Forced expression of vascular endothelial growth factor-A in podocytes decreases mesangial cell numbers and attenuates endothelial cell differentiation in the mouse glomerulus

Abstract

Taken together, the results of this study indicated that the upregulation of podocyte VEGF decreased the number of mesangial cells, likely owing to inhibition of PDGF-B-mediated signaling.

Suppressed ER‐associated degradation by intraglomerular cross talk between mesangial cells and podocytes causes podocyte injury in diabetic kidney disease

“…Furthermore, a recent study, wherein single‐nucleus RNA sequencing analyses of diabetic glomeruli 2 were performed, revealed that some ligand genes are upregulated in diabetic MCs and that their cognate receptors exhibit increased expression in podocytes; the presence of possible pathways of local effector molecules of MCs and podocytes was also proposed. Indeed, podocyte‐specific genetic manipulation can alter the MC phenotype through certain humoral factors in mice 40 . Furthermore, exosomal microRNAs derived from MCs were increased in the urine of diabetic patients 41 .…”

“…Indeed, podocyte-specific genetic manipulation can alter the MC phenotype through certain humoral factors in mice. 40 Furthermore, exosomal microRNAs derived from MCs were increased in the urine of diabetic patients. 41 These findings may support the hypothesis of in situ communication between MCs and podocytes.…”

Efficacy of novel agents in patients with nephropathy associated with POEMS syndrome

“…Mesangiolysis is a glomerular process leading to lesions of continuous endothelial cells and glomerular mesangial cells, endothelial cell proliferation, endothelial swelling and subendothelial widening, endothelial injury caused mesangial interposition, finally mesangial proliferation and mesangial sclerosis [12]. Glomerular endothelial cell proliferation was defined as the endothelial cell number was increased along with enlargement of the subendothelial spaces [13], glomerular subendothelial widening was defined as formation of new layer(s) of basal lamina like double contour basement membrane in capillary of the glomerulus [14]. Three grade evaluation in semi-quantitative analysis based on the percentage of the glomeruli compartment and recorded was mild (1 + , < 25%), moderate (2 + , 26-50%), and severe (3 + , > 50%) [15,16].…”

Identifying Synergistic Mechanisms of Multiple Ingredients in Shuangbai Tablets against Proteinuria by Virtual Screening and a Network Pharmacology Approach

“…e HIF-1 signaling pathway and RAS signaling pathway were identified as mechanisms of SBT against proteinuria from ClueGO results. Studies have reported that high expression of HIF-1A in renal tubular epithelial cells can aggravate glomerular hypertrophy and extracellular matrix accumulation, increasing urinary protein excretion [88]. More importantly, HIF-1 signaling mediated pathways, such as the mitogen-activated protein kinase (MAPK) signaling pathway, and the phosphatidylinositol-3-kinase protein kinase B (PI3K-Akt) signaling pathway [89] both directly damaged renal function through contributing to renal fibrosis or proteinuria-induced renal epithelial-mesenchymal transition [90][91][92].…”

“…Inhibition of RAS can also regulate the high glucoseinduced VEGF signaling pathway [102]. VEGF-A, the most specific and prominent angiogenic factor of VEGF family, has been reported to be involved in the process of angiogenesis, migration, and proliferation of endothelial cells [8,88,103,104]. In addition, autocrine secretion of VEGF was caused by the interactions of AGEs and their receptor RAGE, which were new risk factors in the pathogenesis of end-stage renal disease [105,106].…”