Jyo Y, Sasaki T, Nomura S, Tamai H, Kawai S, Osawa G, Nakao N, Kusakabe M
Department of Medicine, Kawasaki Medical School, Okayama, Japan.
Exp Nephrol. 1997 Sep-Oct;5(5):423-8.
The distribution of tenascin (TN) in the kidneys in relation to embryogenesis, the normal glomerulus and various glomerular diseases has been studied immunohistochemically. However, the existence of TN protein and mRNA simultaneously has never been reported in reversible mesangial proliferative glomerulonephritis (MPGN). In this study, by immunohistochemical methods and in situ hybridization, we investigated the expression of TN in injury to glomerular mesangial cells. Anti-Thy 1.1 mesangial proliferative glomerulonephritis was induced in Wistar rats by injection of antirat thymocyte plasma. After injection, the rats were sacrificed on days 4, 7, 10 and 14. Immunohistochemically, slight staining of TN was detected in normal glomeruli. An increase in staining was observed in the mesangial areas during the mesangial proliferative phase (days 4, 7 and 10). It decreased on day 14. Focal staining of TN in Bowman's capsule and the periglomerular region was also noted during the mesangial proliferative phase. TN mRNA could not be detected in normal glomeruli by in situ hybridization, but it was observed in the mesangial areas during the mesangial proliferative phase. Focal expression of TN mRNA was noted in Bowman's capsular epithelial cells and periglomerular cells after injection. TN mRNA-positive cells were localized to mesangial, Bowman's capsular and periglomerular areas of hypercellularity and were significantly associated with an increase in TN staining areas. In conclusion, the results of this study prove that TN is a component of the normal mesangial matrix, and that it is induced by mesangial, Bowman's capsular and periglomerular cells after mesangial injury. We could not determine the role of TN in Bowman's capsular and periglomerular areas, but a reversible MPGN model has been reported to show an irreversible progressive course in TN knockout mice. In reversible MPGN it is considered that the role of TN in the mesangial areas may be related to the process of mesangial repair.
已采用免疫组织化学方法研究了腱生蛋白（TN）在肾脏中的分布与胚胎发生、正常肾小球及各种肾小球疾病的关系。然而，在可逆性系膜增生性肾小球肾炎（MPGN）中，从未有过TN蛋白和mRNA同时存在的报道。在本研究中，我们通过免疫组织化学方法和原位杂交技术，研究了TN在肾小球系膜细胞损伤中的表达情况。通过注射抗大鼠胸腺细胞血浆，在Wistar大鼠中诱导出抗Thy 1.1系膜增生性肾小球肾炎。注射后，分别于第4、7、10和14天处死大鼠。免疫组织化学结果显示，正常肾小球中可检测到轻微的TN染色。在系膜增生期（第4、7和10天），系膜区染色增强。第14天染色减弱。在系膜增生期，还注意到鲍曼囊和肾小球周围区域有TN的局灶性染色。原位杂交未能在正常肾小球中检测到TN mRNA，但在系膜增生期的系膜区可观察到。注射后，在鲍曼囊上皮细胞和肾小球周围细胞中可观察到TN mRNA的局灶性表达。TN mRNA阳性细胞定位于细胞增多的系膜、鲍曼囊和肾小球周围区域，且与TN染色面积的增加显著相关。总之，本研究结果证明TN是正常系膜基质的组成部分，系膜损伤后由系膜、鲍曼囊和肾小球周围细胞诱导产生。我们无法确定TN在鲍曼囊和肾小球周围区域的作用，但据报道，在TN基因敲除小鼠中，可逆性MPGN模型显示出不可逆的进展过程。在可逆性MPGN中，认为TN在系膜区的作用可能与系膜修复过程有关。
