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This was already demonstrated for mouse kidney endothelial cells.
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Immunohistochemistry analysis of normal mouse kidney showed that immunoreactivity was located on endothelial cells of glomerular capillary loops and peritubular capillaries.
Notably, ESP cells generated endothelial cells that migrated into the mouse kidney parenchyma and formed mature blood vessels.
Furthermore, Kanasaki et al. have recently reported that linagliptin inhibited the endothelial-to-mesenchymal transition in type 1 diabetic mouse kidney, independent of the glucose-lowering effect [ 37].
During mouse kidney development, ephrin-B2 is expressed initially in a subset of podocyte progenitors and subsequently in endothelial cells of the developing glomerulus, while expression of EphB4 was observed in endothelial cells of venous structures [ 94], suggesting the involvement of interaction between ephrin-B2 and EphB in glomerular microvascular assembly.
Mouse kidney progenitor cell.
A conceptual developmental framework has emerged for the mouse kidney.
In an AKI model in which selective kidney endothelial injury is realized, there are evidences for platelet contribution [199].
In the "vascular endothelial type", vessel-like structures consisting of hVm+ cells were dominant, together with some hVm+ cells migrating into the mouse kidney parenchyma (Figure 2C).
In contrast, kidney endothelial cells defined by the latter markers displayed a lower expression of CD146.
Alternatively, C4bp may modulate kidney endothelial cell function in a complement-independent manner.
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