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Objective To clarify the role of transmembrane protein 66(TMEM66) in intima proliferation of carotid artery induced by balloon injury in rats.Methods SD rats were randomly divided into three groups (n=10), including control group, the left carotid artery balloon injury group and injury group added with lentiviruses, respectively.Accordingly, the intima proliferation of carotid artery were detected by H/E staining;the expressions of TMEM66 in carotid artery injuried by balloon were determined by Western blot,q-PCR and immunohistochemistry, and the migration and proliferation of VSMCs were measured by scratch test and CCK8 respectively.Results Compared with control group, the expression of TMEM66 in carotid artery was obviously decreased after balloon injury (P<0.05).Most importantly, the intima proliferation of carotid artery was significantly reversed by overexpression of TMEM66 via specific lentiviruses (P<0.05).Conclusions TMEM66 is able to attenuate the intima proliferation of carotid artery after balloon injury.It could be that upregulation of TMEM66 can alleviate the migration and proliferation of VSMCs by PDGF.
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Objective The purpose of the present study was to investigate the effect of peroxisome proliferator-activated receptors δ（PPAR δ）activation with dietary GW610742X on the expression of tenascin-C in the infarcted and remodeling myocardium.Methods Sixty male Wistar rats were divided into four groups,including control group,sham group,myocardial infarction（MI） group,and MI＋GW610742X（GW）group.The left coronary artery was ligated to establish the MI model.PPAR δ activator GW610742X（100mg/kg/d）was administrated into the rats of GW group.At 3 months after procedure,the expression and distribution of tenascin-C in left ventricular free wall from each group were examined by Western blotting and immunofluorescence,respectively.Results After 3 months following procedure,there were obvious necrosis and fibrosis in left ventricular free wall from MI group.The expression of tenascin-C in MI and GW group was significantly higher than those in control and sham group（P 〈 0.01）.Moreover,tenascin-C expression in GW group was remarkably decreased compared to MI group（P 〈 0.05）.Additionally,tenascin-C expression in sham group was similar to that in control group（P 〉 0.05）.Conclusion The tenascin-C is upregulated in infarcted myocardium during the remodeling process,which can be significantly attenuated by PPAR δ activation.
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Objective To study the long-term effect of administration(6 months) with transient receptor potential vanilloid 1(TRPV1) agonist capsaicin on contractile reactivity of thoracic aorta in C57BL/6J mice.Methods Tow-month-old male C57BL/6J mice were received normal diet group(n=12) or capsaicin group(normal diet plus capsaicin,n=12).Tail-cuff systolic blood pressure(SBP) was examined at the baseline and at the end of the intervention.After 6-month treatment period,carotid artery blood pressure and heart rate were determined by catheterization,and the aortic contractile response was examined using isometric myograph(Danish Myotech Technology,Denmark).Plasma levels of renin,angiotensin Ⅱ(Ang Ⅱ) and aldosterone were determined.Vascular smooth muscle cells(VSMC) were obtained from thoracic aorta of mice and cultured.Angiotensin Ⅱ type 1 receptor(AT1R) protein expression was detected by western blot.Calcium imaging was detected in cultured VSMC using the fluorescent dye technique.Results Systolic blood pressure,invasive carotid artery blood pressure and heart rate have no difference between two groups.No differences was found in PE-induced contraction response in thoracic aorta;while Ang Ⅱ induced contractility of aortic ring was lower in mice with capsaicin than control group [capsaicin:(37.5?1.6)% vs(59.8?1.4)%,P
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Aim To investigate the contribution of cardiac L-and L/T-type Ca 2+ channels blockers on matrix metalloproteinases (MMPs) protein expression and fibronectin (FN) degradation following myocardial infarction(MI). Methods Rat MI model was established by permanent ligation of left coronary artery. Infarcted rats were orally treated with placebo, amlodipine (L-channel blocker, 4 mg?kg -1?d -1) or mibefradil (L/T-Channel blocker, 10 mg?kg -1?d -1) for 7 days before induction of myocardial infarction. Protein levels of MMP-2,3,9 and FN distribution were assayed by immunoflorescence at 1, 3, 7 days post coronary occlusion in left ventricular free wall (LVFW) and myocardium interventricular septum (IS). Results Pathological changes of myocardial tissues in IS and LVFW showed typical myocardial remodeling. The hypertrophy was dominant in IS, but in LVFW the characteristics including disordered alignament, hypertrophy of the myocytes, the discontinuity, dissolving of carediomyofibrills, and the hyperplasia of interstitial tissue were found 7 days after MI. The protein levels of MMP-2,3,9 increased in IS 1,3,7 days post MI gradually, whereas the protein levels of FN decreased gradually, the protein levels of MMP-2,3,9 increased significantly in LVFW 7 days post MI, and the protein levels of FN decreased significantly compared to control group, respectively(P