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.