Qi Zhou

Chongqing Medical University, Ch’ung-ch’ing-shih, Chongqing Shi, China

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Publications (7)29.01 Total impact

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    ABSTRACT: Increased indiscriminate use of pulmonary artery hypertension-targeted drugs has been observed in patients with pulmonary hypertension (PH) secondary to heart failure. We performed a meta-analysis to evaluate the chronic effects of using phosphodiesterase 5 (PDE5) inhibitors to treat patients with PH secondary to chronic systolic heart failure. PubMed, EMBASE, and the Cochrane Library were searched up to October 2013 for randomized controlled trials (RCTs) assessing PDE5 inhibitor treatments in PH patients secondary to chronic heart failure. Six RCTs involving 206 chronic systolic heart failure patients with PH complications were included. Sildenafil was used in all trials. Sildenafil treatment resulted in fewer hospital admissions compared with the placebo treatment (3.15% vs. 12.20%; risk ratio 0.29; 95% confidence interval 0.11-0.77). Various haemodynamic parameters were improved with additional sildenafil treatment, including reduced mean pulmonary artery pressure [weighted mean difference (WMD) -5.71 mmHg, P < 0.05] and pulmonary vascular resistance (WMD -81.5 dynes/cm(-5) , P < 0.00001), increased LVEF (WMD 3.95%, P < 0.01), and unchanged heart rate and blood pressure. The exercise capacity improved (oxygen consumption at peak exercise, WMD 3.20 mL/min(-1) /kg(-1) , P < 0.00001; ventilation to CO2 production slope, WMD -5.89, P < 0.00001), and the clinical symptoms were relieved based on the breathlessness (WMD 7.72, P < 0.00001), fatigue (WMD 2.28, P < 0.05), and emotional functioning (WMD 5.92, P < 0.00001) scores. Additional sildenafil treatment is a potential therapeutic method to improve pulmonary exercise capacity and quality of life by ameliorating PH in patients with chronic systolic heart failure.
    European Journal of Heart Failure 12/2013; · 5.25 Impact Factor
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    ABSTRACT: Impaired regeneration of endothelial cells (EC) and overactivity of vascular smooth muscle cells (VSMC) are hallmarks of the arterial lesions associated with aging. The occurrence of 2 opposing cellular processes in the same arterial milieu makes pharmaceutical treatment difficult to develop. We previously reported that endothelial expression of a Notch ligand (Jagged1) was reduced in aged animals and that growth of the neointima was enhanced in these animals. Similar to aged animals, Tie2-cre(+) Jagged1(lox/+) mice (with heterologous knockout of Jagged1 in EC) showed exaggerated intimal and medial thickening after carotid artery ligation. Unexpectedly, these mice showed little increase of Jagged1 expression not only in EC but also in VSMC, in contrast to a significant upregulation of Jagged1 in wild-type arteries after ligation. Coculture of VSMC with Jagged1-null EC resulted in the transition of VSMC from the contractile to the synthetic phenotype, along with decreased Jagged1 expression by VSMC. Conversely, overexpression of Jagged1 by EC or VSMC was shown to prevent the unfavorable phenotypic transition of VSMC, under both monoculture and coculture conditions. These findings suggest a unidirectional effect of Jagged1 on both EC and VSMC that contributes to inhibition of arterial lesions after vascular injury. Our data also indicate that Jagged1 may be a novel therapeutic target for aging-related vascular diseases.
    Arteriosclerosis Thrombosis and Vascular Biology 06/2011; 31(9):2000-6. · 6.34 Impact Factor
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    ABSTRACT: Endothelial cells of arteries (AEC) have a strikingly greater responsiveness to atherosclerosis factors than venous endothelial cells (VEC). However, the reasons for this phenomenon remain unclear. Chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) plays an important role in regulating embryonic arterial-venous differentiation. We therefore investigate whether COUP-TFII is related to this different susceptibility between AEC and VEC. It is first confirmed that COUP-TFII is expressed in VEC but not in AEC in the adult. Using a siRNA strategy, we identified the expression of Jagged1 and Notch1 in cultured human VEC, which usually exist only in AEC, after knocking down of COUP-TFII. To further elucidate the role of COUP-TFII, we performed DNA microarrays in VEC transfected with the siRNA of COUP-TFII and subsequently stimulated with angiotensin II (AngII) and compared the expression profiles of 112 genes involved in various atherosclerosis-related pathways. The results indicated that expression of atherogenic genes was significantly upregulated after AngII stimulation in VEC transfected with COUP-TFII siRNA. Moreover, in vitro cell functional assay showed that knockdown of COUP-TFII in VEC increased not only basal but also AngII-induced cell adhesions. These results demonstrate that COUP-TFII suppresses the susceptibility of VEC to atherosclerosis through controlling the expression of various atherosclerosis-related molecules.
    Journal of Cellular Biochemistry 11/2010; 112(1):256-64. · 3.06 Impact Factor
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    ABSTRACT: Ageing has been shown to enhance neointima formation due to abnormal growth of vascular smooth muscular cells (VSMC), which is regulated by endothelial functions. The mechanism of how endothelium affects the growth of VSMC in the process remains unclear. We here examined the role of Jagged1, a regulator of cell growth. Male Sprague-Dawley rats at 3 (young) and 22 (old) months of age were subjected to a balloon catheter injury in the thoracic aorta. After 4 weeks, the neointima formation in the injured artery of old rats was more than that of young rats. Compared with the young rats, the increase in Jagged1 expression in the endothelium of old rats after the injury was delayed, weakened, and shortened, suggesting an impaired response of Jagged1 to the injury. In contrast, the increase in the expression of proliferating cell nuclear antigen in the neointima was more significant and maintained longer in old rats than in the young ones. Moreover, the expression of Jagged1 in the cultured arterial endothelial cells (EC) of old animals was less than those of the young ones, which promoted the Platelet-derived growth factor (PDGF)-induced growth and migration of the co-cultured VSMC. Furthermore, suppression of Jagged1 expression by a small interfering RNA in the EC of young rats reduced alpha-smooth muscle actin and calponin expression and also intensified the PDGF-increased growth and migration of the co-cultured VSMC. Ageing enhanced VSMC proliferation, at least in part, through impairing Jagged1 expression in the EC after vascular injury.
    Cardiovascular Research 04/2008; 77(4):800-8. · 5.81 Impact Factor
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    ABSTRACT: Late thrombosis and neointima proliferation after paclitaxel-eluting stents implanting may be related to delayed endothelial cells (ECs) regeneration. This study was to investigate whether mesenchymal stem cells (MSCs) seeding can accelerate endothelial repair and attenuate late smooth muscle cells (SMCs) proliferation after paclitaxel intervention. An ex vivo model of endothelium repair was developed in which rabbit smooth muscle cells were inoculated in the upper chamber and rabbit endothelial cells/human mesenchymal stem cells in the lower chamber of a co-culture system. Paclitaxel (10 nmol/L, 20 min) inhibited smooth muscle cell growth of the confluent endothelial cell group during the observed period. However, increased smooth muscle cells growth was observed in the proliferative endothelial cells group 10 days after paclitaxel intervention. Mesenchymal stem cell seeding inhibited late smooth muscle cell growth incompatible with the effect of proliferative endothelial cells. However, no inhibition on smooth muscle cell growth was observed with mesenchymal stem cell seeding in comparison to the effect of confluent endothelial cells. No vWF but Flk-1 protein was observed in the 25.71% of mesenchymal stem cells after having been co-cultured with rabbit endothelial cells for 5 days. These results indicate that late smooth muscle cell proliferation is closely related to the delayed endothelial cells regeneration after paclitaxel application. Mesenchymal stem cell seeding partly attenuates the late smooth muscle cell proliferation. Mesenchymal stem cells co-cultured with mature endothelial cells have the ability to differentiate toward endothelial cells.
    Journal of Cardiovascular Pharmacology 01/2006; 46(6):779-86. · 2.38 Impact Factor
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    ABSTRACT: Previous studies have shown that mesenchymal stem cells (MSCs) transplantation can promote neovascularization and regenerate damaged myocardium. However, it remains unknown whether MSCs seeding can be used to repair injured cellular components in vascular diseases. In this study we explored the feasibility of applying MSCs to endothelium repair in endothelial damage and vasoproliferative disorders. Ex vivo model of endothelium repair was developed in which rabbit vascular smooth muscle cells (SMCs) were inoculated into the upper chamber and rabbit endothelial cells (ECs)/human MSCs into the lower chamber of a co-culture system. 3H-TdR incorporation and PCNA protein expression were assayed and migrated number of SMCs was calculated to evaluate the effect of MSCs seeding on SMCs growth. Flk-1 and vWF protein expressions were observed to analyze the plasticity of the seeded MSCs along endothelial lineage. In this co-culture system, no vWF protein but Flk-1 protein was observed in the 25.71% of MSCs after having been co-cultured with mature rabbit ECs for 5 days. Compared with the control group, the proliferation and migration of SMCs was significantly increased by proliferative ECs but decreased by confluent ECs (n=6, P<0.01). MSCs seeding decreased the proliferation and migration of SMCs compatible with the effect of proliferative ECs (n=6, P<0.001). However, no inhibition on SMCs growth was observed with MSCs seeding in comparison to the effect of confluent ECs. MSCs seeding can inhibit the proliferation and migration of SMCs. MSCs co-cultured with mature ECs have the ability to undergo milieu-dependent differentiation toward ECs.
    International Journal of Cardiology 12/2005; 105(3):274-82. · 6.18 Impact Factor
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    ABSTRACT: To investigate the effects of paclitaxel combined with bone marrow stromal stem cells (MSCs) implantation on inhibiting the smooth muscle cells (SMCs) growth and promoting endothelial repair by developing an endothelial repair model in vitro. In a cell coculture system, rabbit endothelial cells (ECs) and human MSCs were seeded in the lower chamber and rabbit SMCs were seeded in the upper chamber. 3H-TdR incorporation and PCNA protein expression were used to evaluate SMCs proliferation at the 10th day after paclitaxel application (1, 10, 100 nmol/L; 20 min). Fluorescence immunocytochemistry was employed to observe the Flk-1 and vWF protein expression on MSCs. The SMCs 3H-TdR incorporation of the MSCs implant group was significantly lower than that of the proliferative ECs group (1 nmol/L: 12 265 +/- 991 vs. 14 505 +/- 1013 cpm/well; 10 nmol/L: 8401 +/- 783 vs. 10 511 +/- 934 cpm/well; 100 nmol/L: 5880 +/- 569 vs. 7457 +/- 768 cpm/well, n = 6, P < 0.05), but higher than that of the confluent ECs group (1 nmol/L: 12 265 +/- 991 vs. 8671 +/- 642 cpm/well; 10 nmol/L: 8401 +/- 783 vs. 6175 +/- 743 cpm/well; 100 nmol/L: 5880 +/- 569 vs. 4423 +/- 406 cpm/well, n = 6, P < 0.05). The expression of SMCs PCNA protein in MSCs implant group was lower than that of the proliferative ECs group (1 nmol/L: 0.92 +/- 0.06 vs. 1.15 +/- 0.07; 10 nmol/L: 0.97 +/- 0.07 vs. 1.07 +/- 0.08; 100 nmol/L: 0.91 +/- 0.05 vs. 1.18 +/- 0.11, n = 6, P < 0.05), but higher than that of the confluent ECs group (1 nmol/L: 0.92 +/- 0.06 vs. 0.74 +/- 0.07; 10 nmol/L: 0.97 +/- 0.07 vs. 0.78 +/- 0.06; 100 nmol/L: 0.91 +/- 0.05 vs. 0.71 +/- 0.05, n = 6, P < 0.05). The MSCs did not express vWF or Flk-1 protein before coculture. Although none cell expressed vWF, some of the MSCs began to express Flk-1 protein after cocultured with mature ECs for 10 days. MSCs implantation can partly inhibit the delayed SMCs proliferation. The MSCs cocultured with paclitaxel-treated mature ECs have the ability to differentiate into ECs.
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 05/2005; 33(5):464-8.