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Giang Nguyen So Young Park Cong Thuc Le Won Sun Park Dae Hee Choi Eun-Hee Cho 《Biochemical and biophysical research communications》2018,495(4):2649-2656
Background
Chronic liver disease is becoming a major cause of morbidity and mortality worldwide. During liver injury, hepatic stellate cells (HSCs) trans-differentiate into activated myofibroblasts, which produce extracellular matrix.Succinate and succinate receptor (G-protein coupled receptor91, GPR91) signaling pathway has now emerged as a regulator of metabolic signaling. A previous study showed that succinate and its specific receptor, GPR91, are involved in the activation of HSCs and the overexpression of α-smooth muscle actin (α-SMA).Metformin, a well-known anti-diabetic drug, inhibits hepatic gluconeogenesis in the liver. Many studies have shown that metformin not only prevented, but also reversed, steatosis and inflammation in a nonalcoholic steatohepatitis (NASH) animal model. However, the role of metformin in HSC activation and succinate-GPR91 signaling has not been clarified.Methods
The immortalized human HSCs, LX-2?cells, were used for the in vitro study. For the in vivo study, male C57BL/J6 mice were randomly divided into 3 groups and were fed with a methionine-choline-deficient diet (MCD diet group) as a nonalcoholic steatohepatitis (NASH) mouse model with or without 0.1% metformin for 12 weeks, or were fed a control methionine-choline-sufficient diet (MCS diet group).Results
In our study, metformin and 5-aminoimidazole-4-carboxamide 1-β-d-ribofuranoside (AICAR), which is an analog of adenosine monophosphate, were shown to suppress α-SMA expression via enhanced phosphorylation of AMP-activated protein kinase (AMPK) and inhibition of succinate-GPR91 signaling in activated LX-2?cells induced by palmitate- or succinate. Metformin and AICAR also reduced succinate concentration in the cell lysates when LX-2?cells were treated with palmitate. Moreover, metformin and AICAR reduced interleukin-6 and, transforming growth factor-β1 production in succinate-treated LX-2?cells. Both metformin and AICAR inhibited succinate-stimulated HSC proliferation and cell migration.Mice fed a MCD diet demonstrated increased steatohepatitis and liver fibrosis compared to that of mice fed control diet. Metformin ameliorated steatohepatitis, liver fibrosis, inflammatory cytokine production and decreased α -SMA and GPR91expression in the livers of the MCD diet-fed mice.Conclusion
This study shows that metformin can attenuate activation of HSCs by activating the AMPK pathway and inhibiting the succinate-GPR91 pathway. Metformin has therapeutic potential for treating steatohepatitis and liver fibrosis. 相似文献3.
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Xu Gao Avirup Guha Benjamin Buck Dilesh Patel Melissa J. Snider Michael Boyd Muhammad Afzal Auroa Badin Hemant Godara Zhenguo Liu Jaret Tyler Raul Weiss Steven Kalbfleisch John Hummel Ralph Augostini Mahmoud Houmsse Emile G. Daoud 《Indian pacing and electrophysiology journal》2018,18(2):68-72
Background
Expert opinion recommends performing exercise testing with initiation of Class Ic antiarrhythmic medication.Objective
To evaluate the rate and reason for discontinuation of Ic agent within the first year of follow up, with particular attention to rate of proarrhythmia and the value of routine treadmill testing.Methods
This is a single center retrospective cohort study including consecutive patients with atrial arrhythmias who were initiated on a Class Ic agent from 2011 to 2016. Data was collated from chart review and pharmacy database.Results
The study population included 300 patients (55% male, mean age 61; mean ejection fraction, 56%) started on flecainide (n = 153; 51%) and propafenone (n = 147; 49%). Drug initiation was completed while hospitalized on telemetry and the staff electrophysiologists directed dosing. There was one proarrhythmic event during initiation (0.3%). The primary reason for not being discharged on Ic agent was due to detection of proarrhythmia (n = 15) or ischemia (n = 1) with treadmill testing (5.3%). Exercise testing was the single significant variable to affect the decision to discontinue Ic drug, p < 0.0001 (95% CI: 1.89–6.08%). During follow up, the primary reason for discontinuation of Ic agent was lack of efficacy, 32%.Conclusions
With proper screening, initiation of Class Ic agent is associated with very low rate of proarrhythmia. Treadmill testing is of incremental value and should be completed in all patients after loading Class Ic antiarrhythmic. 相似文献5.
Mohammad El Garhy Marc-Alexander Ohlow Bernward Lauer 《Indian pacing and electrophysiology journal》2018,18(1):20-24
Aims
Shock coil interaction in patients with multiple implantable cardioverter defibrillator (ICD) leads is occasionally observed. We aimed to evaluate the incidence of shock coil interaction and its clinical relevance.Methods and results
All ICD patients (646 patients) who came to follow up control in our ICD ambulance between January 1, 2011, and December 31, 2011 in the department of cardiology in Bad Berka hospital were retrospectively evaluated in this study. All baseline demographic, clinical, and procedural characteristics and postoperative chest x ray in postero-anterior and lateral view as well as clinical and ICD follow up data were evaluated.Among 646 patients 42 had multiple ICD leads (6.5%) of whom 36 patients (5.5% of total cohort patients and 85.7% of patients with multiple ICD leads) had shock coil interaction and presented the study group (Group I). The control group (Group II) consisted of 610 patients without coil-coil interaction including patients with single shock lead (604 patients) or patients with multiple leads but without interaction between shock coils (6 patients).Inappropriate anti-tachycardia therapies and RV lead revisions were more frequent in patients with interaction between shock coils (Group I vs Group II: 27.7% and 5.7%; p = 0.049 and 30.6% vs 6.4; p = 0.0001, respectively).Conclusions
Interaction between shock coils may be one of possible causes of lead failure and resulted in inappropriate therapies and subsequent lead revision. 相似文献6.
U. Boles E.E. Gul L. Fitzgerald F. Sadiq Ali C. Nolan K. Aldworth-Gaumond D.R. Redfearn A. Baranchuk B. Glover C. Simpson H. Abdollah K.A. Michael 《Indian pacing and electrophysiology journal》2018,18(2):56-60
Background
Current algorithms and device morphology templates have been proposed in current Implantable Cardioverter-Defibrillators (ICDs) to minimize inappropriate therapies (ITS), but this has not been completely successful.Aim
Assess the impact of a deliberate strategy of using an atrial lead implant with standardized parameters; based on all current ICD discriminators and technologies, on the burden of ITS.Method
A retrospective single-centre analysis of 250 patients with either dual chamber (DR) ICDs or biventricular ICDs (CRTDs) over a (41.9 ± 27.3) month period was performed. The incidence of ITS on all ICD and CRTD patients was chronicled after the implementation of standardized programming.Results
39 events of anti-tachycardial pacing (ATP) and/or shocks were identified in 20 patients (8% incidence rate among patients). The total number of individual therapies was 120, of which 34% were inappropriate ATP, and 36% were inappropriate shocks. 11 patients of the 250 patients received ITS (4.4%). Of the 20 patients, four had ICDs for primary prevention and 16 for a secondary prevention. All the episodes in the primary indication group were inappropriate, while seven patients (43%) of the secondary indication group experienced inappropriate therapies.Conclusions
The burden of ITS in the population of patients receiving ICDs was 4.4% in the presence of atrial leads. The proposed rationalized programming criteria seems an effective strategy to minimize the burden of inappropriate therapies and will require further validation. 相似文献7.
Taichi Ikedo Manabu Minami Hiroharu Kataoka Kosuke Hayashi Manabu Nagata Risako Fujikawa Fumiyoshi Yamazaki Mitsutoshi Setou Masayuki Yokode Susumu Miyamoto 《Biochemical and biophysical research communications》2018,495(1):332-338
Object
The wall thickness of intracranial aneurysms (IAs) is heterogeneous. Although thinning of the IA wall is thought to contribute to IA rupture, the underlying mechanism remains poorly understood. Recently, imaging mass spectroscopy (IMS) has been used to reveal the distribution of phospholipids in vascular diseases. To investigate the feature of phospholipid composition of IA walls, we conducted IMS in a rat model of experimentally induced IA.Material and methods
IAs were surgically induced in 7-week-old male rats and analyzed by IMS in negative-ion mode.Results
A molecule at m/z 885.5 was more abundant in the thickened wall than in the thinned wall (P = 0.03). Multiple-stage mass spectroscopy revealed the molecule to be phosphatidylinositol containing stearic acid and arachidonic acid (PI 18:0/20:4). Immunohistochemistry indicated that vascular smooth muscle cells (SMCs) in the thickened wall had dedifferentiated phenotypes. To investigate the relationship between accumulation of PI (18:0/20:4) and phenotypic changes in SMCs, we subjected primary mouse aortic SMCs to liquid chromatography–tandem mass spectrometry. Notably, dedifferentiated SMCs had 1.3-fold more PI (18:0/20:4) than partly differentiated SMCs.Conclusions
Our study demonstrated the heterogeneity in phospholipid composition of the aneurysmal walls using experimentally induced IAs. PI (18:0/20:4) accumulated at high levels in the thickened aneurysmal wall where synthetic dedifferentiated SMCs exist, suggesting that this phospholipid may be involved in the phenotypic switching of medial SMCs in the IA wall. 相似文献8.
Pan Zhang Jingwei Feng Yunjun Liao Junrong Cai Tao Zhou Mingliang Sun Jianhua Gao Kai Gao 《Biochemical and biophysical research communications》2018,495(3):2249-2256
Background
Flap necrosis due to insufficient blood supply is a common postoperative complication in random pattern flaps. Stem cell therapies have emerged as promising biologics for tissue ischemia. A novel fat derived product, stromal vascular fraction gel (SVF-gel), can be prepared with lipoaspirate through simple mechanical processing, removing only the lipid content. SVF-gel enriches adipose-derived stem cells and potentially beneficial for flap necrosis.Methods
Nude mice ischemic flaps were treated with human SVF-gel, stromal vascular fraction (SVF) cell suspension or saline (n = 10). They were injected to the flap recipient beds, and necrosis and vascularization was assessed on postoperative day 14. We harvested the necrosis-free distal to evaluated skin healthiness and neovasculogenesis by Masson's trichrome stain and immunofluorescence, etc. Pro-angiogenic factors were assessed with tissue qRT-PCR. Finally, we traced the grafted human tissue with immunofluorescence.Results
SVF-gel-treated flaps have the smallest necrotic zones (22.05% ± 0.0438) compared with the saline controls (53.78% ± 0.1412) or SVF-treated ones (35.54% ± 0.0850, p = 0.039). Numerous functional musculocutaneous perforators were developed around SVF-gel grafts. The SVF-gel-treated skin had the best fat restoration (231.3 ± 48.1 μm) among three groups (F = 10.83, p = 0.0102) while saline-treated flap distal appeared fibrotic. SVF-gel-treated flaps also had ～43% more CD31 + capillaries (p = 0.0152) with ～3 folds more gene expression of angiogenic cytokines of VEGF and bFGF (p = 0.0310 and 0.0303, respectively) than saline-treated controls. Furthermore, we found hSVF-gel cells (hGolgi+) had directly engrafted as vessel component (α-smooth muscle actin, α-SMA+) to the flap.Conclusion
Adipose cellular matrix enhanced flap neovascularization partly by direct incorporation, improved flap survival and fat restoration. The composition-selective fat grafting with SVF-gel demonstrated efficacy comparable with stem cell therapy and is especially valuable for clinical translation. 相似文献9.
Jem D. Lane Sarah Whittaker-Axon Richard J. Schilling Martin D. Lowe 《Indian pacing and electrophysiology journal》2019,19(2):49-54
Background
Implantable cardioverter-defibrillator (ICD) lead parameters may deteriorate due to right ventricular (RV) disease such as arrhythmogenic right ventricular cardiomyopathy (ARVC), with implications for safe delivery of therapies. We compared ICD and CRT-D (cardiac resynchronisation therapy-defibrillator) lead parameters in patients with ARVC and dilated cardiomyopathy (DCM).Methods
RV lead sensing (R wave amplitude) and pacing (threshold and amplitude-pulse width product (APWP)), left ventricular (LV) pacing (APWP), and imaging parameter trends were assessed in 18 patients with ARVC and 18 with DCM.Results
R wave amplitude did not change significantly over time in either group (over 5 years, ARVC -0.4 mV, 95% CI -3.8–3.0 mV; DCM -1.8 mV, 95% CI -5.0–1.3 mV). Within ARVC group, divergent trends were seen according to lead position. DCM patients experienced an increase in RV lead threshold (+1.1 V over 5 years, 95% CI + 0.5 to +1.7 V) and RV APWP (+0.48 Vms over 5 years, 95% CI + 0.24 to +0.71 Vms); ARVC patients had no change. ARVC patients had a higher LVEF at baseline than DCM patients (52 vs 20%, p < 0.001), though LVEF decreased over time for the former, while increasing for the latter. TAPSE did not change over time for ARVC patients.Conclusions
Lead parameters in ARVC patients were stable over medium-term follow up. In DCM patients, RV lead threshold and RV and LV APWP increased over time. These differential responses for DCM and ARVC were not explained by imaging indices, and may reflect distinct patterns of disease progression. 相似文献10.
Amirfarjam Fazelifar Fatemeh Jorfi Majid Haghjoo 《Indian pacing and electrophysiology journal》2018,18(1):13-19
Background
With increasing use of cardiac resynchronization therapy (CRT), treating physicians should be familiar with different electrocardiographic (ECG) patterns of left ventricular (LV) lead and biventricular (BiV) pacing. However, there are a few publications on ECG patterns during BiV pacing.Purpose
This study was sought to determine different ECG patterns in patients with BiV pacing.Methods
Twelve-lead ECGs during BiV pacing (right ventricular leads at apex and LV leads in one of the lateral coronary veins) were analyzed in 181 consecutive patients (121 male; mean age, 62.0 ± 13.5 years) with advanced heart failure and baseline left bundle branch block pattern after at least 6-month of uncomplicated CRT.Results
During BiV pacing, 65% of the patients showed a dominant R wave in V1. There was a right axis deviation in 57% in frontal plane. However, a left superior axis emerged in 34% and normal frontal plane axis in 9%. Sequential BiV pacing (73% vs. 58%, P = 0.04) and pacing from posterolateral coronary vein (80% vs. 60%, p = 0.045) were more likely to present with a dominant R wave in V1. In sequential pacing, AV interval was significantly longer in patients with negative complex in V1 than in those with positive complex (124 ± 21 vs. 116 ± 8.0, p = 0.005). A Q/q wave was detected in 85% of patients in lead I and 78% in lead aVL.Conclusions
BiV pacing from lateral coronary venous branches and right ventricular apex characteristically presented with dominant R wave in V1, Q/q wave in leads I and aVL, and right or left superior axis. However, a negative complex in V1, QRS axis in other quadrants, and lack of Q/q wave in leads I and aVL did not necessarily indicate a problem. 相似文献11.
Kaori Ueda Akishi Onishi Shin-ichiro Ito Makoto Nakamura Masayo Takahashi 《Biochemical and biophysical research communications》2018,495(4):2595-2601
Purpose
Three-dimensional retinal organoids can be differentiated from embryonic stem cells/induced pluripotent stem cells (ES/iPS cells) under defined medium conditions. We modified the serum-free floating culture of embryoid body-like aggregates with quick reaggregation (SFEBq) culture procedure to obtain retinal organoids expressing more rod photoreceptors and S- and M-cone opsins.Methods
Retinal organoids differentiated from mouse Nrl-eGFP iPS cells were cultured in various mediums during photoreceptor development. To promote rod photoreceptor development, organoids were maintained in media containing 9-cis retinoic acids (9cRA). To obtain retinal organoids with M-opsin expression, we cultured in medium with 1% fetal bovine serum (FBS) supplemented with T3, BMP4, and DAPT. Section immunohistochemistry was performed to visualize the expression of photoreceptor markers.Results
In three-dimensional (3D) retinas exposed to 9cRA, rhodopsin was expressed earlier and S-cone opsins were suppressed. We could maintain 3D retinas up to DD 35 in culture media with 1% FBS. The 3D retinas expressed rhodopsin, S- and M-opsins, but most cone photoreceptors expressed either S- or M-opsins.Conclusion
By modifying culture conditions in the SFEBq protocol, we obtained rod-dominated 3D retinas and S- and M-opsin expressing 3D retinas. 相似文献12.
Muhammad Umer Nisar Muhammad Bilal Munir Michael S. Sharbaugh Floyd W. Thoma Andrew D. Althouse Samir Saba 《Indian pacing and electrophysiology journal》2018,18(1):6-12
Aims
Atrial fibrillation (AF) is the most common sustained arrhythmia encountered in clinical practice. Patients presenting with AF are often admitted to hospital for rhythm or rate control, symptom management, and/or anticoagulation. We investigated temporal trends in AF hospitalizations in United States from 1996 to 2010.Methods
Data were obtained from the National Hospital Discharge Survey (NHDS), a national probability sample survey of discharges conducted annually by National Center for Health Statistics. Because of the survey design, sampling weights were applied to the raw NHDS data to produce national estimates. Hospitalizations with a primary diagnosis of AF were identified using International Classification of Diseases, 9th Revision, Clinical Modification (ICD-9-CM) code of 427.31. Weighted least squares regression was used to test for linear trends in the number of AF admissions, length of stay, and inpatient mortality. We further stratified AF admissions based on patients' age, gender, and race.Results
Admissions for a primary diagnosis of AF increased from approximately 286,000 in 1996 to about 410,000 in 2010 with a significant linear trend (β = 9470 additional admissions per year, p < 0.001). The trend of increased AF admissions was uniform across patient sub-groups. Overall, mean length of stay for AF admissions was 3.75 days, and this remained relatively stable over time (β = 0.002 days, p = 0.884). Inpatient mortality was 0.96% and also remained stable over time (β = 0.031%, p = 0.181).Conclusion
Our data demonstrate an increase in the number of AF admissions but constant length of stay and mortality over time. 相似文献13.
Shanjie Wang Yanhong Fan Xinyu Feng Chuang Sun Zhaofeng Shi Tian Li Jianjun Lv Zhi Yang Zhijing Zhao Dongdong Sun 《Biochemical and biophysical research communications》2018,495(1):292-299
Background
Cardiomyocyte autophagy and apoptosis are crucial events underlying the development of cardiac abnormalities and dysfunction after myocardial infarction (MI). A better understanding of the cell signaling pathways involved in cardiac remodeling may support the development of new therapeutic strategies for the treatment of heart failure (HF) after MI.Methods
A cardiac MI injury model was constructed by ligating the left anterior descending (LAD) coronary artery. Neonatal cardiomyocytes were isolated and cultured to investigate the mechanisms underlying the protective effects of nicorandil on MI-induced injury.Results
Nicorandil reduced cardiac enzyme release, mitigated left ventricular enlargement and cardiac dysfunction after MI, as evaluated by echocardiography and hemodynamic measurements. According to the results of the western blot analysis and immunofluorescence staining, nicorandil enhanced autophagic flux and reduced apoptosis in cardiomyocytes subjected to hypoxic injury. Interestingly, nicorandil increased Mst1 and p-Mst1 levels in cardiomyocytes subjected to MI injury. Mst1 knockout abolished the protective effects of nicorandil on cardiac remodeling and dysfunction after MI. Mst1 knockout also abolished the beneficial effects of nicorandil on cardiac enzyme release and cardiomyocyte autophagy and apoptosis.Conclusions
Nicorandil alleviates post-MI cardiac dysfunction and remodeling. The mechanisms were associated with enhancing autophagy and inhibiting apoptosis through Mst1 inhibition. 相似文献14.
Tomohiro Ueda Tomohisa Takagi Kazuhiro Katada Takaya Iida Katsura Mizushima Osamu Dohi Tetsuya Okayama Naohisa Yoshida Kazuhiro Kamada Kazuhiko Uchiyama Osamu Handa Takeshi Ishikawa Hideyuki Konishi Yuji Naito Yukio Nagasaki Yoshito Itoh 《Biochemical and biophysical research communications》2018,495(2):2044-2049
Background
Intestinal ischemia-reperfusion (I-R) injury is a serious abdominal condition leading to multiple organ failure with high mortality. However, no reliable treatment is available. A redox nanoparticle (RNPO) was recently developed, and its efficacy for several intestinal inflammatory conditions has been reported. To this end, the aim of this study was to investigate the therapeutic effects of RNPO on intestinal I-R injury in mice.Methods
Ischemia was induced in the small intestine of C57BL/6 mice by occluding the superior mesenteric artery for 45 min under anesthesia followed by reperfusion for 4 h. Mice were orally administered the vehicle or RNPO 1 h before ischemia. Inflammatory markers such as histological findings, thiobarbituric acid (TBA)-reactive substances as an index of lipid peroxidation, myeloperoxidase (MPO) activity as an index of neutrophil infiltration, and expression of pro-inflammatory cytokine mRNA in the intestinal mucosa were assessed.Results
Induction of I-R caused a significant increase in inflammatory markers (histological scores, TBA-reactive substances, MPO activity, and expression of keratinocyte chemoattractant mRNA). These changes were significantly attenuated in RNPO-treated mice as compared to vehicle-treated mice.Conclusion
Orally administered RNPO attenuated intestinal I-R injury in mice in association with reductions in neutrophil infiltration and lipid peroxidation, suggesting the possibly potential of RNPO as a therapeutic agent for intestinal I-R injury. 相似文献15.
Iskra H. Bayraktarova Milko K. Stoyanov Boyan T. Kunev Tchavdar N. Shalganov 《Indian pacing and electrophysiology journal》2018,18(2):49-53
Purpose
To study the correlation between the sudden prolongations of the atrio-Hisian (AH) interval with ≥50 ms during burst and programmed atrial stimulation, and to define whether the AH jump during burst atrial pacing is a reliable diagnostic criterion for dual AV nodal physiology.Methods
Retrospective data on 304 patients with preliminary ECG diagnosis of AV nodal reentrant tachycardia (AVNRT), confirmed during electrophysiological study, was analyzed for the presence of AH jump during burst and programmed atrial stimulation, and for correlation between the pacing modes for inducing the jump. Wilcoxon signed-ranks test and Spearman's bivariate correlation coefficient were applied, significant was P-value <0.05.Results
The population was aged 48.5 ± 15.7 (12-85) years; males were 38.5%. AH jump occurred during burst atrial pacing in 81% of the patients, and during programmed stimulation – in 78%, P = 0.366. In 63.2% AH jump was induced by both pacing modes; in 17.8% – only by burst pacing; in 14.8% – only by programmed pacing; in 4.2% there was no inducible jump. There was negative correlation between both pacing modes, ρ = –0.204, Р<0.001.Conclusion
Burst and programmed atrial stimulation separately prove the presence of dual AV nodal physiology in 81 and 78% of the patients with AVNRT, respectively. There is negative correlation between the two pacing modes, allowing the combination of the two methods to prove diagnostic in 95.8% of the patients. 相似文献16.
Yuyu Li Zhiai Hu Chenchen Zhou Yang Xu Li Huang Xin Wang Shujuan Zou 《BMC cell biology》2017,18(1):19
Background
External root resorption, commonly starting from cementum, is a severe side effect of orthodontic treatment. In this pathological process and repairing course followed, cementoblasts play a significant role. Previous studies implicated that parathyroid hormone (PTH) could act on committed osteoblast precursors to promote differentiation, and inhibit apoptosis. But little was known about the role of PTH in cementoblasts. The purpose of this study was to investigate the effects of intermittent PTH on cementoblasts and its influence after mechanical strain treatment.Results
Higher levels of cementogenesis- and differentiation-related biomarkers (bone sialoprotein (BSP), osteocalcin (OCN), Collagen type I (COL1) and Osterix (Osx)) were shown in 1–3 cycles of intermittent PTH treated groups than the control group. Additionally, intermittent PTH increased alkaline phosphatase (ALP) activity and mineralized nodules formation, as measured by ALP staining, quantitative ALP assay, Alizarin red S staining and quantitative calcium assay. The morphology of OCCM-30 cells changed after mechanical strain exertion. Expression of BSP, ALP, OCN, osteopontin (OPN) and Osx was restrained after 18 h mechanical strain. Furthermore, intermittent PTH significantly increased the expression of cementogenesis- and differentiation-related biomarkers in mechanical strain treated OCCM-30 cells.Conclusions
Taken together, these data suggested that intermittent PTH promoted cementum formation through activating cementogenesis- and differentiation-related biomarkers, and attenuated the catabolic effects of mechanical strain in immortalized cementoblasts OCCM-30.17.
Shilu Zhao Mingfang Li Weizhu Ju Lingyun Gu Fengxiang Zhang Hongwu Chen Kai Gu Bing Yang Minglong Chen 《Indian pacing and electrophysiology journal》2018,18(3):95-99
Background
Atrial tissue fibrosis can cause electrical or structural remodeling in patients with atrial fibrillation. Transforming growth factor beta 1(TGF-β1) signaling acts as a central role in fibroblast activation. In this report, we aimed to investigate the relationship between serum level of TGF-β1 and mean left atrial voltage in patients with chronic atrial fibrillation (CAF).Methods
A total of 16 consecutive adult patients with CAF who underwent catheter ablation were enrolled. Blood samples for measurement of TGF-β1 were collected from periphery veins and coronary sinus before pulmonary vein isolation. The measurement was performed with a commercially available ELISA kit. Cardiac indices were measured using echocardiography. The left atrial electroanatomic mapping was performed after pulmonary vein isolation.Results
Serum level of TGF-β1 in peripheral blood was higher than that in coronary sinus (p < 0.001). TGF-β1 serum level in coronary sinus negatively correlated with mean left atrial voltage (r = -0.650, p = 0.012), While periphery TGF-β1 level tended to be negatively correlated with mean left atrial voltage(r = -0.492, p = 0.053). Patients who treated with angiotensin II receptor antagonists had lower coronary sinus TGF-β1 serum level than those who did not treated with angiotensin II receptor antagonists (p = 0.046).Conclusion
Level of TGF-β1 in peripheral serum is higher than that in coronary sinus, and serum level of TGF-β1 in coronary sinus is negatively associated with mean left atrial voltage in patients with CAF, angiotensin II receptor antagonists could affect TGF-β1 serum level. 相似文献18.
Jamie L. Kuck Julie A. Bastarache Ciara M. Shaver Joshua P. Fessel Sergey I. Dikalov James M. May Lorraine B. Ware 《Biochemical and biophysical research communications》2018,495(1):433-437
Background
Increased endothelial permeability is central to shock and organ dysfunction in sepsis but therapeutics targeted to known mediators of increased endothelial permeability have been unsuccessful in patient studies. We previously reported that cell-free hemoglobin (CFH) is elevated in the majority of patients with sepsis and is associated with organ dysfunction, poor clinical outcomes and elevated markers of oxidant injury. Others have shown that Vitamin C (ascorbate) may have endothelial protective effects in sepsis. In this study, we tested the hypothesis that high levels of CFH, as seen in the circulation of patients with sepsis, disrupt endothelial barrier integrity.Methods
Human umbilical vein endothelial cells (HUVEC) were grown to confluence and treated with CFH with or without ascorbate. Monolayer permeability was measured by Electric Cell-substrate Impedance Sensing (ECIS) or transfer of 14C-inulin. Viability was measured by trypan blue exclusion. Intracellular ascorbate was measured by HPLC.Results
CFH increased permeability in a dose- and time-dependent manner with 1 mg/ml of CFH increasing inulin transfer by 50% without affecting cell viability. CFH (1 mg/ml) also caused a dramatic reduction in intracellular ascorbate in the same time frame (1.4 mM without CFH, 0.23 mM 18 h after 1 mg/ml CFH, p < 0.05). Pre-treatment of HUVECs with ascorbate attenuated CFH induced permeability.Conclusions
CFH increases endothelial permeability in part through depletion of intracellular ascorbate. Supplementation of ascorbate can attenuate increases in permeability mediated by CFH suggesting a possible therapeutic approach in sepsis. 相似文献19.
Shuilian Luo Yuhang Chen Rui He Yujun Shi Li Su 《Biochemical and biophysical research communications》2018,495(1):607-613
Objective
The decreased expression of muscle-specific microRNA-1 (miR-1) has been found in many cardiovascular diseases and is considered to contribute to heart failure (HF). Here we investigated the role of miR-1 in myocardium protection by infusion of miR-1 in a cardiac global miRNA-deficient mouse.Methods
We generated a cardiac-selective miRNA-deficient mouse by crossing Dicerflox/flox mice with mice expressing tamoxifen-inducible Cre recombinase under the control of a mouse αMHC promoter. When Dicer gene was removed following tamoxifen injection, the mice were treated with micrONTM mmu-miR-1a-3p agomir (agomir-1). The mice were subjected to echocardiography measurement, and the heart tissue specimens were stained with hematoxylin and eosin (H&E) and Sirius red. Terminal deoxynucleotidyl transferase-mediated dUTP nickend labeling assay and Ki67 immunofluorescence were used to determine apoptosis and proliferation.Results
Dicer deletion resulted in extensive decrease in cardiac miRNAs in the mice. In echocardiography, the mice developed rapid and dramatic left ventricular enlargement. In histology, apparent cardiomyocyte hypertrophy, myofiber disarray, ventricular fibrosis, inflammatory infiltration, and severe ventricular remodeling were exhibited. When the mice were treated with agomir-1, they did not show any significant abnormalities in heart structure and histology in response to Dicer ablation.Conclusion
The proper expression of miRNAs plays vital roles in the maintenance of heart histology and function. Among these miRNAs, miR-1 is critical to inhibit myocyte hypertrophy and extracellular matrix deposition, thereby preventing cardiac remodeling in cardiac-selective Dicer deficient mice. 相似文献20.
Chi Liu Ping Zhu Masayuki Fujino Yoshitaka Isaka Hidenori Ito Kiwamu Takahashi Motowo Nakajima Tohru Tanaka Jian Zhuang Xiao-Kang Li 《Biochemical and biophysical research communications》2019,508(2):583-589