Bone marrow cells contribute to regeneration of damaged glomerular endothelial cells.Background. There is accumulating evidence that adult bone marrow (BM) cells show unexpected plasticity, and can differentiate into a wide range of specialized cells. In the case of intrinsic renal glomerular cells, BM-derived cells have been reported to differentiate into both mesangial cells and podocytes. However, there is controversy on recruitment of glomerular endothelial cells, although endothelial cells in other tissues are known to be recruited from the BM.Methods. Sprague-Dawley (SD) rats and SD rats made chimeric by transplantation of bone marrow cells from enhanced green fluorescent protein (EGFP) transgenic littermate rats, were injected with anti-Thy-1.1 antibody, followed by unilateral nephrectomy (1-kidney model). Chimeric rats used in 1-kidney model were sacrificed for histologic examination at weeks 2, 4, 8, and 11. We examined isolated glomeruli and frozen sections of kidneys from rats of each group at weeks 2 and 11 by confocal laser scan microsopy (CLSM), both immunohistologically and three dimensionally.Results. In the 1-kidney group, using chimeric rats transplanted with EGFP(+) bone marrow cells, most rats died, presumably of uremia, after 8 to 11 weeks. A CLSM study using isolated glomeruli and frozen sections of kidneys revealed that bone marrow-derived PECAM-1(+), RECA-1(+) cells, and OX-7(+) cells contributed to the structural support for the glomerular capillaries during the chronic course. Global glomerular sclerotic lesions and diffuse tubular atrophic changes, with interstitial cell infiltration, were remarkable at weeks 8 and 11.Conclusion. Bone marrow-derived endothelial progenitor cells participated in glomerular endothelial cell turnover after severe damage. Treatment that could target bone marrowderived endothelial progenitor cells and promote angiogenesis in regions of progressive glomerular lesions may be a promising therapeutic approach for preventing end-stage renal disease.

Progressive glomerulosclerosis can be induced in the rat by a one shot injection of anti-Thy 1.1 monoclonal antibody followed by unilateral nephrectomy. This model shows that there is a positive association between impairment of vascular regeneration and the development of glomerulosclerosis.

This study investigated a potential role of nitric oxide (NO) in the regulation of gap junctional intercellular communication (GJIC).

Abstract-A change in intracellular Ca2ϩ is considered to be the common final signaling pathway through which renin secretion is governed. Therefore, information relating to the generation, control, and processing of Ca 2ϩ signaling in juxtaglomerular cells (JG) will be critical for understanding JG cell behavior. In this study, we investigated the means by which JG cells harmonize their intracellular Ca 2ϩ signals and explored the potential role of these mechanisms in renin secretion. Mechanical stimulation of a single JG cell initiated propagation of an intercellular Ca 2ϩ wave to up to 11.9Ϯ4.1 surrounding cells, and this was prevented in the presence of the ATP-degrading enzyme, apyrase (1.7Ϯ0.