Notice of Retraction: In Vivo Study of Adenovirus Mediated Transgenic HIF-1alpha and Its Protective Effects on Cardiac Function - Biochemical, Cellular, Molecular and Tissue Engineering

2011 ◽  
Author(s):  
Dong-Ye Li ◽  
Yan Yan ◽  
Hong Zhu ◽  
Yi-Na Liu ◽  
Chuang Liu ◽  
...  
Keyword(s):  
Tissue Engineering ◽  
Cardiac Function ◽  
In Vivo Study ◽  
Protective Effects

Abstract 144: Post-myocardial Infarction Therapeutics Using Cardiovascular Progenitor Cells (PC) Derived from Induced Pluripotent Stem Cells (iPSC)

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Yigang Wang
Keyword(s):  
Cardiac Function ◽  
Heart Function ◽  
Vessel Density ◽  
Protective Effects ◽  
Paracrine Factors ◽  
Beneficial Effects ◽  
The Third ◽  
Simplex Virus ◽  
Patch Group

Objective: We sought to assess the cardiac protective effects after MI of (1) PC differentiated directly into cardiomyocytes (CM) and endothelial cells (EC) to the site of injury, or (2) paracrine factors released from PC. Methods: These concepts were evaluated by using iPSC-derived PC genetically modified to express the herpes simplex virus thymidine kinase (TK) under the control of cardiomyocyte (NCX1) or endothelial cell (VE-cadherin) specific promoters. PC expressing the TK permitted ablation at the first week or the third week by iv ganciclovir (GCV). If GCV applied at the first week, but not at the third week, altered cardiac function, we would conclude that myocardial contractile recovery depends on CM and EC-derived from iPSC. If the beneficial effects on cardiac function persisted after GCV was given at the third week, we would surmise that the PC effect was via by a paracrine action. MI created by ligation of LAD, the cell patch with PC was applied to the scarred myocardium. Rats were treated with GCV at 1 or 3 weeks to ablate implanted PC. Echocardiography, vessel density, and histological analysis were used to obtain endpoints for this study. Result: In vivo : The levels of IGF-1α and VEGF released from ischemic tissues were significant higher in the cell patch group. Heart function, infarction size, and vessel density were significantly improved after cell patch treatment. However, this beneficial effect on cardiac function was completely abolished in the group given GCV at week 1, but only partially abolished in the group given GCV at week 3 compared to the untreated cell patch group. Conclusions: Taken together, these data support our conclusion that iPSC-derived cardiovascular lineages (CM and EC) contribute directly to an improved cardiac performance and attenuated remodeling, and that paracrine factors also play a supporting role in the restoration of heart function after MI.

scholarly journals Reduction of cardiomyocyte S-nitrosylation by S-nitrosoglutathione reductase protects against sepsis-induced myocardial depression

2013 ◽  
Vol 304 (8) ◽  
pp. H1134-H1146 ◽  
Author(s):  
Patrick Y. Sips ◽  
Tomoya Irie ◽  
Lin Zou ◽  
Shohei Shinozaki ◽  
Michihiro Sakai ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Ex Vivo ◽  
Myocardial Dysfunction ◽  
Endotoxic Shock ◽  
Protein S ◽  
Septic Cardiomyopathy ◽  
Protective Effects ◽  
Myocardial Depression ◽  
Lps Challenge

Myocardial depression is an important contributor to morbidity and mortality in septic patients. Nitric oxide (NO) plays an important role in the development of septic cardiomyopathy, but also has protective effects. Recent evidence has indicated that NO exerts many of its downstream effects on the cardiovascular system via protein S-nitrosylation, which is negatively regulated by S-nitrosoglutathione reductase (GSNOR), an enzyme promoting denitrosylation. We tested the hypothesis that reducing cardiomyocyte S-nitrosylation by increasing GSNOR activity can improve myocardial dysfunction during sepsis. Therefore, we generated mice with a cardiomyocyte-specific overexpression of GSNOR (GSNOR-CMTg mice) and subjected them to endotoxic shock. Measurements of cardiac function in vivo and ex vivo showed that GSNOR-CMTg mice had a significantly improved cardiac function after lipopolysaccharide challenge (LPS, 50 mg/kg) compared with wild-type (WT) mice. Cardiomyocytes isolated from septic GSNOR-CMTg mice showed a corresponding improvement in contractility compared with WT cells. However, systolic Ca2+ release was similarly depressed in both genotypes after LPS, indicating that GSNOR-CMTg cardiomyocytes have increased Ca2+ sensitivity during sepsis. Parameters of inflammation were equally increased in LPS-treated hearts of both genotypes, and no compensatory changes in NO synthase expression levels were found in GSNOR-overexpressing hearts before or after LPS challenge. GSNOR overexpression however significantly reduced total cardiac protein S-nitrosylation during sepsis. Taken together, our results indicate that increasing the denitrosylation capacity of cardiomyocytes protects against sepsis-induced myocardial depression. Our findings suggest that specifically reducing protein S-nitrosylation during sepsis improves cardiac function by increasing cardiac myofilament sensitivity to Ca2+.

A Poly(lactic-co-glycolic acid) Knitted Scaffold for Tendon Tissue Engineering: An In Vitro and In Vivo Study

2010 ◽  
Vol 21 (13) ◽  
pp. 1737-1760 ◽  
Author(s):  
Cédryck Vaquette ◽  
Saïd Slimani ◽  
Cyril J. F. Kahn ◽  
Nguyen Tran ◽  
Rachid Rahouadj ◽  
...  
Keyword(s):  
Tissue Engineering ◽  
Glycolic Acid ◽  
In Vivo Study ◽  
Tendon Tissue ◽  
Tendon Tissue Engineering

scholarly journals Possible Role of Interaction between PPARαand Cyclophilin D in Cardioprotection of AMPK againstIn VivoIschemia-Reperfusion in Rats

PPAR Research ◽  
2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Giselle Barreto-Torres ◽  
Sabzali Javadov
Keyword(s):  
Cardiac Function ◽  
Mitochondrial Function ◽  
Mitochondrial Permeability Transition ◽  
Synergistic Effects ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
Simultaneous Administration ◽  
Cyclophilin D ◽  
Ptp Opening

Activated AMPK protects the heart from cardiac ischemia-reperfusion (IR) injury and is associated with inhibition of mitochondrial permeability transition pore (PTP) opening. On the other hand, pharmacological inhibition of the PTP reduces infarct size and improves cardiac function. However, it is unclear whether beneficial effects of AMPK are mediated through the PTP and, if they are not, whether simultaneous activation of AMPK and inhibition of the PTP exert synergistic protective effects against cardiac IR injury. Here, we examined the effects of the AMPK activator, A-769662 in combination with the PTP inhibitor, sanglifehrin A (SfA) onin vivocardiac IR. Cardiac dysfunction following IR injury was associated with decreased activity of the mitochondrial electron transport chain (ETC) and increased mitochondrial ROS and PTP opening. Administration of A-769662 or SfA individually upon reperfusion improved cardiac function, reduced infarction size, and inhibited ROS production and PTP opening. However, simultaneous administration of SfA and A-769662 did not provide synergistic improvement of postischemic recovery of cardiac and mitochondrial function, though both compounds disrupted IR-induced interaction between PPARαand CyP-D. In conclusion, A-769662 or SfA prevents PPARαinteraction with CyP-D, improving cardiac outcomes and increasing mitochondrial function, and simultaneous administration of the drugs does not provide synergistic effects.

scholarly journals Novel layered double hydroxides-hydroxyapatite/gelatin bone tissue engineering scaffolds: Fabrication, characterization, and in vivo study

2017 ◽  
Vol 76 ◽  
pp. 701-714 ◽  
Author(s):  
Fateme Fayyazbakhsh ◽  
Mehran Solati-Hashjin ◽  
Abbas Keshtkar ◽  
Mohammad Ali Shokrgozar ◽  
Mohammad Mehdi Dehghan ◽  
...  
Keyword(s):  
Tissue Engineering ◽  
Bone Tissue Engineering ◽  
Bone Tissue ◽  
Layered Double Hydroxides ◽  
In Vivo Study ◽  
Tissue Engineering Scaffolds ◽  
Double Hydroxides

scholarly journals Protective effects of Salidroside on cardiac function in mice with myocardial infarction

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Pengsheng Chen ◽  
Jia Liu ◽  
Hongyun Ruan ◽  
Miaomiao Zhang ◽  
Peng Wu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Normal Saline ◽  
Myocardial Inflammation ◽  
Coronary Artery Ligation ◽  
Protective Effects ◽  
Myocardial Remodeling ◽  
Artery Ligation ◽  
Post Surgery

AbstractSalidroside (SAL) is the major ingredient of Rhodiola rosea, and has been traditionally used in Chinese medicine for decades. Numerous studies have demonstrated the protective effects of SAL for myocardial ischemia. However, it is yet to be deciphered whether SAL has cardioprotective effects after myocardial infarction (MI) in vivo. In the present study, we established a mouse MI model via coronary artery ligation. The aim was to investigate whether SAL treatment could reduce mortality, improve cardiac function and attenuate myocardial remodeling in MI mice. Post-surgery, mice were randomly administered SAL or normal saline. After 21 days, SAL was found to significantly reduce mortality, improve cardiac function, reduce fibrosis and infarct size compared to normal saline. In addition, oral administration of SAL could attenuate myocardial inflammation and apoptosis and promote angiogenesis. SAL down-regulated the expression levels of TNF-α, TGF-β1, IL-1β, Bax and up-regulate the expression of Bcl-2, VEGF, Akt and eNOS. These results indicated that SAL could alleviate the pathological processes of myocardial remodeling in MI mice, and may be a potentially effective therapeutic approach for the management of clinical ischemic cardiovascular diseases.

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