Unwrapping the origins and roles of the renal endothelium

Stolz, Donna B.; Sims‐Lucas, Sunder

doi:10.1007/s00467-014-2798-3

Cited by 35 publications

(29 citation statements)

References 69 publications

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“…Recent studies have suggested that VEGF and VEGF-eNOS axis bioavailability decreased progressively in stenotic kidneys. Administration of VEGF can induce renal angiogenesis and alleviate renal fibrosis, and therefore VEGF therapy could provide a novel clinical approach in the treatment of chronic kidney disease (He et al, 2013;Stolz et al, 2015). By immunohistochemistry, expressions of VEGF and VEGFR2 were found to decrease in obstructed kidney of unilateral ureteral obstruction mice, and shenkang injection was found to increase expressions of VEGF/ VEGFR2 in this study.…”

Section: Discussionsupporting

confidence: 53%

Effects of shenkang injection on renal angiogenesis in mice with unilateral ureteral obstruction

Pan

Zhang

Liu

et al. 2020

Bangladesh J Pharmacol

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This study aimed to investigate effects of shenkang injection on angiogenesis in mice with renal fibrosis. C57BL/6J mice after unilateral ureteral obstruction were administrated with different doses of shenkang injection for two weeks. Losartan-administrated mice and Sham-operation mice were as positive and negative controls, respectively. Renal function and vasculature changes were observed, and expressions of VEGF and VEGFR2 were detected. Shenkang injection reduced serum levels of urea nitrogen, creatinine and cystatin C. Shenkang injection alleviated the loss of microvessels, decreased the deposition of collagen fibers, and increased expressions of VEGF and VEGFR2 in the obstructed kidney. These findings indicate that shenkang injection alleviates renal dysfunction and fibrotic changes in mice with renal fibrosis by regulating renal angiogenesis. Video Clip of Methodology: Renal Vasculature by Angiography: 6 min 41 sec: Full Screen Alternate

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Section: Discussionsupporting

confidence: 53%

Effects of shenkang injection on renal angiogenesis in mice with unilateral ureteral obstruction

Pan

Zhang

Liu

et al. 2020

Bangladesh J Pharmacol

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“…The blood that is filtered exits via the efferent arterioles that are juxtaposed to the afferent arterioles. We could visualize these arterioles with their brightly stained borders, as these arterioles have an actin filament‐rich smooth muscle lining (their locations are marked as ‘A’ in Fig. C).…”

Section: Resultsmentioning

confidence: 99%

Identification and classification of epithelial cells in nephron segments by actin cytoskeleton patterns

Kumaran

Hanukoglu

2019

The FEBS Journal

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The basic functional unit in a kidney is the nephron, which is a long and morphologically segmented tubule. The nephron begins with a cluster of capillaries called glomerulus through which the blood is filtered into the Bowman's space. The filtrate flows through the nephron segments. During this flow, electrolytes and solutes are reabsorbed by channels and transport systems into the capillaries wrapped around the nephron. Many questions related to renal function focus on identifying the sites of expression of these systems. In this study, we mapped whole kidney sections by confocal microscopic imaging of fluorescent phalloidin, which binds to actin filaments. In tile scans (composed of hundreds of images) of these sections, the cortex and the medullary regions (outer and inner stripes of the outer medulla, and inner medulla) could be easily identified by their cytoskeletal patterns. At a higher resolution, we identified distinct features of the actin cytoskeleton in the apical, basal, and lateral borders of the cells. These features could be used to identify segments of a nephron (the proximal tubule, thin and thick segments of Henle's loop, and distal tubule), the collecting duct system, the papillary ducts in the papilla, and the urothelium that covers the pelvis. To verify our findings, we used additional markers, including aquaporin isoforms, cytokeratin 8‐18, and WGA lectin. This study highlights the power of high‐resolution confocal microscopy for identifying specific cell types using the simple probe of F‐actin‐binding phalloidin.

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“…The renal vasculature is formed by both angiogenesis (vessel sprouting from an existing vessel) and vasculogenesis (new vessel formation from EPCs) [52]. In adulthood, EPCs have been described to reside in the bone marrow, circulating blood, and blood vessels, whereas incompetence of resident EPCs has been reported in human CKD and several kidney injury models [33].…”

Section: Angiogenesis-based Treatment Of Kidney Diseasementioning

confidence: 99%

Hypoxia and Dysregulated Angiogenesis in Kidney Disease

Tanaka

Nangaku

2015

Kidney Dis

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Background: Accumulating evidence has demonstrated that renal hypoxia has a crucial role in the pathogenesis of acute kidney injury (AKI), chronic kidney disease (CKD), and AKI-to-CKD transition, ultimately culminating in end-stage kidney disease. Renal hypoxia in progressive CKD is intricately linked to persisting capillary loss, which is mainly due to dysregulated angiogenesis. Summary: In CKD, hypoxia-inducible factor (HIF) accumulates in the ischemic tubulointerstitium but fails to sufficiently stimulate angiogenic responses, partly because of blunted activation of HIF, which is best exemplified in diabetic kidney disease. In addition, vascular endothelial growth factor (VEGF) expression is downregulated, possibly because injured tubules are not able to express sufficient VEGF and inflammatory circumstances inhibit VEGF expression. The upregulation of antiangiogenic factors and the incompetence of endothelial progenitor cells (EPCs) may also play some roles in the inadequacy of capillary restoration. Administration of VEGF or angiopoietin-1 maintains peritubular capillaries in several kidney diseases; however, administration of a single angiogenic factor may lead to the formation of abnormal vessels and induce inflammation, resulting in worsening of hypoxia and tubulointerstitial fibrosis. HIF stabilization, which aims to achieve the formation of mature and stable vessels by inducing coordinated angiogenesis, is a promising strategy. Given that the effect of systemic HIF activation is highly context-dependent, further studies are needed to elucidate the precise roles of HIF in various kidney diseases. The adoptive transfer of EPCs or mesenchymal stem cells (MSCs) is a fascinating alternative strategy to restore the peritubular capillaries. Key Messages: Suppressed HIF activation and VEGF expression may be responsible for the dysregulated angiogenesis in progressive CKD. Administration of a single angiogenic factor can cause abnormal vessel formation and inflammation, leading to a detrimental result. Although further studies are warranted, HIF stabilization and adoptive transfer of EPCs or MSCs appear to be promising strategies to restore normal capillaries.

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Unwrapping the origins and roles of the renal endothelium

Cited by 35 publications

References 69 publications

Effects of shenkang injection on renal angiogenesis in mice with unilateral ureteral obstruction

Effects of shenkang injection on renal angiogenesis in mice with unilateral ureteral obstruction

Identification and classification of epithelial cells in nephron segments by actin cytoskeleton patterns

Hypoxia and Dysregulated Angiogenesis in Kidney Disease

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