Abstract:Renin, a key component in the regulation of blood pressure in mammals, is produced by the rare and highly specialized juxtaglomerular (JG) cells of the kidney. Chronic stimulation of renin release results in a recruitment of new JG cells by the apparent conversion of adjacent smooth muscle cells along the afferent arterioles. Because JG cells rapidly de-differentiate when removed from the kidney, their developmental origin and the mechanism that explains their phenotypic plasticity remain unclear. To overcome … Show more
“…Clearly therefore, hypoxia-inducible genes are essential for normal development and physiologic adaptation of RPC. The upregulated PDGFR-β expression in these cells is in full agreement with the results from the human reninoma studies showing that the PDGFB-PDGFR-β pathway downregulates renin expression [ 64 ].…”
Section: Plasticity and Regenerationsupporting
confidence: 87%
“… Fig. 2 The ‘recruitment’ phenomenon, illustrated by a schematic illustration ( a , c ) and immunofluorescence and fluorescent in situ hybridization data from control and captopril-treated mice ( b , d , modified from [ 64 ]). In adult kidneys, renin is produced by the juxtaglomerular (JG) cells located within the afferent arterioles at the entrance of the glomeruli.…”
Section: The Recruitment Phenomenonmentioning
confidence: 99%
“…Martini et al performed RNA transcriptome analysis on human reninomas, as an approach to further understand JGC biology [ 64 ]. Reninomas are rare, renin-producing tumors, arising from a proliferation of JGC in the kidney cortex, and are often detected because of the appearance of fulminant hypertension in young patients [ 65 , 66 ].…”
Section: Jgc Signature: the Myo-endocrine Profilementioning
confidence: 99%
“…Renin, α-smooth muscle actin (αSMA) and interleukin-6 (IL-6) gene expression are also provided. Data (mean ± SEM of n = 5–11) are modified from [ 64 ], and have been expressed as a percentage of the levels in cells exposed to medium of control-transfected cells, i.e., cells treated with the transfection mix, but without cDNA. *P < 0.05. b , c As4.1 cells under control conditions and after exposure to PDGFB (×10 magnification) …”
Section: Jgc Signature: the Myo-endocrine Profilementioning
confidence: 99%
“…Indeed, in a mesangiolysis murine model, renin lineage cells repopulated the intraglomerular mesangium [ 80 ]. Interestingly, these cells stopped producing renin and expressed PDGFR-β, i.e., the receptor linked to renin downregulation [ 64 ]. Furthermore, Stefanska et al established that pericytes are RPC in the human kidney [ 81 ].…”
Renin is the first and rate-limiting step of the renin-angiotensin system. The exclusive source of renin in the circulation are the juxtaglomerular cells of the kidney, which line the afferent arterioles at the entrance of the glomeruli. Normally, renin production by these cells suffices to maintain homeostasis. However, under chronic stimulation of renin release, for instance during a low-salt diet or antihypertensive therapy, cells that previously expressed renin during congenital life re-convert to a renin-producing cell phenotype, a phenomenon which is known as “recruitment”. How exactly such differentiation occurs remains to be clarified. This review critically discusses the phenotypic plasticity of renin cells, connecting them not only to the classical concept of blood pressure regulation, but also to more complex contexts such as development and growth processes, cell repair mechanisms and tissue regeneration.
“…Clearly therefore, hypoxia-inducible genes are essential for normal development and physiologic adaptation of RPC. The upregulated PDGFR-β expression in these cells is in full agreement with the results from the human reninoma studies showing that the PDGFB-PDGFR-β pathway downregulates renin expression [ 64 ].…”
Section: Plasticity and Regenerationsupporting
confidence: 87%
“… Fig. 2 The ‘recruitment’ phenomenon, illustrated by a schematic illustration ( a , c ) and immunofluorescence and fluorescent in situ hybridization data from control and captopril-treated mice ( b , d , modified from [ 64 ]). In adult kidneys, renin is produced by the juxtaglomerular (JG) cells located within the afferent arterioles at the entrance of the glomeruli.…”
Section: The Recruitment Phenomenonmentioning
confidence: 99%
“…Martini et al performed RNA transcriptome analysis on human reninomas, as an approach to further understand JGC biology [ 64 ]. Reninomas are rare, renin-producing tumors, arising from a proliferation of JGC in the kidney cortex, and are often detected because of the appearance of fulminant hypertension in young patients [ 65 , 66 ].…”
Section: Jgc Signature: the Myo-endocrine Profilementioning
confidence: 99%
“…Renin, α-smooth muscle actin (αSMA) and interleukin-6 (IL-6) gene expression are also provided. Data (mean ± SEM of n = 5–11) are modified from [ 64 ], and have been expressed as a percentage of the levels in cells exposed to medium of control-transfected cells, i.e., cells treated with the transfection mix, but without cDNA. *P < 0.05. b , c As4.1 cells under control conditions and after exposure to PDGFB (×10 magnification) …”
Section: Jgc Signature: the Myo-endocrine Profilementioning
confidence: 99%
“…Indeed, in a mesangiolysis murine model, renin lineage cells repopulated the intraglomerular mesangium [ 80 ]. Interestingly, these cells stopped producing renin and expressed PDGFR-β, i.e., the receptor linked to renin downregulation [ 64 ]. Furthermore, Stefanska et al established that pericytes are RPC in the human kidney [ 81 ].…”
Renin is the first and rate-limiting step of the renin-angiotensin system. The exclusive source of renin in the circulation are the juxtaglomerular cells of the kidney, which line the afferent arterioles at the entrance of the glomeruli. Normally, renin production by these cells suffices to maintain homeostasis. However, under chronic stimulation of renin release, for instance during a low-salt diet or antihypertensive therapy, cells that previously expressed renin during congenital life re-convert to a renin-producing cell phenotype, a phenomenon which is known as “recruitment”. How exactly such differentiation occurs remains to be clarified. This review critically discusses the phenotypic plasticity of renin cells, connecting them not only to the classical concept of blood pressure regulation, but also to more complex contexts such as development and growth processes, cell repair mechanisms and tissue regeneration.
Juxtaglomerular cell tumor (JGT) is a relatively rare, benign reninproducing tumor that causes hypertension, hyperaldosteronism, and hypokalemia due to excessive renin secretion. Here, we report a case of malignant JGT with pulmonary metastases. A 7-year-old male child patient was referred to the hospital for proteinuria found during a school medical checkup. An ultrasound examination revealed a tumor
The protease renin, the key enzyme of the renin–angiotensin–aldosterone system, is mainly produced and secreted by juxtaglomerular cells in the kidney, which are located in the walls of the afferent arterioles at their entrance into the glomeruli. When the body’s demand for renin rises, the renin production capacity of the kidneys commonly increases by induction of renin expression in vascular smooth muscle cells and in extraglomerular mesangial cells. These cells undergo a reversible metaplastic cellular transformation in order to produce renin. Juxtaglomerular cells of the renin lineage have also been described to migrate into the glomerulus and differentiate into podocytes, epithelial cells or mesangial cells to restore damaged cells in states of glomerular disease. More recently, it could be shown that renin cells can also undergo an endocrine and metaplastic switch to erythropoietin-producing cells. This review aims to describe the high degree of plasticity of renin-producing cells of the kidneys and to analyze the underlying mechanisms.
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