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1.
Andreas Böttcher Alfred Böttcher Gerd Schmitz Petra Schling 《Central European Journal of Biology》2006,1(2):203-220
Angiotensin-converting enzyme (ACE, kininase II) is a plasma membrane zinc metallopeptidase that acts as a key enzyme for
the extracellular conversion of vasoactive peptides. Recently, ACE outside-in signalling in endothelial cells has been described.
The present study tested the hypothesis that ACE signalling is not restricted to endothelial cells and may act as an additional
peptide receptor on human preadipocytes and adipocytes. ACE protein levels were not changed during adipose conversion of human
primary preadipocytes. The enzyme was primarily localized to the non-detergent-resistant fraction of the membrane and phosphorylated
in non-dividing cells. Antibody arrays of whole cell lysate detected putative ACE-interacting proteins, which all share important
roles in cell cycle control and/or apoptosis. These findings suggest that ACE is a versatile molecule, involved both in the
regulation of extracellular peptide concentrations and direct intracellular signalling. In human adipose cells ACE may potentially
influence exit from the cell cycle, differentiation, and programmed cell death signalling. 相似文献
2.
《Bioscience, biotechnology, and biochemistry》2013,77(12):3232-3236
We found human renin inhibitory activity in soybean and isolated the active compound, soybean renin inhibitor (SRI). The physico-chemical data on the isolated SRI were identical with those of soyasaponin I. SRI showed significant inhibition against recombinant human renin, with an IC50 value of 30 μg/ml. Kinetic studies with SRI indicated partial noncompetitive inhibition, with a Ki value of 37.5 μM. On the other hand, SRI weakly inhibited pepsin, papain, and bromeline activities, but did not inhibit other proteinases, such as trypsin, kallikrein, angiotensin converting enzyme, and aminopeptidase M. Moreover, a significant (p<0.05) decrease in the systolic blood pressure of spontaneously hypertensive rats was observed when partially purified SRI was orally administrated at 40 mg/kg/d for 7 weeks. This is the first demonstration of a renin inhibitor from soybean, soyasaponin I. 相似文献
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肾素(原)受体在大鼠肾小球系膜细胞和肾脏的表达 总被引:1,自引:0,他引:1
近年发现的肾素(原)受体(renin/prorenin receptor,RnR)已被证明具有生物学功能,在心、肾及多种细胞表达。本文旨在观察RnR在体外培养的大鼠肾小球系膜细胞(mesangial cells,MCs)和肾脏中是否表达,及其表达的细胞部位,并用RnR的多肽阻断剂肾素原“柄区肽”(handle region peptide,HRP)与RnR结合后观察受体复合物进入细胞的过程与定位。结果显示,RnR主要存在于大鼠肾脏皮质肾小球系膜区和体外培养的MCs的细胞核周围胞浆和细胞膜。将FITC标记的HRP(FITC-HRP)加入细胞培养液后30S到30min期间,可观察到FITC-HRP由培养液转移到胞浆内并进入细胞核。用免疫荧光和激光共聚焦技术观察到,HRP与RnR的共定位主要位于细胞膜和细胞核周围胞浆;在30min时,一部分HRP已进入细胞核,而RnR没有进入细胞核内,仍主要位于细胞核周围胞浆。上述结果提示,RnR与其配基结合后进入细胞内并发挥生物学效应。 相似文献
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Wu SN Huang HC Yeh CC Yang WH Lo YC 《Biochemical and biophysical research communications》2011,(3):508-513
Experimental and clinical data support the notion that peroxisome proliferator-activated receptor γ (PPARγ) activation is associated with anti-atherosclerosis as well as anti-diabetic effect. Telmisartan, an angiotensin receptor blocker (ARB), acts as a partial PPARγ agonist. We hypothesized that telmisartan protects against diabetic vascular complications, through PPARγ activation. We compared the effects of telmisartan, telmisartan combined with GW9662 (a PPARγ antagonist), and losartan with no PPARγ activity on vascular injury in obese type 2 diabetic db/db mice. Compared to losartan, telmisartan significantly ameliorated vascular endothelial dysfunction, downregulation of phospho-eNOS, and coronary arterial remodeling in db/db mice. More vascular protective effects of telmisartan than losartan were associated with greater anti-inflammatory effects of telmisartan, as shown by attenuation of vascular nuclear factor kappa B (NFκB) activation and tumor necrosis factor α. Coadministration of GW9662 with telmisartan abolished the above mentioned greater protective effects of telmisartan against vascular injury than losartan in db/db mice. Thus, PPARγ activity appears to be involved in the vascular protective effects of telmisartan in db/db mice. Moreover, telmisartan, but not losartan, prevented the downregulation of vascular PPARγ in db/db mice and this effect of telmisartan was cancelled by the coadministration of GW9662. Our data provided the first evidence indicating that PPARγ activity of telmisartan contributed to the protective effects of telmisartan against diabetic vascular complication. PPARγ activity of telmisartan was involved in the normalization of vascular PPARγ downregulation in diabetic mice. Thus, telmisartan seems to exert vascular protective effects in hypertensive patients with diabetes. 相似文献
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Dobrian AD Lieb DC Cole BK Taylor-Fishwick DA Chakrabarti SK Nadler JL 《Progress in lipid research》2011,50(1):115-131
The 12/15-lipoxygenase enzymes react with fatty acids producing active lipid metabolites that are involved in a number of significant disease states. The latter include type 1 and type 2 diabetes (and associated complications), cardiovascular disease, hypertension, renal disease, and the neurological conditions Alzheimer’s disease and Parkinson’s disease. A number of elegant studies over the last thirty years have contributed to unraveling the role that lipoxygenases play in chronic inflammation. The development of animal models with targeted gene deletions has led to a better understanding of the role that lipoxygenases play in various conditions. Selective inhibitors of the different lipoxygenase isoforms are an active area of investigation, and will be both an important research tool and a promising therapeutic target for treating a wide spectrum of human diseases. 相似文献
8.
Tschöpe C Westermann D Dhayat N Dhayat S Altmann C Steendijk P Schultheiss HP Walther T 《Cell biochemistry and biophysics》2005,43(1):45-52
Hearts of normotensive angiotensin II type 2 receptor (AT2)-deficient mice do not develop fibrosis after angiotensin II-induced chronic hypertension. Thus, the goal of our study was
to clarify whether AT2 knockouts (KOs) are also characterized by altered left ventricular (LV) function and modified remodeling of the extracellular
matrix (ECM) after induction of myocardial infarction (MI). MI was induced in 5-mo-old female AT2-deficient mice and controls by occlusion of the left coronary artery. Time-matched sham-operated animals served as controls.
After 48 h, the first sets of mice were hemodynamically characterized using a pressure-tip catheter (n=8/group). We also obtained pressure volume loops using a microconductance catheter in additional sets of animals 3 wk after
induction of MI (n=7/group). Finally, the collagen index was illustrated by Sirius red staining and quantified by digital analysis. Whereas
the LV function of sham-operated animals did not differ between both genotypes, the collagen index was 44% lower in KO animals.
Forty-eight hours and 3 wk post-MI, systolic and diastolic LV function were impaired in both AT2-deficient and wild-type (WT) animals to the same extent by approx 45%. No differences were found between the two genotypes
with respect to LV hypertrophy and the fibrosis index in the infarcted and noninfarcted areas 3 wk post-MI. While AT2-KO mice had less cardiac collagen content under basal conditions, the receptor deficiency had no significant influence on
LV function at the two investigated time points after induction of MI or on the remodeling of ECM at the latter time point.
Thus, hypetension-induced fibrosis is probably triggered by other control mechanisms than fibrosis induced by MI. 相似文献
9.
Local renin-angiotensin systems 总被引:6,自引:0,他引:6
A. H. Jan Danser 《Molecular and cellular biochemistry》1996,157(1-2):211-216
The existence of a local cardiovascular renin-angiotensin system (RAS) is often invoked to explain the long-term beneficial effects of RAS inhibitors in heart failure and hypertension. The implicit assumption is that all components of the RAS are synthesized in situ, so that local angiotensin II formation may occur independently of the circulating RAS. Evidence for this assumption however is lacking. The angiotensin release from isolated perfused rat hearts or hindlimbs depends on the presence of renal renin. When calculating the in vivo angiotensin production at tissue sites in humans and pigs, taking into account the extensive regional angiotensin clearance by infusing radiolabeled angiotensin I or II, it was found that angiotensin production correlated closely with plasma renin activity. Moreover, in pigs the cardiac tissue levels of renin and angiotensin were directly correlated with their respective plasma levels, and both in tissue and plasma the levels were undetectably low after nephrectomy. Similarly, rat vascular renin and angiotensin decrease to low or undetectable levels within 48 h after nephrectomy. Aortic renin has a longer half life than plasma renin, suggesting that renin may be bound by the vessel wall. In support of this assumption, both renin receptors and renin-binding proteins have been described. Like ACE, renin was enriched in a purified membrane fraction prepared from cardiac tissue. Binding of renin to cardiac or vascular membranes may therefore be part of a mechanism by which renin is taken up from plasma. It appears that the concept of a local RAS needs to be reassessed. Local angiotensin formation in heart and vessel wall does occur, but depends, at least under normal circumstances, on the uptake of renal renin from the circulation. Tissues may regulate their local angiotensin concentrations by varying the number of renin receptors and/or renin-binding proteins, the ACE level, the amount of metabolizing enzymes and the angiotensin receptor density.Abbreviations RAS
renin-angiotensin system
- ANG
angiotensin
- ACE
angiotensin-converting enzyme
- PRA
plasma renin activity 相似文献
10.
《Bioscience, biotechnology, and biochemistry》2013,77(7):1367-1371
The local tissue-specific renin-angiotensin system (RAS) was identified. The aim of this study was to investigate the role of local bone RAS in the osteoporosis of aging mice. Twelve-month-old and two-month-old male mice were respectively assigned to the ageing and young groups. The tibias and femurs were collected for an analysis of histomorphology, bone mass, and gene and protein expression. H&E staining and micro-CT measurement showed a loss of the trabecular bone network and decrease of bone mineral density in the proximal tibial metaphysis of the aged mice. The PCR results indicated the significant up-regulation of renin and angiotensinogen (AGT) mRNA expression in both the tibia and femur of the ageing mice. Western blotting data showed that the tibial angiotensin II protein expression was significantly increased in the ageing group. The enhancement of renin and AGT expression in the bone tissue resulted in the increased production of angiotensin II which plays an important role in the pathology of age-related osteoporosis. 相似文献