Xuzhou Cardiovascular Disease Institute

Tongshan, China

Xuzhou Cardiovascular Disease Institute

Tongshan, China
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Shan Y.,Nanjing Southeast University | Gong H.-B.,Nanjing Southeast University | Gong H.-B.,Xuzhou Cardiovascular Disease Institute | Gong H.-B.,Xuzhou Central Hospital | And 9 more authors.
Journal of Clinical Rehabilitative Tissue Engineering Research | Year: 2010

BACKGROUND: Previous studies have found that cardiocytes overexpressing β-adrenergic receptors (β-AR) can improve its contractile function in transgenic mice, rats and other small animals, but experimental reports about the large mammals are few. OBJECTIVE: To observe changes and mechanisms of contractile function following cardiocytes overexpressing β2-AR in canines. METHODS: Canine cardiocytes were isolated by collagenase II and transfected by adenovirus β2AR. The expression of β2AR protein of cardiocytes, the level of intracellular cyclic adenosine monophosphate (cAMP) at basic state and maximum systolic states, and the changes of contractile function were observed at 48 hours after operation. RESULTS AND CONCLUSION: Compared with the control group, the expression of β2AR protein of cardiocytes and the level of the intracellular cAMP in the adenovirus β2AR group were increased (P < 0.05). The basal contraction amplitude of cadiocytes in adenovirus β2- AR group was also increased significantly (P < 0.05), but the max contraction amplitude of cardiocytes was not changed significantly between two groups. The study suggested that the over-expression of β2AR could increase the level of intracellular cAMP and improved the contractile function of cadiocytes in canines.


Paur H.,Imperial College London | Wright P.T.,Imperial College London | Sikkel M.B.,Imperial College London | Tranter M.H.,Imperial College London | And 15 more authors.
Circulation | Year: 2012

Background-Takotsubo cardiomyopathy is an acute heart failure syndrome characterized by myocardial hypocontractility from the mid left ventricle to the apex. It is precipitated by extreme stress and can be triggered by intravenous catecholamine administration, particularly epinephrine. Despite its grave presentation, Takotsubo cardiomyopathy is rapidly reversible, with generally good prognosis. We hypothesized that this represents switching of epinephrine signaling through the pleiotropic β 2-adrenergic receptor (β 2AR) from canonical stimulatory G-protein-activated cardiostimulant to inhibitory G-protein-activated cardiodepressant pathways. Methods and Results-We describe an in vivo rat model in which a high intravenous epinephrine, but not norepinephrine, bolus produces the characteristic reversible apical depression of myocardial contraction coupled with basal hypercontractility. The effect is prevented via Gi inactivation by pertussis toxin pretreatment. β 2AR number and functional responses were greater in isolated apical cardiomyocytes than in basal cardiomyocytes, which confirmed the higher apical sensitivity and response to circulating epinephrine. In vitro studies demonstrated high-dose epinephrine can induce direct cardiomyocyte cardiodepression and cardioprotection in a β 2AR- Gi-dependent manner. Preventing epinephrine-Gi effects increased mortality in the Takotsubo model, whereas β-blockers that activate β 2AR- Gi exacerbated the epinephrine-dependent negative inotropic effects without further deaths. In contrast, levosimendan rescued the acute cardiac dysfunction without increased mortality. Conclusions-We suggest that biased agonism of epinephrine for β 2AR-Gs at low concentrations and for Gi at high concentrations underpins the acute apical cardiodepression observed in Takotsubo cardiomyopathy, with an apical-basal gradient in β 2ARs explaining the differential regional responses. We suggest this epinephrine-specific β 2AR-Gi signaling may have evolved as a cardioprotective strategy to limit catecholamine-induced myocardial toxicity during acute stress. © 2012 American Heart Association, Inc.


Chen B.,Xuzhou Medical College | Lyu Q.,Xuzhou Cardiovascular Disease Institute | Zhang M.,Xuzhou Medical College | Liu W.,Xuzhou Medical College | Zhu S.,Xuzhou Medical College
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology | Year: 2015

OBJECTIVE: To explore the effect of leptin on the transdifferentiation of human lung fibroblast to myofibroblast and its mechanism.METHODS: Human embryonic lung fibroblasts (HFL-1) were cultured in vitro and treated with 50, 100, 200 ng/mL recombinant human leptin (rHL) alone or in combination with 5 ng/mL transforming growth factor-β1 (TGF-β1). The protein levels of α-smooth muscle actin (α-SMA), total protein kinase B (AKT) and phosphorylated AKT (p-AKT) in HFL-1 were detected by Western blotting. The proliferation activity of HFL-1 was evaluated by the cell counting kit-8 (CCK-8). The level of collagen type 1 in supernatant fluid of HFL-1 was detected by ELISA.RESULTS: After treatment with 50, 100 and 200 ng/mL rHL for 48 hours, α-SMA protein expression in HFL-1 was significantly raised as compared with control group. Co-stimulation with 200 ng/mL rHL and 5 ng/mL TGF-β1 increased α-SMA protein expression in HFL-1 remarkably as compared with the treatment with 200 ng/mL rHL or 5 ng/mL TGF-β1 alone. Leptin promoted the expression of p-AKT in HFL-1, and this effect was blocked by PI3K inhibitor LY294002. There was no significant difference in cell viability between HFL-1 treated with 12.5, 25, 50, 100 and 200 ng/mL rHL and without rHL. After treatment with 50, 100 and 200 ng/mL rHL for 48 hours, the level of collagen type 1 in supernatant fluid of HFL-1 significantly increased as compared with control group.CONCLUSION: Leptin can induce human lung fibroblast to differentiate into myofibroblast and its mechanism is related to the activation of PI3K/AKT signaling.


PubMed | Xuzhou Cardiovascular Disease Institute and Xuzhou Medical College
Type: Journal Article | Journal: Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology | Year: 2015

To explore the effect of leptin on the transdifferentiation of human lung fibroblast to myofibroblast and its mechanism.Human embryonic lung fibroblasts (HFL-1) were cultured in vitro and treated with 50, 100, 200 ng/mL recombinant human leptin (rHL) alone or in combination with 5 ng/mL transforming growth factor-1 (TGF-1). The protein levels of -smooth muscle actin (-SMA), total protein kinase B (AKT) and phosphorylated AKT (p-AKT) in HFL-1 were detected by Western blotting. The proliferation activity of HFL-1 was evaluated by the cell counting kit-8 (CCK-8). The level of collagen type 1 in supernatant fluid of HFL-1 was detected by ELISA.After treatment with 50, 100 and 200 ng/mL rHL for 48 hours, -SMA protein expression in HFL-1 was significantly raised as compared with control group. Co-stimulation with 200 ng/mL rHL and 5 ng/mL TGF-1 increased -SMA protein expression in HFL-1 remarkably as compared with the treatment with 200 ng/mL rHL or 5 ng/mL TGF-1 alone. Leptin promoted the expression of p-AKT in HFL-1, and this effect was blocked by PI3K inhibitor LY294002. There was no significant difference in cell viability between HFL-1 treated with 12.5, 25, 50, 100 and 200 ng/mL rHL and without rHL. After treatment with 50, 100 and 200 ng/mL rHL for 48 hours, the level of collagen type 1 in supernatant fluid of HFL-1 significantly increased as compared with control group.Leptin can induce human lung fibroblast to differentiate into myofibroblast and its mechanism is related to the activation of PI3K/AKT signaling.

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