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These data indicate that Ang II-AT2R (show AGTR2 Proteins) regulates human bone marrow MSC (show MSC Proteins) migration by signaling through the FAK (show PTK2 Proteins) and RhoA (show RHOA Proteins)/Cdc42 (show CDC42 Proteins) pathways.
Data suggest that up-regulaton of Ang-(1 (show ANGPT1 Proteins)-7) levels in follicular fluid correlates with increases in number of mature oocytes retrieved upon ovarian stimulation in preparation for in vitro fertilization.
Urinary angiotensinogen and renin (show REN Proteins) excretion are elevated in CKD patients. Both parameters are negatively associated with eGFR (show EGFR Proteins) and these associations are independent of urinary albumin (show ALB Proteins) excretion
Reduced IL-18 (show IL18 Proteins) serum concentration in children after HUS (show CFH Proteins) with no difference in its urine concentration may indicate a loss of the protective effects of this cytokine on renal function due to previously occurred HUS (show CFH Proteins).
Angiotensin II initiates hepatocyte epithelial-mesenchymal transition by activating the NOX-derived H2O2-mediated NLRP3 (show NLRP3 Proteins) inflammasome/IL-1ss/Smad (show SMAD1 Proteins) circuit.
present study has demonstrated, for the first time, that high glucose augments AGT (show AGXT Proteins) in human RPTCs through HNF-5, which provides a potential therapeutic target for diabetic nephropathy
AngII-dependent phosphorylation of LCP1 (show LCP1 Proteins) in cultured podocytes was mediated by the kinases ERK (show EPHB2 Proteins), p90 (show CANX Proteins) ribosomal S6 kinase (show RPS6KB1 Proteins), PKA, or PKC (show PRRT2 Proteins). LCP1 (show LCP1 Proteins) phosphorylation increased filopodia formation.
Autosomal dominant polycystic kidney disease (ADPKD), uniquely increases urinary angiotensinogen and renin (show REN Proteins) excretion despite their circulating levels being comparable with those in non-ADPKD chronic kidney disease.
Quaternary interactions and supercoiling modulate the cooperative DNA binding of AGT (show AGXT Proteins).
results show that SNPs in the Hap (show SAFB Proteins)-I of the hAGT gene promote high-fat diet-induced binding of transcription factors GR, CEBP-beta (show CEBPB Proteins) and STAT3 (show STAT3 Proteins), which lead to elevated expression of the hAGT gene in hepatic and adipose tissues
NLRP3 (show NLRP3 Proteins) gene deletion attenuates Ang II-induced NLRP3 (show NLRP3 Proteins) inflammasome activation, phenotypic transformation from a contractile phenotype to a synthetic phenotype and proliferation in primary mice Vascular Smooth Muscle Cells.
adipocyte-derived Agt (show AGXT Proteins) has essentially no contribution to the plasma concentration and no impact on blood pressure compared to liver-derived Agt (show AGXT Proteins).
Lung ischemia-reperfusion injury causes a dysregulation of circulating Ang 2 (show ANGPT2 Proteins) levels and plasma PREP (show PREP Proteins) activity, although no direct link between both phenomena could be shown.
Inhibition of TLR4 (show TLR4 Proteins) ameliorates AngII-impaired cavernosal relaxation, decreases TNF-alpha (show TNF Proteins) levels, and restores Nitric Oxide bioavailability, demonstrating that TLR4 (show TLR4 Proteins) partly mediates AngII-induced cavernosal dysfunction.
Our study is the first to show the important role of IL-6 (show IL6 Proteins) in regulating cardiac pathogenesis via inflammation and apoptosis during AngII-induced hypertension. We also provide a novel link between IL-6 (show IL6 Proteins)/STAT3 (show STAT3 Proteins) and EndoG (show ENDOG Proteins)/MEF2A (show MEF2A Proteins) pathway that affects cardiac hypertrophy during AngII stimulation.
this study demonstrated that Ang II could increase TRPC6 (show TRPC6 Proteins) induced Ca(2 (show CA2 Proteins)+) influx and enhance autophagy through increasing reactive oxygen species levels in podocytes, and autophagy could protect Ang II-treated podocytes.
These results implied that AngII could effectively induce EpiCs to differentiate into vascular smooth muscle-like cells through the AT1 receptor (show AGTRAP Proteins).
Results suggest the involvement of angiotensin II (Ang II), through its angiotensin type-1 receptor (AT1R (show AGTRAP Proteins)) in the inflammation induced by Aah (show ASPH Proteins) venom, in the heart and the aorta.
Angiotensin II stimulates PYY secretion, in turn inhibiting epithelial anion fluxes, thereby reducing net fluid secretion into the colonic lumen.
expression of spinal ACE (show ACE Proteins) increased in streptozotocin-induced diabetic mice, which in turn led to an increase in Ang II levels and tactile allodynia.
In conclusion, endothelial vWF (show VWF Proteins) knockdown prevented angiotensin II-induced ET-1 (show EDN1 Proteins) upregulation through attenuation of NOX-mediated O2- production.
Data suggest that intra-adrenal metabolism of Ang II to Ang III is required for zona glomerulosa cell-mediated relaxation of adrenal arterioles but not for aldosterone secretion.
NADPH oxidase (show NOX1 Proteins) plays an important role in proMMP-2 expression and activation and MMP-2 (show MMP2 Proteins) mediated SMC (show DYM Proteins) proliferation occurs through the involvement of Spm (show NPC1 Proteins)-Cer (show CBLN1 Proteins)-S1P (show MBTPS1 Proteins) signaling axis under ANG II stimulation of PASMCs
The metabolism of angiotensin II (Ang II) to angiotensin III (Ang III) and its role in the vasorelaxation response in adrenal arteries are reported.
The study identified the serine phosphorylation (p-Ser (show SIGLEC1 Proteins)) sites induced by PKC-Beta (show PRKCB Proteins) activation or AGT, which inhibits insulin (show INS Proteins)-induced p-Tyr (show TYR Proteins) sites on IRS2 (show IRS2 Proteins) and its signals in endothelial cells.
Data suggest up-regulation of AGT in granulosa cells and of Ang II in follicular fluid during preovulatory period; Ang II appears to amplify stimulatory effects of luteinizing hormone on secretion of progesterone/prostaglandins by granulosa cells.
Data suggest that angiotensin II promotes uptake/accumulation of iron (non-transferrin (show Tf Proteins) bound iron) into vascular endothelial cells; such iron accumulation appears to depend on activation of angiotensin type 1 receptor and promotes oxidative stress.
a critical role for H(2)O(2) in angiotensin-II signaling to the endothelial cytoskeleton in a novel pathway that is critically dependent on MARCKS, Rac1, and c-Abl.
The objective of this study was to characterize the profiles of Ang-(1-7), MAS receptor, ACE(2), NEP and PEP during the ovulatory process in cattle.
Fetal adrenal cells in primary culture respond to angiotensin-II by increasing aldosterone production and aldosterone synthase (show CYP11B2 Proteins) [P450c18/CYP11B2 (show CYP11B2 Proteins)] activity.
ANG II inhibits bTREK-1 K(+) channels by a Ca(2+)-dependent mechanism that does not require the depletion of membrane-associated PIP(2).
The protein encoded by this gene, pre-angiotensinogen or angiotensinogen precursor, is expressed in the liver and is cleaved by the enzyme renin in response to lowered blood pressure. The resulting product, angiotensin I, is then cleaved by angiotensin converting enzyme (ACE) to generate the physiologically active enzyme angiotensin II. The protein is involved in maintaining blood pressure and in the pathogenesis of essential hypertension and preeclampsia. Mutations in this gene are associated with susceptibility to essential hypertension, and can cause renal tubular dysgenesis, a severe disorder of renal tubular development. Defects in this gene have also been associated with non-familial structural atrial fibrillation, and inflammatory bowel disease.
alpha-1 antiproteinase, antitrypsin
, angiotensin I
, angiotensin II
, serine (or cysteine) proteinase inhibitor
, serpin A8
, angiotensin ll
, angiotensinogen (PAT)
, zC8A9.1 (angiotensinogen )
, Serpin A8