The phenotypic modulation in renal arteriolar smooth muscles and the glomerular mesangial cells.

在本研究中，我们证明了在高血压和各种肾小球疾病的发展过程中，表型调制发生在肾小动脉平滑肌和肾小球细胞中。盐负荷的易卒中自发性高血压大鼠（SHRSP）发展为恶性高血压。在肾脏中，SM 2（肌肉型肌球蛋白重链异构体）和α-肌动蛋白的表达根据血管损伤的程度而降低。由于SM 2被认为在高度分化的具有强收缩性的平滑肌中表达，因此SM 2表达的降低可能导致小动脉的功能异常，这加速了高血压肾小球损伤。肾小球系膜细胞表达非肌性肌球蛋白、SmMember和α-肌动蛋白。在各种肾小球疾病中，表型调节发生在上皮细胞和系膜细胞中。这些表型的调制证实了免疫电镜和北方分析的信使RNA。在抗-thy-1肾小球肾炎，系膜细胞表达α-肌动蛋白从早期的疾病和Smember在后期阶段。在残肾中，SmMemf在早期肾小球系膜细胞表达，而在晚期肾小球肥大时，在上皮细胞表达。在抗肾小球基底膜肾炎和链脲佐菌素诱导的糖尿病肾脏中，上皮细胞和系膜细胞均表达Smember。在残余肾、抗GBM肾小球肾炎或糖尿病肾中，α-肌动蛋白根本不表达。因此，肾小球细胞的表型调节发生不均匀，以及在不同的方式。目前，肾小球细胞表型调节的功能意义尚不清楚。

In the present study we demonstrated that the phenotypic modulation occurred in smooth muscles of renal arterioles and in glomerular cells during development of hypertension and various glomerular diseases. Salt-loaded stroke-prone-spontaneously hypertensive rats (SHRSP) developed malignant hypertension. In the kidney, the expression of SM2 (muscle-type myosin heavy chain isoform) and alpha-actin was decreased according to the degree of vascular damages. As SM2 is regarded to be expressed in highly differentiated smooth muscles of strong contractility, the decrease in SM2 expression might result in functional abnormalities in arterioles, which accelerates hypertensive glomerular damage. The mesangial cells expressed non-muscle myosin, Smemb, and alpha-actin. In various glomerular diseases, the phenotypic modulation took place in the epithelial cells and in the mesangial cells. These phenotypic modulations were confirmed by the immunoelectron microscopy and also by the northern analysis of messenger RNA.In the anti-thy-1 glomerulonephritis, mesangial cells express alpha-actin from the earlier stage of the disease and also Smemb in the later stage. In the remnant kidney, Smemb was expressed in the mesangial cells at the earlier stage, but in the epithelial cells at the later stage, when the glomerular hypertrophy developed. In the anti-glomerular basement membrane glomerulonephritis and the streptozotocin-induced diabetic kidney, both the epithelial and mesangial cells expressed Smemb. In the remnant kidney, the anti-GBM glomerulonephritis or diabetic kidney, alpha-actin was not expressed at all. Thus, the phenotypic modulation of glomerular cells took place heterogeneously as well as in the varying manner. At present, the functional meaning of the phenotypic modulation of glomerular cells is unknown.