Glomerular cell proliferation and apoptosis in uninephrectomized spontaneously hypertensive rats

Rodrı́guez-López, Ana M.; Flores, Olga; Arévalo, Miguel; López‐Novoa, José M.

doi:10.1046/j.1523-1755.1998.06810.x

Cited by 40 publications

(20 citation statements)

References 21 publications

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“…30 Recently, increased apoptosis has been reported in the normotensive and SHR with a remnant kidney. 31,32 In the nonsclerotic glomerulus of the L-NAME-treaded SHR, which we report herein, the apoptosis labeling index was also increased in association with a reduced glomerular cell number. Although the GIS increased with the higher dose of L-NAME, apoptosis was not associated with a reduced PCNA index.…”

Section: Discussionsupporting

confidence: 69%

Apoptosis and Glomerular Injury After Prolonged Nitric Oxide Synthase Inhibition in Spontaneously Hypertensive Rats

Ono

Ono²,

Takanohashi³

et al. 2001

Hypertension

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Abstract-This study was designed to investigate the relationship between apoptosis and glomerular injury in spontaneously hypertensive rats (SHR) with hypertensive disease that was exacerbated by inhibition of NO synthesis. Development of glomerular cell apoptosis was evaluated by assessment of renal hemodynamics, glomerular morphometric changes, and participation of the renin-angiotensin system. Three groups of 20-week-old SHR were investigated: control male SHR and 2 similar groups given 2 doses of N G -nitro-L-arginine methyl ester (L-NAME, 50 or 80 mg/L, respectively) for 3 weeks. Mean arterial pressure and renal vascular resistance increased, whereas effective renal plasma flow and glomerular filtration rate were diminished by L-NAME. The small artery wall/lumen ratio increased as the glomerular-tuft area diminished. Renal cortical tissue levels of angiotensin II increased in response to the L-NAME, thereby inducing afferent arteriolar injury. Apoptosis and proliferative index (PCNA) of nonsclerotic glomeruli were induced by the low-dose L-NAME as the glomerular cell number decreased. In contrast, the PCNA index was downregulated with the high-dose L-NAME. These results indicate that angiotensin II activation, induced by L-NAME, was related to glomerular cell deletion and apoptosis together with the pathophysiological changes of severe nephrosclerosis and impaired renal dynamics. (Hypertension. 2001;38:1300-1306.)

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Section: Discussionsupporting

confidence: 69%

Apoptosis and Glomerular Injury After Prolonged Nitric Oxide Synthase Inhibition in Spontaneously Hypertensive Rats

Ono

Ono²,

Takanohashi³

et al. 2001

Hypertension

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“…This result is in line with the major role of tubular epithelial cells in the progression of CRF [24], based on the regulation of inflammatory processes [25]. Tubular CD146 expression is also associated with age and male sex, two risk factors for CRF according to, respectively, an impaired tubular function [26] and the androgen effects [27]. The pathogenesis for CD146 tubular de novo expression reflects the plasticity of these cells.…”

Section: Discussionsupporting

confidence: 65%

Tubular CD146 Expression in Nephropathies Is Related to Chronic Renal Failure

Daniel¹,

Bardin

Moal

et al. 2005

Nephron Exp Nephrol

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Background: CD146, a member of the immunoglobulin superfamily, is mainly expressed at the endothelial junction. The soluble form of CD146 is increased in the serum of patients with chronic renal failure. The aim of the study was to investigate CD146 expression on biopsies of normal kidney and nephropathies. Methods: We did an immunohistochemical analysis of 10 normal renal tissues and 126 patients with nephropathies. Results: The mean age of the patients was 47.5 ± 18 years with 65% of men. At the time of the biopsy, 73 patients (57.9%) had a renal failure and the mean proteinuria was 3.3 ± 2.9 g/24 h. Inflammatory syndrome was present in 60 (47.6%) patients. Fibrous interstitial changes from minimal lesions to diffuse lesions were seen in 105 (83.3%) biopsies; the mean glomerulosclerosis index was 16.9 ± 19.7%. Normal kidneys showed CD146 staining on endothelial cells, smooth muscle cells, and mesangium. Normal tubular cells were not stained. If endocapillary proliferation was present, the mesangial CD146 expression was higher. This mesangial expression correlated with proteinuria (p = 0.007) and not with renal failure (p = 0.07). A de novo expression on tubular cells was found in 53 patients (42%) and this expression correlated with age (p < 0.001), male sex (p = 0.04), glomerulosclerosis (p < 0.001), interstitial fibrosis (p < 0.001), and renal failure (p < 0.001). Conclusion: Renal CD146 expression is of interest for determining the pathogenesis of mesangial alterations during glomerular injuries and of tubular phenotypic changes during chronic renal failure.

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“…ROS are involved in many of the physiological and pathological processes observed in hypertension, since it is capable of inducing oxidation and damage of macromolecules contributing to cellular damage and, consequently, cell death through apoptosis (Lavi et al, 2010;Endtmann et al, 2011;Worou et al, 2011). These processes have been documented in different cell systems (Rodriguez-Lopez et al, 1998;Rizzoni et al, 2000;Liu et al, 2003), but apoptosis in the 2K1C hypertension model is not completely understood. In the present study, we examined the hypothesis that DNA fragmentation and apoptosis are consequences of ROS production and determined whether these events also occur in BM cells.…”

Section: Apoptosismentioning

confidence: 99%

Renovascular Hypertension Leads to DNA Damage and Apoptosis in Bone Marrow Cells

Campagnaro

Tonini

Doche

et al. 2013

DNA and Cell Biology

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Angiotensin II (Ang II), which plays a pivotal role in the pathophysiology of the two-kidney, one-clip (2K1C) Goldblatt hypertension, has been associated with augmented generation of reactive oxygen species (ROS) in some cells and tissues. In the present study, we evaluated the influence of 2K1C hypertension on oxidative stress, DNA fragmentation, and apoptosis of bone marrow (BM) cells. Two weeks after the renal artery clipping or Sham operation, flow cytometry analysis showed a higher production of superoxide anions (approximately sixfold) and hydrogen peroxide (approximately twofold) in 2K1C hypertensive than in Sham normotensive mice. 2K1C mice also showed an augmented DNA fragmentation (54%) and apoptotic cells (21%). Our data show that the 2K1C renovascular hypertension is characterized by an increased production of ROS, DNA damage, and apoptosis of BM, which is a fundamental source of the cells involved in tissue repair.

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Glomerular cell proliferation and apoptosis in uninephrectomized spontaneously hypertensive rats

Cited by 40 publications

References 21 publications

Apoptosis and Glomerular Injury After Prolonged Nitric Oxide Synthase Inhibition in Spontaneously Hypertensive Rats

Apoptosis and Glomerular Injury After Prolonged Nitric Oxide Synthase Inhibition in Spontaneously Hypertensive Rats

Tubular CD146 Expression in Nephropathies Is Related to Chronic Renal Failure

Renovascular Hypertension Leads to DNA Damage and Apoptosis in Bone Marrow Cells

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