A Collagen-Chitosan Injectable Hydrogel Improves Vascularization and Cardiac Remodeling in a Mouse Model of Chronic Myocardial Infarction

2013 ◽  
Vol 29 (10) ◽  
pp. S203-S204 ◽  
Author(s):  
A. Ahmadi ◽  
B. Vulesevic ◽  
M. Ruel ◽  
E.J. Suuronen
Keyword(s):  
Myocardial Infarction ◽  
Mouse Model ◽  
Cardiac Remodeling ◽  
Chronic Myocardial Infarction ◽  
Injectable Hydrogel

A Collagen-Chitosan Injectable Hydrogel Improves Cardiac Remodeling in a Mouse Model of Myocardial Infarction

2014 ◽  
Vol 4 (11) ◽  
pp. 886-894 ◽  
Author(s):  
Ali Ahmadi ◽  
Branka Vulesevic ◽  
Nick J. R. Blackburn ◽  
Joanne Joseph Marc Ruel ◽  
Erik J. Suuronen
Keyword(s):  
Myocardial Infarction ◽  
Mouse Model ◽  
Cardiac Remodeling ◽  
Injectable Hydrogel

Cardiomyocyte transplantation does not reverse cardiac remodeling in rats with chronic myocardial infarction

2002 ◽  
Vol 74 (1) ◽  
pp. 25-30 ◽  
Author(s):  
Yutaka Sakakibara ◽  
Keiichi Tambara ◽  
Fanglin Lu ◽  
Takeshi Nishina ◽  
Noritoshi Nagaya ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Remodeling ◽  
Chronic Myocardial Infarction ◽  
Reverse Cardiac Remodeling

scholarly journals Beneficial effects of muscone on cardiac remodeling in a mouse model of myocardial infarction

2014 ◽  
Vol 34 (1) ◽  
pp. 103-111 ◽  
Author(s):  
XIAOYAN WANG ◽  
HAOYU MENG ◽  
PENGSHENG CHEN ◽  
NAIQUAN YANG ◽  
XIN LU ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Mouse Model ◽  
Cardiac Remodeling ◽  
Beneficial Effects

scholarly journals miR155 Deficiency Reduces Myofibroblast Density but Fails to Improve Cardiac Function after Myocardial Infarction in Dyslipidemic Mouse Model

2021 ◽  
Vol 22 (11) ◽  
pp. 5480
Author(s):  
David Schumacher ◽  
Adelina Curaj ◽  
Sakine Simsekyilmaz ◽  
Andreas Schober ◽  
Elisa A. Liehn ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Mouse Model ◽  
Cardiac Remodeling ◽  
Left Ventricular ◽  
Cardiomyocyte Hypertrophy ◽  
Cardiac Inflammation ◽  
Infarction Size ◽  
Adverse Remodeling ◽  
And Function

Myocardial infarction remains the most common cause of heart failure with adverse remodeling. MicroRNA (miR)155 is upregulated following myocardial infarction and represents a relevant regulatory factor for cardiac remodeling by engagement in cardiac inflammation, fibrosis and cardiomyocyte hypertrophy. Here, we investigated the role of miR155 in cardiac remodeling and dysfunction following myocardial infarction in a dyslipidemic mouse model. Myocardial infarction was induced in dyslipidemic apolipoprotein E-deficient (ApoE−/−) mice with and without additional miR155 knockout by ligation of the LAD. Four weeks later, echocardiography was performed to assess left ventricular (LV) dimensions and function, and mice were subsequently sacrificed for histological analysis. Echocardiography revealed no difference in LV ejection fractions, LV mass and LV volumes between ApoE−/− and ApoE−/−/miR155−/− mice. Histology confirmed comparable infarction size and unaltered neoangiogenesis in the myocardial scar. Notably, myofibroblast density was significantly decreased in ApoE−/−/miR155−/− mice compared to the control, but no difference was observed for total collagen deposition. Our findings reveal that genetic depletion of miR155 in a dyslipidemic mouse model of myocardial infarction does not reduce infarction size and consecutive heart failure but does decrease myofibroblast density in the post-ischemic scar.

scholarly journals Role of kallistatin in prevention of cardiac remodeling after chronic myocardial infarction

2008 ◽  
Vol 88 (11) ◽  
pp. 1157-1166 ◽  
Author(s):  
Lin Gao ◽  
Hang Yin ◽  
Robert S Smith ◽  
Lee Chao ◽  
Julie Chao
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Remodeling ◽  
Chronic Myocardial Infarction

P629Voluntary exercise associated with myokine production ameliorates cardiac remodeling and inflammation in a myocardial infarction mouse model

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
T Kadoguchi ◽  
K Shimada ◽  
A Hamad ◽  
T Aikawa ◽  
S Ouchi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Mouse Model ◽  
Cardiac Remodeling ◽  
Plasma Levels ◽  
Left Ventricular ◽  
Fibroblast Growth Factor 21 ◽  
Mrna Levels ◽  
Tnf Α ◽  
Anti Inflammatory

Abstract Background Left ventricular (LV) remodeling, through excessive inflammation, leads to heart failure. Exercise (Ex) training is associated with a risk reduction in heart failure through direct and indirect mechanisms by which Ex contributes an anti-inflammatory effect. During Ex, contracting muscle fibers release myokines, including interleukins (ILs), tumor necrosis factor α (TNF-α), follistatin-like protein 1 (FSTL-1), and fibroblast growth factor 21 (FGF-21), into the bloodstream. These myokines may have beneficial effects on other damaged organs, such as an infarcted myocardium, through anti-inflammatory effects. However, the exact mechanisms of the anti-inflammatory effects of voluntary Ex in myocardial infarction (MI) are poorly understood. Therefore, we investigated the effect of voluntary Ex on cardiac remodeling and inflammation, the relationship between cardiac remodeling and skeletal muscle (SKM) response, and circulating myokine levels in a mouse model of MI. Methods Twelve-week-old male C57BL/6J mice were used and divided into the following 4 groups: sham operation (Sham), MI, Sham+Ex, and MI+Ex. MI was induced by ligation of the left anterior descending coronary artery. Ex groups began voluntary wheel running for 4 weeks after the operation. An echocardiography was performed at baseline and 4 weeks after the operation. The mRNA levels in the LV infarcted area and SKM were measured with RT-PCR and western blot analysis. Plasma levels of myokines were also measured with immunoassays. Results Four weeks after MI induction, echocardiographic evaluation showed that the MI mice had a larger LV end-diastolic diameter (LVEDD) and end-systolic diameter (LVESD) than the Sham mice. The MI mice also showed higher mRNA levels of TNF-α, IL-1β, IL-6, and IL-10 in the LV tissue when compared to the Sham mice. These changes were significantly ameliorated in the MI+Ex mice. Interestingly, in the MI+Ex mice, mRNA levels of IL-6, IL-1β, FSTL-1, and FGF-21 in the SKM were significantly higher than in the MI mice, while there were no significant differences in TNF-α and IL-10 levels in all groups. Similarly, protein expression levels of peroxisome proliferator-activated receptor gamma coactivator 1-alpha, sirtuin-1, and mitochondrial transcriptional factor A of mitochondrial function markers in SKM were also significantly higher in the MI+Ex mice than in the MI mice. Furthermore, there were significant correlations between plasma levels of IL-1β, but not other myokines, and LVEDD, and LVESD. In addition, there was also a significant correlation between the SKM IL-1β level and LVESD in the Sham+Ex mice (all, P<0.05). Conclusions Amelioration of cardiac remodeling and inflammation by voluntary Ex is associated with increased myokines, especially IL-1β, in a MI mouse model. These results suggest that increased myokine levels, through voluntary exercise, may play an important role in the prevention of cardiac remodeling after MI.

P5390Adipolin/C1q/Tnf-related protein 12 attenuates adverse cardiac remodeling in a mouse model of myocardial infarction

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
T Takikawa ◽  
K Ohashi ◽  
L Fang ◽  
H Kawanishi ◽  
N Otaka ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Body Weight ◽  
Heart Disease ◽  
Mouse Model ◽  
Ischemic Heart Disease ◽  
Cardiac Remodeling ◽  
Ischemic Heart ◽  
Myocardial Remodeling ◽  
Myocardial Apoptosis ◽  
Cultured Cardiomyocytes

Abstract Background Ischemic heart disease is one of leading causes of death worldwide. Obesity is closely linked to the development of cardiovascular diseases including ischemic heart disease. Adipose tissue produces various secretory bioactive proteins called as adipokines, and dysregulation of adipokine production contributes to the pathogenesis of obesity-related complications. Previously we identified adipolin, also referred to as C1q/Tnf-related protein12, as an insulin-sensitizing adipokine that is down-regulated in obesity. Here, we investigated the effects of adipolin on cardiac remodeling in a mouse model of myocardial infarction (MI). Method Male adipolin-knockout (APL-KO) and wild-type (WT) mice were subjected to the permanent ligation of the left anterior descending coronary artery to create MI. Echocardiographic and histological analyses were performed to evaluate cardiac function and myocardial remodeling at 4 weeks after MI. Apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Cardiomyocyte cross sectional area was evaluated by Wheat Germ Agglutinin staining. Perivascular fibrosis was assessed by Masson's trichrome staining. Neonatal rat ventricular myocytes were used as cultured cardiac myocytes for in vitro study. Results APL-KO mice exhibited increased ratios of the heart weight/body weight and lung weight/body weight after MI compared with WT mice. APL-KO mice showed increased left ventricular diastolic diameter and decreased fractional shortening after MI compared with WT mice. APL-KO mice had increases in myocardial apoptosis, cardiomyocyte hypertrophy and perivascular fibrosis at the remote zone of infarct hearts as compared with WT mice. Treatment of cultured cardiomyocytes with adipolin protein reduced apoptosis in response to 24 hours of hypoxia. Treatment with adipolin protein also increased the phosphorylation of Akt in cardiomyocytes. Inhibition of PI3 kinase/Akt signaling by LY294002 reversed the anti-apoptotic effects of adipolin in cultured cardiomyocytes. Conclusion Our data indicate that adipolin prevents pathological myocardial remodeling after chronic ischemia, at least in part, by suppressing myocardial apoptosis through an Akt-dependent mechanism.

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