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[PMID]: 29523869
[Au] Autor:Mogi M; Kohara K; Tabara Y; Tsukuda K; Igase M; Horiuchi M
[Ad] Address:Department of Molecular Cardiovascular Biology and Pharmacology, Ehime University, Graduate School of Medicine, Tohon, Japan. mmogi@m.ehime-u.ac.jp.
[Ti] Title:Correlation between the 24-h urinary angiotensinogen or aldosterone level and muscle mass: Japan shimanami health promoting program study.
[So] Source:Hypertens Res;, 2018 Mar 09.
[Is] ISSN:1348-4214
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Our previous report indicated that sarcopenia is associated with arterial stiffness and cardiovascular death. The renin-angiotensin system (RAS) plays an important role in cardiovascular disease and its activation may be correlated with sarcopenia according to basic research. However, few clinical studies have assessed the correlation between skeletal muscle loss and RAS component concentrations in healthy subjects. The purpose of this study was to investigate the relationships between the excretion of angiotensinogen (AGT) and aldosterone (Ald) in 24-h urine samples and clinical and sarcopenic indices. A total of 344 people participated in a voluntary medical check-up program, "Anti-Aging Doc", and underwent measurement of their sarcopenia-related indices. Urine samples were collected for 24-h within 8 weeks after a medical check-up using a partition cup and a proportional sampling method. Urine AGT and Ald levels were evaluated by enzyme-linked immunosorbent assay (ELISA). After compensating for possible confounding parameters, including baPWV, the 24-h urinary excretion of AGT was independently and negatively associated with the thigh muscle cross-sectional area. On the other hand, urinary Ald excretion was not associated with sarcopenia-related indices after compensation, even though it showed a modest but significantly positive association with sarcopenic indices in single regression analysis. Urinary AGT was related to sarcopenic indices and may be involved in the pathogenesis of sarcopenia. On the other hand, urinary Ald was not related to sarcopenic indices when considering other risk factors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1038/s41440-018-0021-9

  2 / 5079 MEDLINE  
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[PMID]: 29521315
[Au] Autor:Örsçelik Ö; Özkan B; Arslan A; Sahin EE; Sakarya O; Sürmeli OA; Balci Fidanci S; Çelik A; Çimen BY; Özcan IT
[Ad] Address:Department of Cardiology, Faculty of Medicine, Mersin University; Mersin-Turkey. ozcanorscelik@yahoo.com.
[Ti] Title:Relationship between intrarenal renin-angiotensin activity and re-hospitalization in patients with heart failure with reduced ejection fraction.
[So] Source:Anatol J Cardiol;19(3):205-212, 2018 Mar.
[Is] ISSN:2149-2271
[Cp] Country of publication:Turkey
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Heart failure (HF) is a clinical syndrome resulting from structural or functional damages. Although clinical trials have shown that the plasma renin-angiotensin system (RAS) activation decreases HF functional status and increases hospitalization for HF patients, the effect of intrarenal RAS activity is still unknown. In this study, we investigated the relationship between the New York Heart Association (NYHA) class, duration, and number of hospitalizations in the previous year and urinary angiotensinogen (UAGT) in patients with HF with reduced ejection fraction (HFrEF). METHODS: This study included 85 patients who had an ejection fraction of <40% and were receiving optimal medical treatment. Among these, 22 were excluded from the study for various reasons. Demographically and biochemically, the remaining 63 patients were compared according to the NYHA functional classes and re-hospitalization status. RESULTS: When the groups were compared in terms of N-terminal pro-B-type natriuretic peptide (NT-proBNP), UAGT, and high-sensitivity C-reactive protein (Hs-CRP), it was found that these parameters were significantly higher in patients who were hospitalized more than two times in the previous year [p<0.001; p=0.007; p<0.001, respectively]. There was a significant correlation between number of hospitalizations and NT-proBNP (r=0.507, p<0.001), Hs-CRP (r=0.511, p<0.001), hemoglobin (r=-0.419, p=0.001), serum sodium (r=-0.26, p=0.04), and systolic blood pressure (r=-0.283, p=0.02). When the independence of multiple correlations was assessed using multiple linear regression analysis, NT-proBNP, Hs-CRP, and hemoglobin levels were independent predictors of re-hospitalization, but this was not the same for UAGT. CONCLUSION: Although UAGT levels are high in patients with poor NYHA functional class and repeated hospitalizations, this marker is not valuable for predicting repeated hospitalization in patients with HFrEF.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.14744/AnatolJCardiol.2018.68726

  3 / 5079 MEDLINE  
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[PMID]: 29514038
[Au] Autor:Zavrsnik M; Letonja J; Makuc J; Seruga M; Cilensek I; Petrovic D
[Ad] Address:Department for Diabetes and Metabolic Diseases, Clinic for Internal Medicine, University Medical Centre Maribor, Maribor, Slovenia. matej.zavrsnik1@guest.arnes.si.
[Ti] Title:Interleukin-4 gene (IL4) polymorphism rs2243250 is not associated with diabetic nephropathy (DN) in Caucasians with type 2 diabetes mellitus (T2DM).
[So] Source:Bosn J Basic Med Sci;, 2018 Mar 07.
[Is] ISSN:1840-4812
[Cp] Country of publication:Bosnia and Herzegovina
[La] Language:eng
[Ab] Abstract:Diabetic nephropathy (DN) is a microvascular complication that affects up to 40% of diabetic patients and can lead to end-stage kidney disease. Inflammatory cytokines such as interleukin 1 (IL-1), IL-6, IL-18 and tumor necrosis factor-α have been linked to the development and progression of DN. The aim of our study was to examine the relationship between rs2243250 polymorphism of the interleukin 4 gene (IL4) and DN in patients with type 2 diabetes mellitus (T2DM). This study is a continuation of our previous research on the association between angiotensinogen (AGT) gene polymorphisms and DN in patients with T2DM. We included 651 unrelated Slovenian (Caucasian) patients who had had T2DM for at least 10 years. The participants were classified into a group of T2DM patients with DN (276 cases) and a group without DN (375 controls). IL4 rs2243250 polymorphism was analyzed using a TaqMan SNP genotyping assay and StepOne Real-Time PCR System. The frequencies of rs2243250 TT, CT and CC (wild type) genotypes were 3.2%, 29.4% and 67.4%, respectively in patients with DN, and 2.7%, 34.4% and 62.9%, respectively in controls. Our logistic regression analysis adjusted for gender, age, diabetes duration, and glycosylated hemoglobin showed no association between rs2243250 and the risk for DN (OR 1.06; CI 0.37-3.05; p = 0.9). IL4 rs2243250 is not associated with DN in our subset of Slovenian patients with T2DM.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:Publisher
[do] DOI:10.17305/bjbms.2018.2688

  4 / 5079 MEDLINE  
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[PMID]: 29513563
[Au] Autor:Webster LM; Gill C; Seed PT; Bramham K; Wiesender C; Nelson-Piercy C; Myers JE; Chappell LC
[Ad] Address:Women's academic Health Centre, King's College London, United Kingdom.
[Ti] Title:Chronic hypertension in pregnancy: the impact of ethnicity and superimposed preeclampsia on placental, endothelial and renal biomarkers.
[So] Source:Am J Physiol Regul Integr Comp Physiol;, 2018 Mar 07.
[Is] ISSN:1522-1490
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Black ethnicity is associated with worse pregnancy outcomes in women with chronic hypertension. Pre-existing endothelial and renal dysfunction, and poor placentation may contribute but pathophysiological mechanisms underpinning increased risk are poorly understood. This cohort study aimed to investigate the relationship between ethnicity, superimposed pre-eclampsia and longitudinal changes in markers of endothelial, renal and placental dysfunction in women with chronic hypertension. Plasma concentrations of placental growth factor (PlGF), syndecan-1, renin, aldosterone, and urinary angiotensinogen:creatinine ratio (AGTCR), protein:creatinine ratio (PCR) and albumin:creatinine ratio (ACR) were quantified during pregnancy and postpartum in women with chronic hypertension. Comparisons of longitudinal biomarker concentrations were made using log-transformation and random effects logistic regression allowing for gestation. Of 117 women, superimposed preeclampsia was diagnosed in 21% (n=25), with 24% (n=6) having an additional diagnosis of diabetes. The cohort included 63 (54%) women who self-identified as of Black ethnicity. PlGF concentrations were 67% lower (95% CI -79% to -48%), and AGTCR, PCR and ACR were higher over gestation, in women with subsequent superimposed preeclampsia (compared to those without superimposed preeclampsia). PlGF <100 pg/mL at 20-23.9 weeks' gestation predicted subsequent birthweight <3rd centile with 88% sensitivity (95% CI 47%-100%) and 83% specificity (95% CI 70%-92%). Black women had 43% lower renin (95% CI -58% to -23%) and 41% lower aldosterone (95%CI -45% to -15%) concentrations over gestation. Changes in placental (PlGF) and renal (AGTCR/PCR/ACR) biomarkers predated adverse pregnancy outcome. Ethnic variation in the renin-angiotensin-aldosterone system exists in women with chronic hypertension in pregnancy and may be important in treatment selection.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:Publisher
[do] DOI:10.1152/ajpregu.00139.2017

  5 / 5079 MEDLINE  
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[PMID]: 29432515
[Au] Autor:Sato E; Wang AY; Satoh M; Nishikiori Y; Oba-Yabana I; Yoshida M; Sato H; Ito S; Hida W; Mori T
[Ad] Address:Division of Nephrology, Endocrinology, and Vascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
[Ti] Title:Urinary angiotensinogen excretion level is associated with elevated blood pressure in the normotensive general population.
[So] Source:Am J Hypertens;, 2018 Feb 08.
[Is] ISSN:1941-7225
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Background: Inflammation, intrarenal renin-angiotensin system activation, oxidative stress, and carbonyl stress have been postulated to play a fundamental role in controlling blood pressure. However, little is known about the association among renal renin-angiotensin system activation, carbonyl stress, and blood pressure elevation. Methods: We evaluated the relationship between blood pressure elevation and either renal renin-angiotensin system activity or carbonyl stress in the general population (N=355) in Japan. To minimize the effect of anti-hypertensive drug therapy, we divided participants into three groups (normotensive, hypertensive-with-non-medication, and hypertensive-with-medication). Intrarenal renin-angiotensin system activity and carbonyl stress were indicated by the urinary angiotensinogen and carbonyl compound excretion levels, respectively. Results: The urinary angiotensinogen and carbonyl compound excretion levels were significantly associated with blood pressure. Using a stepwise multiple regression analysis, we found that the urinary angiotensinogen excretion levels were strongly associated with blood pressure elevation, compared with inflammation, oxidative stress, and carbonyl stress markers, in all groups. Urinary carbonyl compound excretion was significantly associated with blood pressure in only the hypertensive-without-medication group. Furthermore, blood pressure was significantly increased in these participants, and both the urinary angiotensinogen and carbonyl compound levels were high. The urinary angiotensinogen excretion levels were strongly associated with elevated blood pressure in normotensive people, and inappropriate renal renin-angiotensin system activity and carbonyl stress independently contributed to the development of hypertension. Conclusions: These findings suggest that renin-angiotensin system activation, particularly renal renin-angiotensin system activation exert a fundamental role in the pathogenesis of hypertension in the general population.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1093/ajh/hpy020

  6 / 5079 MEDLINE  
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[PMID]: 29425341
[Au] Autor:Leifheit-Nestler M; Kirchhoff F; Nespor J; Richter B; Soetje B; Klintschar M; Heineke J; Haffner D
[Ad] Address:Department of Pediatric Kidney, Liver and Metabolic Diseases, Pediatric Research Center, Hannover Medical School, Hannover, Germany.
[Ti] Title:Fibroblast growth factor 23 is induced by an activated renin-angiotensin-aldosterone system in cardiac myocytes and promotes the pro-fibrotic crosstalk between cardiac myocytes and fibroblasts.
[So] Source:Nephrol Dial Transplant;, 2018 Feb 07.
[Is] ISSN:1460-2385
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Background: Fibroblast growth factor 23 (FGF23) is discussed as a new biomarker of cardiac hypertrophy and mortality in patients with and without chronic kidney disease (CKD). We previously demonstrated that FGF23 is expressed by cardiac myocytes, enhanced in CKD and induces cardiac hypertrophy via activation of FGF receptor 4 independent of its co-receptor klotho. The impact of FGF23 on cardiac fibrosis is largely unknown. Methods: By conducting a retrospective case-control study including myocardial autopsy samples from 24 patients with end-stage CKD and in vitro studies in cardiac fibroblasts and myocytes, we investigated the pro-fibrotic properties of FGF23. Results: The accumulation of fibrillar collagens I and III was increased in myocardial tissue of CKD patients and correlated with dialysis vintage, klotho deficiency and enhanced cardiac angiotensinogen (AGT) expression. Using human fibrosis RT2 Profiler PCR array analysis, transforming growth factor (TGF)-ß and its related TGF-ß receptor/Smad complexes, extracellular matrix remodeling enzymes and pro-fibrotic growth factors were upregulated in myocardial tissue of CKD patients. FGF23 stimulated cell proliferation, migration, pro-fibrotic TGF-ß receptor/Smad complexes and collagen synthesis in cultured cardiac fibroblasts. In isolated cardiac myocytes, FGF23 enhanced collagen remodeling, expression of pro-inflammatory genes and pro-survival pathways and induced pro-hypertrophic genes. FGF23 stimulated AGT expression in cardiac myocytes and angiotensin II and aldosterone, as components of the renin-angiotensin-aldosterone system (RAAS), induced FGF23 in cardiac myocytes. Conclusions: Our data demonstrate that activated RAAS induces FGF23 expression in cardiac myocytes and thereby stimulates a pro-fibrotic crosstalk between cardiac myocytes and fibroblasts, which may contribute to myocardial fibrosis in CKD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1093/ndt/gfy006

  7 / 5079 MEDLINE  
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[PMID]: 29507351
[Au] Autor:Ohashi N; Isobe S; Matsuyama T; Ishigaki S; Tsuji N; Fujikura T; Tsuji T; Kato A; Yasuda H
[Ad] Address:Internal Medicine 1, Hamamatsu University School of Medicine, 1-20-1 Handayama Higashi-ku, 431-3192, Hamamatsu, Japan. ohashi-n@hama-med.ac.jp.
[Ti] Title:Night-time activation of the intrarenal renin-angiotensin system due to nocturnal hypertension is associated with renal arteriosclerosis in normotensive IgA nephropathy patients.
[So] Source:Hypertens Res;, 2018 Mar 05.
[Is] ISSN:1348-4214
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Intrarenal renin-angiotensin system (RAS) activation plays an important role in the development of hypertension and renal damage. However, the association between daytime and night-time intrarenal RAS activation and renal structural damage in normotensive IgA nephropathy patients is unclear. We investigated the relationships between urinary angiotensinogen (U-AGT) excretion, which reflects intrarenal RAS activity, and renal structural damage (i.e., endocapillary and mesangial cell hypercellularity, arteriolar hyalinosis and arteriosclerosis levels, and global glomerulosclerosis and tubulointerstitial fibrosis percentages) in 27 normotensive IgA nephropathy patients (age 39.2 ± 13.6 years, 10 men and 17 women, estimated glomerular filtration rate (eGFR) 74.0 ± 17.3 ml/min/1.73 m , urinary protein excretion 0.58 ± 0.50 g/day, and U-AGT excretion 64.9 ± 100.6 µg/day). The arteriosclerosis level had a significant positive association with the daytime and night-time U-AGT excretion levels. By contrast, the endocapillary and mesangial cell hypercellularity and arteriolar hyalinosis levels and global glomerulosclerosis and tubulointerstitial fibrosis percentages did not correlate with the daytime and night-time U-AGT excretion levels. The daytime and night-time U-AGT excretion levels were higher in patients with arteriosclerotic changes than in patients without these changes. Multiple linear regression analysis revealed that the arteriosclerosis levels had a significant positive association with the U-AGT excretion levels at night after adjusting for age, sex, body mass index, and the eGFR. However, when diastolic BP was added as an independent variable, the relationship between U-AGT excretion and arteriosclerosis at night disappeared. In normotensive IgA nephropathy patients, intrarenal RAS activation at night due to nocturnal hypertension may be associated with arteriosclerosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:Publisher
[do] DOI:10.1038/s41440-018-0026-4

  8 / 5079 MEDLINE  
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[PMID]: 29506687
[Au] Autor:Liu B; Zhang R; Wei S; Yuan Q; Xue M; Hao P; Xu F; Wang J; Chen Y
[Ad] Address:Department of Emergency, Qilu Hospital, Shandong University, Jinan, China; Chest Pain Center, Qilu Hospital, Shandong University, Jinan, China; Key Laboratory of Emergency and Critical Care Medicine of Shandong Province, Qilu Hospital, Shandong University, Jinan, China; Institute of Emergency and Cr
[Ti] Title:ALDH2 protects against alcoholic cardiomyopathy through a mechanism involving the p38 MAPK/CREB pathway and local renin-angiotensin system inhibition in cardiomyocytes.
[So] Source:Int J Cardiol;257:150-159, 2018 Apr 15.
[Is] ISSN:1874-1754
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: Angiotensin II (Ang II) in the local cardiac renin-angiotensin system (RAS) is closely associated with alcoholic cardiomyopathy (ACM). Inhibition of local cardiac RAS has great significance in the treatment of ACM. Although aldehyde dehydrogenase 2 (ALDH2) has been demonstrated to protect against ACM through detoxification of aldehydes, the precise mechanisms are largely unknown. In the present study, we determined whether ALDH2 improved cardiac damage by inhibiting the local RAS in ACM and investigated the related regulatory mechanisms. METHODS AND RESULTS: Adult male mice were fed with 5% ethanol or a control diet for 2months, with or without the ALDH2 activator Alda-1. Heavy ethanol consumption induced cardiac damage, increased angiotensinogen (AGT) and Ang II and decreased myocardial ALDH2 activity in hearts. ALDH2 activation improved ethanol-induced cardiac damage and decreased AGT and Ang II in hearts. In vitro, ALDH2 activation or overexpression decreased AGT and Ang II in cultured cardiomyocytes treated with 400mmol/L ethanol for 24h. Furthermore, p38 MAP kinase (p38 MAPK)/cyclic adenosine monophosphate response element-binding protein (CREB) pathway activation by ethanol increased AGT and Ang II in cardiomyocytes. In addition, ALDH2 activation or overexpression inhibited the p38 MAPK/CREB pathway leading to decreased AGT and Ang II in cardiomyocytes. We also found that p38 MAPK activation effectively mitigated Alda-1-decreased AGT and Ang II, the effect of which was reversed by inhibition of CREB. CONCLUSIONS: ALDH2 decreased AGT and Ang II in the local cardiac RAS via inhibiting the p38 MAPK/CREB pathway in ACM, thus improving ethanol-induced cardiac damage.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:In-Data-Review

  9 / 5079 MEDLINE  
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[PMID]: 29371216
[Au] Autor:Chang L; Xiong W; Zhao X; Fan Y; Guo Y; Garcia-Barrio M; Zhang J; Jiang Z; Lin JD; Chen YE
[Ad] Address:Frankel Cardiovascular Center, Department of Internal Medicine, University of Michigan, Ann Arbor, MI.
[Ti] Title:Bmal1 in Perivascular Adipose Tissue Regulates Resting Phase Blood Pressure Through Transcriptional Regulation of Angiotensinogen.
[So] Source:Circulation;, 2018 Jan 25.
[Is] ISSN:1524-4539
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:-The perivascular adipose tissue (PVAT), surrounding vessels, constitutes a distinct functional integral layer of the vasculature required to preserve vascular tone under physiological conditions. However, there is little information regarding the relationship between PVAT and blood pressure regulation, including its potential contributions to circadian blood pressure variation. -Using unique brown adipocyte-specific aryl hydrocarbon receptor nuclear translocator-like protein 1 (Bmal1) and angiotensinogen (Agt) knock out mice we determined the vasoactivity of homogenized PVAT in aortic rings and how brown-adipocyte peripheral expression of Bmal1 and Agt in PVAT regulate the amplitude of diurnal change in blood pressure in mice. -We uncovered a peripheral clock in PVAT and demonstrated that loss of Bmal1 in PVAT reduces blood pressure in mice during the resting phase leading to a super-dipper phenotype. PVAT extracts from wild type mice significantly induced contractility of isolated aortic rings in an endothelium independent manner. This property was impaired in PVAT from brown adipocyte-selective Bmal1 deficient mice (BA-Bmal1-KO). The PVAT contractile properties are mediated by local angiotensin II (Ang II), operating through angiotensin II type 1 receptor-dependent signaling in the isolated vessels and is linked to PVAT circadian regulation of Agt. Indeed, Agt mRNA and Ang II levels in PVAT of BA-Bmal1-KO mice were significantly reduced. Systemic infusion of Ang II, in turn, reduced Bmal1 expression in PVAT while eliminating the hypotensive phenotype during the resting phase in BA-Bmal1-KOmice. Agt, highly expressed in PVAT, shows circadian expression in PVAT and selective deletion of Agt in brown adipocytes recapitulates the phenotype of selective deletion of Bmal1 in brown adipocytes. Furthermore, Agt is a transcriptional target of Bmal1 in PVAT. -These data indicate that local Bmal1 in PVAT regulates Agt expression and the ensuing increase in Ang II, which acts on smooth muscle cells (SMCs) in the vessel walls to regulate vasoactivity and blood pressure on a circadian fashion during the resting phase. These findings will contribute to better understand cardiovascular complications of circadian disorders, alterations in the circadian dipping phenotype and the crosstalk between systemic and peripheral regulation of blood pressure.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180303
[Lr] Last revision date:180303
[St] Status:Publisher

  10 / 5079 MEDLINE  
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[PMID]: 29488353
[Au] Autor:Liu TT; Hao Q; Zhang Y; Li ZH; Cui ZH; Yang W
[Ad] Address:Department of Ophthalmology, First Hospital of Jilin University, Changchun, China.
[Ti] Title:Effects of microRNA-133b on retinal vascular endothelial cell proliferation and apoptosis through angiotensinogen-mediated angiotensin II- extracellular signal-regulated kinase 1/2 signalling pathway in rats with diabetic retinopathy.
[So] Source:Acta Ophthalmol;, 2018 Feb 28.
[Is] ISSN:1755-3768
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:PURPOSE: This study aimed to explore the effects of microRNA-133b (miR-133b) on diabetic retinopathy (DR) by targeting angiotensinogen (AGT) through the angiotensin-II (AngII) extracellular signal-regulated kinase 1/2 (ERK1/2) signalling pathway in rats. METHODS: The DR rat model was established using retinal tissues of DR rats and normal rats. Immunohistochemistry was performed to detect the protein expressions of AGT and CD34 in retinal tissues. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were applied to detect miR-133b expression, AGT, AngII, ERK1/2 mRNA, and protein expressions in tissues and cells after transfection. Retinal vascular endothelial cells were cultured and divided into normal, blank, miR-133b mimics, miR-133b mimics negative control (NC), miR-133b inhibitors, miR-133b inhibitors NC, siRNA NC, siRNA-AGT, and miR-133b inhibitors + siRNA-AGT groups. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay was performed to detect cell proliferation. Cell cycle and apoptosis were evaluated using flow cytometry. RESULTS: Compared with normal rats, AGT and CD34 were expressed more frequently in DR rats. MicroRNA (miR)-133b expression was downregulated but AGT, AngII, ERK1 and ERK2 mRNA expressions were upregulated in retinal tissues of DR rats. When compared to the normal group, all other groups displayed decreased cell proliferation, increased cell number in G0/G1, decreased cell number in S stage, increased cell apoptosis rate and declined miR-133b expression. As well, significant increased expressions of AGT and the AngII-ERK1/2 pathway-related proteins were observed in retinal vascular endothelial cells in all groups except the normal group. The miR-133b mimics and siRNA-AGT groups had increased cell proliferation, decreased cell number in the G0/G1 phase, increased cell number in S stage, decreased cell apoptosis rate and decreased expressions of AGT and AngII-ERK1/2 pathway-related proteins than the miR-133b inhibitors + siRNA-AGT group. The miR-133b inhibitors group exhibited opposite trends compared with the miR-133b mimics and siRNA-AGT groups. CONCLUSION: The study provides data to suggest that miR-133b induces proliferation and inhibits apoptosis of retinal vascular endothelial cells by targeting AGT through the AngII-ERK1/2 signalling pathway in DR rats.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180228
[Lr] Last revision date:180228
[St] Status:Publisher
[do] DOI:10.1111/aos.13715


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