Expression of TrkB in the murine kidney.

Neurotrophins acting through Trk signal-transducing receptors play essential roles in the nervous system, and probably in some nonneuronal tissues. In the present study we used Western-blot and immunohistochemistry to investigate the occurrence and cellular localization of TrkB in the mouse kidney. Furthermore, the structure and ultrastructure of the kidney in mice carrying a mutation in the trkB gene were analyzed. TrkB in the kidney was identical to the cerebral one (145 kDa). Since the antibody used recognize a sequence within the tyrosine-kinase domain of TrkB, the renal TrkB receptor identified here must be regarded as able to mediate biological effects of their ligands. TrkB immunoreactivity was restricted to the juxtaglomerular apparatus, including differentiated vascular cells and extaglomerular mesangial cells. In these cells, TrkB colocalized with renin. The structural analysis revealed no major changes in the kidney structure of TrkB-deficient mice, with the exception of a significant reduction of the glomerular area. Nevertheless, in these animals there was an apparent increase in the number of extraglomerular mesangial cells (which retain the ability to synthesize renin) and absence of the macula densa. Taken together, these results strongly suggest a role of TrkB and their ligands in the control of the normal development and maintenance of the juxtaglomerular apparatus.