EXPRESSION OF TENASCIN IN MESANGIAL INJURY IN EXPERIMENTAL GLOMERULONEPHRITIS

Citation
Y. Jyo et al., EXPRESSION OF TENASCIN IN MESANGIAL INJURY IN EXPERIMENTAL GLOMERULONEPHRITIS, Experimental nephrology, 5(5), 1997, pp. 423-428
Citations number
29
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
10187782
Volume
5
Issue
5
Year of publication
1997
Pages
423 - 428
Database
ISI
SICI code
1018-7782(1997)5:5<423:EOTIMI>2.0.ZU;2-U
Abstract
The distribution of tenascin (TN) in the kidneys in relation to embryo genesis, the normal glomerulus and various glomerular diseases has bee n studied immunohistochemically. However, the existence of TN protein and mRNA simultaneously has never been reported in reversible mesangia l proliferative glomerulonephritis (MPGN). In this study, by immunohis tochemical methods and in situ hybridization, we investigated the expr ession of TN in injury to glomerular mesangial cells. Anti-Thy 1.1 mes angial 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 stai ning of TN was detected in normal glomeruli. An increase in staining w as 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 duri ng 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 expre ssion of TN mRNA was noted in Bowman's capsular epithelial cells and p eriglomerular cells after injection. TN mRNA-positive cells were local ized to mesangial, Bowman's capsular and periglomerular areas of hyper cellularity and were significantly associated with an increase in TN s taining 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 mesangi al injury. We could not determine the role of TN in Bowman's capsular and periglomerular areas, but a reversible MPGN model has been reporte d to show an irreversible progressive course in TN knockout mice. In r eversible MPGN it is considered that the role of TN in the mesangial a reas may be related to the process of mesangial repair.