Capillary neoformation is important in repair of glomerular injury of various origins. VEOF was shown to be crucial for glomerular capillary repair in glomerulonephritis (ON). We reasoned that other angiogenic factors are likewise involved in glomerular capillary remodeling and found angiopoietin 1 and -2 (ANGI and ANG2). mRNA to be upregulated in cDNA microarrays of microdissected glomeruli of anti-Thy 1.1 ON of the rat. We then studied glomerular in situ gene and protein expression of ANG1 and ANG2 and their receptor Tie-2 in the course of anti- Thyl.! ON, which was induced by injection of OX-7 antibody. Animals were perfusion fixed at days 6 and 12 after ON induction and compared with nonnephritic controls receiving PBS. Capillary damage and repair were quantitatively analyzed using stereological techniques. Gene and protein expression of ANOI and ANO2 and their receptor Tie-2 was analyzed using real-time quantitative PCR from microdissected glomeruli, nonradioactive in situ hybridization, double immunofluorescence, and Western blot analysis. Glomerular capillarization assessed as length density was significantly lower at day 6 of anti-Thyl.1 ON than in controls; it was back to normal values at day 12. ANGI and ANG2 gene expression was markedly upregulated at day 6 of the disease compared with controls. Protein expression of ANO1 and ANO2 was confined to podocytes and that of Tie-2 to endothelial cells. At day 12 of anti-Thyl.1 ON when capillary restoration was nearly completed, ANO1 and ANO2 gene expression returned to basal levels, whereas Tie-2 expression was still high. With the use of a combined molecular and in situ approach, the spatial and temporal gene and protein expression of the angiopoietins and their receptor was analyzed in anti-Thyl.l ON. The results indicate that glomerular expression of ANO I and ANG2 and Tie-2 is differentially regulated and may contribute to healing and endothelial cell stabilization in experimental ON. [ABSTRACT FROM AUTHOR]