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  • (A) Representative M-mode echocardiographic tracings of wild-type (WT) and Rad−/− mice 4 weeks after myocardial infarction (MI). (B,C) Ejection fraction and fractional shortening for sham and MI (circles and squares, respectively) WT (closed) and Rad−/− (open) mice. (D,E) Left ventricular interior dimension values for WT (closed) and Rad−/− (open) at diastole (LVIDd; D) and systole (LVIDs; E). (F) Left ventricular posterior wall thickness at diastole (LVPWd). (G) Left ventricular anterior wall thickness at diastole (LVAWd). N = 19 MI and 28 sham Rad−/− and 30 MI and 38 sham WT mice per group. *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001 versus WT MI.
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  • (A) HASMCs were incubated for 24 h with the indicated concentrations of TSG-6 and were harvested for immunoblotting analyses of collagen-1, collagen-3, TIMP-2, MMP-2, MMP-9, fibronectin, elastin, and α-tubulin. (Top) Representative results of protein expression of each molecule. (Bottom) Densitometric data of each molecule after normalization relative to α-tubulin. n = 4 to 7; *p = 0.025; †p = 0.015; ‡p = 0.047; #p < 0.01 vs. 0 ng/ml of TSG-6. (B) HASMCs were incubated for 24 h in serum-free conditioned medium with the indicated concentrations of TSG-6. In the culture supernatant, MMP-2 and -9 activities were determined by the gelatin zymography. n = 5 to 6; §p = 0.049; ¶p = 0.031; @p = 0.011; &p < 0.0001 vs. 0 ng/ml of TSG-6. All values are presented as mean ± SEM. ECM = extracellular matrix; M = matrix metalloproteinase marker; MMP = matrix metalloproteinase; S = sample; TIMP = tissue inhibitor of metalloproteinase; VSMC = vascular smooth muscle cell; other abbreviations as in Figure 1.
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  • Protocol 1 assesses the therapeutic effects of 5-week chronic vagal nerve stimulation (VNS) delivered by an implantable neurostimulator in free-moving rats with pulmonary arterial hypertension (PAH). Protocol 2 assesses the effects of 90-min acute VNS delivered by an external stimulation device in anesthetized rats with advanced PAH. CTRL = control; O2 = oxygen; SS = sham stimulation.
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  • Smooth muscle (SM)-specific conditional and inducible knock-out (KO) of mTOR attenuates hypoxia-induced pulmonary hypertension in mTORSM−/− mice. (A) Schematic strategy for the generation of mTORSM−/− mice (a) and the timeline indicating the time for injection of tamoxifen (Tam) (to induce mTOR KO), hypoxic exposure (for inducing pulmonary hypertension) and experimental measurements (b). (B) Representative immunofluorescence images showing cell nuclei (4′,6′-diamidino-2-phenylindole [DAPI]; blue), smooth muscle cells (smooth muscle actin [SMA]; red), and mammalian target of rapamycin (mTOR; green) in the cross-section of small pulmonary artery (PA) in lung tissues from wild-type (WT) (mTOR-Oil) and mTORSM−/− (mTOR-Tam) mice (a). Summarized data (mean ± SE; n = 5 in each group) for DAPI, SMA, and mTOR fluorescence intensity are shown in panels b. It is noted that the mTOR (green) expression is almost abolished in the SMA-positive PA wall in mTOR-Tam mice but preserved in the mTOR-Oil mice. Student’s t-test (DAPI and SMA level) and Welch’s t-test (mTOR level), **p < 0.01 and ***p < 0.001 versus mTOR-Oil. (C) Representative record of right ventricular pressure (RVP) in WT and mTORSM−/− mice exposed to normoxia (room air, 21% oxygen) and hypoxia (10% oxygen for 3 weeks) (a). Summarized data (mean ± SE) showing the peak value of right ventricular systolic pressure (RVSP) (b) (Kruskal-Wallis test, p < 0.001) and the Fulton index (the ratio of weight of the right ventricle divided by weight of the left ventricle plus the septum [RV/(LV + S)]) (c) (Kruskal-Wallis test, p = 0.005) in WT and mTORSM−/− mice exposed to normoxia and hypoxia. Dunn test, *p < 0.05, ***p < 0.001 versus Normoxia-WT; ##p < 0.01 versus Hypoxia-WT. (D) Representative hematoxylin and eosin images (a) of the cross-section of small PA and summarized data (mean ± SE) (b) showing the PA wall thickness in WT and mTORSM−/− mice under normoxic and hypoxic conditions. Kruskal-Wallis test, p < 0.001; Dunn test, **p < 0.01, *p < 0.05 versus Normoxia-WT, ##p < 0.01 versus Hypoxia-WT. (E) Summarized data (mean ± SE) showing the number of red blood cells (RBC) (Kruskal-Wallis test, p = 0.04), hemoglobin concentration (HGB) (Kruskal-Wallis test, p = 0.01), and hematocrit percentage (HCT) (Kruskal-Wallis test, p = 0.01) in WT and mTORSM−/− mice exposed to normoxia and hypoxia. Analysis of variance, **p < 0.01, *p < 0.05 versus Normoxia-WT; #p < 0.05 versus Hypoxia-WT. The numbers of experiments (n) for each group are indicated in each bar.
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  • Image on the left shows a stent within main pulmonary artery (MPA). Image on the right is an angiogram taken after successful transcatheter implantation of pulmonary valve. PA = pulmonary artery; TOF = tetralogy of Fallot.
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  • Effects of ATP versus dATP in ex vivo human cardiac tissue from end-stage HF patients demonstrating dATP increases force. (A) Representative isometric force trace of demembranated tissue at pCa 5.6 with ATP or dATP. (B) Force measured at pCa 5.6 with 10%, 25%, 50%, and 100% dATP compared with 100% ATP (n = 4 at each dATP concentration). Measurements are mean ± SEM. *p < 0.05 compared with 100% ATP by paired Student t test.
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  • (A) Improvement of left ventricular developed pressure (LVDP) by perfusion with dialysates of human plasma obtained after RIPC compared to dialysates of human plasma obtained at baseline. (B) Coronary flow was not affected. Data are median with interquartile ranges of n = 20 at each time point; *p < 0.05 versus baseline. d = day; CF = coronary flow.
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  • CAD = coronary artery disease; CNS = central nervous system; CVA = cerebrovascular accident; CXCL = chemokine ligand; IGFBP-5 = insulin-like growth factor binding protein; NEMO = nuclear factor kappa B essential modulator; PAD = peripheral artery disease; PAI = plasminogen activator inhibitor; SMA = smooth muscle actin; SPRY = sprout homolog; TLR = Toll-like receptor; vWF = von Willebrand factor; XIAP = X-linked inhibitor of apoptosis.
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  • Functional differences between groups at the 4.5-month time point using FunRich software are shown. Abbreviations as in Figure 2.
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  • Blood was either pre-incubated with no supplement, buffer, aspirin (ASA) (300 μg/ml), GPVI-Fc (333 nM), or GPVI-Fc*Fab2-XL (333 nM) before transfer to collagen/adenosine diphosphate (ADP) or collagen/epinephrine cartridges and determination of the in vitro closure time with the platelet function analyzer PFA-200. Mean ± SD; n = 6. ***p < 0.001 by repeated measures analysis of variance and secondary pair-wise comparison of ASA versus all other conditions. Abbreviations as in Figure 2.
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