糸球体　

WordNet

a small intertwined group of capillaries in the malpighian body; it filters the blood during urine formation
of or relating to glomeruli

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/06/17 03:24:43」(JST)

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1. 糸球体の免疫障害の機序 mechanisms of immune injury of the glomerulus
2. 高血圧におけるACE阻害剤の腎への効果 renal effects of ace inhibitors in hypertension
3. 降圧療法と慢性腎臓病の進行：実験的研究 antihypertensive therapy and progression of chronic kidney disease experimental studies
4. 一酸化窒素と腎臓 nitric oxide and the kidney
5. 腎でのマグネシウム処理における利尿剤の有効性 effect of diuretics on magnesium handling by the kidney

English Journal

Using gold nanorods core/silver shell nanostructures as model material to probe biodistribution and toxic effects of silver nanoparticles in mice.

Meng J1, Ji Y, Liu J, Cheng X, Guo H, Zhang W, Wu X, Xu H.Author information 1Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College , Beijing , P. R. China.AbstractThe aim of this work was to probe the biodistribution and toxic effects of silver nanoparticles (NPs) with powerful anti-bacterial and anti-virus activities. For this purpose, novel silver NPs with gold nanorod (NR) core and silver shell (Au@Ag NRs) were developed and employed as a model material. The inner gold core provided an excellent internal reference for tracking the NRs in vivo. After subcutaneous injection of Au@Ag NRs, silver and gold contents in the subcutis and organs were examined by inductively coupled plasma mass spectrometry at different time points within 28 days. Histological analysis, physiological function and complement faction 3 (C3) and 5a (C5a) measurement were performed over time to reveal the toxic effect of Au@Ag NRs in vivo. Experimental results showed that majority of the Au@Ag NRs remained in the injection site except for a small amount migrating into the lymph nodes. The silver shell was dissolved in the subcutaneous tissue and released silver ions rapidly, which resulted in detectable silver accumulation in most of the organs. The accumulated silver ions in the kidney not only interacted with the kidney cells membrane but also induced a rapid increase of complement fraction C3 followed by a significant consumption and C3a and C5a production significantly in the serum, which resulted in kidney oxidative damage and eventually led to the morphological changes and filtration function impairment of the glomerulus. The released silver ions also caused oxidative injury of subcutaneous tissue in the injection site.
Nanotoxicology.Nanotoxicology.2014 Sep;8(6):686-96. doi: 10.3109/17435390.2013.822593. Epub 2013 Jul 29.
The aim of this work was to probe the biodistribution and toxic effects of silver nanoparticles (NPs) with powerful anti-bacterial and anti-virus activities. For this purpose, novel silver NPs with gold nanorod (NR) core and silver shell (Au@Ag NRs) were developed and employed as a model material. T
PMID 23837638

Renal protection by low dose irbesartan in diabetic nephropathy is paralleled by a reduction of inflammation, not of endoplasmic reticulum stress.

Hartner A1, Cordasic N2, Klanke B2, Menendez-Castro C3, Veelken R2, Schmieder RE2, Hilgers KF2.Author information 1Department of Pediatrics and Adolescent Medicine, University of Erlangen-Nürnberg, Loschgestrasse 15, D-91054 Erlangen, Germany. Electronic address: andrea.hartner@uk-erlangen.de.2Department of Nephrology and Hypertension, University of Erlangen-Nürnberg, Loschgestrasse 8, D-91054 Erlangen, Germany.3Department of Pediatrics and Adolescent Medicine, University of Erlangen-Nürnberg, Loschgestrasse 15, D-91054 Erlangen, Germany.AbstractDiabetes can disrupt endoplasmic reticulum (ER) homeostasis which leads to ER stress. ER stress-induced renal apoptosis seems to be involved in the development of diabetic nephropathy. The present study was designed to investigate the contribution of reduced ER stress to the beneficial effects of an angiotensin receptor blocker. Insulin-dependent diabetes mellitus was induced by streptozotocin injections to hypertensive mRen2-transgenic rats. After 2weeks animals were treated with 0.7mg/kg/day irbesartan. Blood glucose, blood pressure and protein excretion were assessed. Expression of ER stress markers was measured by real-time PCR. Immunohistochemistry was performed to detect markers of ER stress, renal damage and infiltrating cells. Glomerulosclerosis and apoptosis were evaluated. Diabetic mRen2-transgenic rats developed renal injury with proteinuria, tubulointerstitial cell proliferation as well as glomerulosclerosis and podocyte injury. Moreover, an increase in inflammation, podocyte ER stress and apoptosis was detected. Irbesartan somewhat lowered blood pressure and reduced proteinuria, tubulointerstitial cell proliferation and glomerulosclerosis. Podocyte damage was ameliorated but markers of ER stress (calnexin, grp78) and apoptosis were not reduced by irbesartan. On the other hand, inflammatory cell infiltration in the tubulointerstitium and the glomerulus was significantly attenuated. We conclude that irbesartan reduced renal damage even in a very low dose. The beneficial effects of low dose irbesartan were paralleled by a reduction of blood pressure and inflammation but not by a reduction of ER stress and apoptosis. Thus, sustained endoplasmic reticulum stress in the kidney does not necessarily lead to increased inflammation and tubulointerstitial or glomerular injury.
Biochimica et biophysica acta.Biochim Biophys Acta.2014 Apr;1842(4):558-65. doi: 10.1016/j.bbadis.2014.01.001. Epub 2014 Jan 10.
Diabetes can disrupt endoplasmic reticulum (ER) homeostasis which leads to ER stress. ER stress-induced renal apoptosis seems to be involved in the development of diabetic nephropathy. The present study was designed to investigate the contribution of reduced ER stress to the beneficial effects of an
PMID 24418215

RGS2 regulates urotensin II-induced intracellular Ca2+ elevation and contraction in glomerular mesangial cells.

Adebiyi A.Author information Department of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee.AbstractUrotensin II (UII), a vasoactive peptide modulates renal hemodynamics. However, the physiological functions of UII in glomerular cells are unclear. In particular, whether UII alters mesangial tone remains largely unknown. The present study investigates the physiological effects of UII on glomerular mesangial cells (GMCs). This study also tested the hypothesis that the regulator of G-protein signaling (RGS) controls UII receptor (UTR) activity in GMCs. RT-PCR, Western immunoblotting, and immunofluorescence revealed UTR expression in cultured murine GMCs. Mouse UII (mUII) stimulated Ca(2+) release from intracellular stores and activated store-operated Ca(2+) entry (SOCE) in the cells. mUII also caused a reduction in planar GMC surface area. mUII-induced [Ca(2+)]i elevation and contraction were attenuated by SB 657510, a UTR antagonist, araguspongin B, an inositol 1,4,5-trisphosphate receptor antagonist, thapsigargin, a sarco/endoplasmic reticulum Ca(2+)-ATPase inhibitor, and La(3+), a store-operated Ca(2+) channel blocker, but not nimodipine, an L-type Ca(2+) channel blocker. In situ proximity ligation assay indicated molecular proximity between endogenous RGS2 and UTR in the cells. Treatment of GMCs with mUII elevated plasma membrane expression of RGS2 by ∼2-fold. mUII also increased the interaction between RGS2 and UTR in the cells. siRNA-mediated knockdown of RGS2 in murine GMCs increased mUII-induced [Ca(2+)]i elevation and contraction by ∼35 and 31%, respectively. These findings indicate that mUII-induced SOCE results in murine GMC contraction. These data also suggest that UTR activation stimulates RGS2 recruitment to GMC plasma membrane as a negative feedback mechanism to regulate UTR signaling.
Journal of cellular physiology.J Cell Physiol.2014 Apr;229(4):502-11. doi: 10.1002/jcp.24470.
Urotensin II (UII), a vasoactive peptide modulates renal hemodynamics. However, the physiological functions of UII in glomerular cells are unclear. In particular, whether UII alters mesangial tone remains largely unknown. The present study investigates the physiological effects of UII on glomerular
PMID 24105430