胞数量没有增加。至于细胞周期蛋白激酶抑制剂（CKI）家族，它抑制细胞周期从g1期向S期的转移，p21和p27已被确定。关于足细胞中p27阳性细胞的数量，未观察到FGF2引起的变化，但注意到p21阳性足细胞的增加。这些发现表明，大多数足细胞停留在GL晚期的原因可能是p21的上调。此外，FGF2诱导与转运细胞周期相关的足细胞损伤。对比两组PAN大鼠，FGF2组brdu阳性细胞数量明显增加。这一发现表明，少数足细胞进入DNA合成阶段。计数双核或多核足细胞的数量。我们的假设是足细胞进入S期与fgf2引起的细胞损伤有关。我们已经表明，TGF-B亚型和受体随着各种肾小球损伤模型的足细胞增加而增加。smad家族最近在TGF-B的信号传导中被分离和鉴定。在各种肾小球损伤模型足细胞中观察到smad家族的表达。TGF-B增加p21在体外某些细胞中的表达。综上所述，足细胞中p21表达的增加可能是由于TGF-B的上调。我们认为p21通过阻止受损细胞进入细胞周期来保护足细胞免受损伤。

Podocytes are mostly present in the late G1 phase of the cell cycle even in the proliferative state, and there is no increase in the number of cells. As for the cyclin kinase inhibitor (CKI) family, which suppresses shifting of the cell cycle from the G i to the S phase, p21 and p27 have been identified. Regarding the number of p27-positive cells in podocytes, changes due to administration of FGF2 were not observed, but an increase in p21-positive podocytes was noted. These findings suggest that the reason most podocytes remain in the late GL phase might be upregulation of p21. Furthermore, FGF2 induced podocyte injury related to the transit cell cycle. When two sets of PAN rats were compared, the number of BrdU-positive cells was clearly greater in the rats administered FGF2. This finding demonstrated that a few podocytes entered the DNA synthesis phase. The number of bi - or multi- nucleated podocytes was counted in these rats. Our hypothesis is that podocytes entering the S phase are associated with FGF2-idced cell damage. We have shown that TGF-B isoforms and receptors increase with the podocytes of various glomerular injury models. The smad family was recently isolated and identified in the signalling of TGF-B.Expression of the smad family was observed in the podocytes of various glomerular injury models. TGF-B increases the expression of p21 in certain cells in vitro. Taken together, increases in p21 expression in podocytes may be due to the upregulation of TGF-B.We propose that p21 protects podocytes against damage by preventing damaged cells from entering the cell cycle.