Galectin-3 is expressed in the myocardium very early post–myocardial infarction

Hashmi, Satwat; Al-Salam, Suhail

doi:10.1016/j.carpath.2014.12.001

Cited by 49 publications

(41 citation statements)

References 72 publications

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“…23 reported that the mRNA expression of galectin‐3 in the infarcted area was the highest at 1 week after myocardial infarction and then gradually decreased in the next few weeks. Hashmi and Al‐Salam 24 also showed significantly upregulated mRNA and protein expressions of galectin‐3 at 60 min and 24 h after myocardial infarction in mice. Our group recently demonstrated that inflammation might participate in the worsening cardiorenal functions and remodelling processes post aortocaval fistula in unilateral nephrectomized rats 25, and significant upregulation of galectin‐3 expression in the hearts and kidney was evidenced in this model 26.…”

Section: Introductionmentioning

confidence: 92%

Ticagrelor attenuates myocardial ischaemia–reperfusion injury possibly through downregulating galectin‐3 expression in the infarct area of rats

Liu

et al. 2018

Brit J Clinical Pharma

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AimsThe full benefits of myocardial revascularization strategies applied to acute myocardial infarction patients might be reduced by myocardial ischaemia and reperfusion (I/R) injury. It is known that inflammation plays an important role in the pathogenesis of I/R injury and galectin‐3, a known inflammatory factor, is actively involved in ischaemia‐induced inflammation and fibrosis of various organs. Previous studies demonstrated that anti‐platelets therapy with ticagrelor, a new P2Y12 receptor antagonist, could effectively attenuate myocardial I/R injury and I/R injury‐related inflammatory responses. It remains unknown whether the cardioprotective effects of ticagrelor are also mediated by modulating myocardial galectin‐3 expression.MethodsWe determined the ratio of infarct area (IA)/area at risk (AAR), expression of galectin‐3, TNF‐α and IL‐6 in infarct area of rats treated with placebo (equal volume saline per gastric gavage immediately after LAD ligation, then once daily till study end) or ticagrelor (150 mg kg−1 dissolved in saline per gastric gavage immediately after LAD ligation, then once daily till study end) at 24 h, 3 and 7 days post I (45 min)/R injury. Sham‐operated rats served as control.ResultsOur results showed that ticagrelor treatment significantly reduced IA/AAR ratio at 3 and 7 days post I/R, downregulated mRNA and protein expression of galectin‐3, as well as mRNA expression of TNF‐α and IL‐6 in infarct area at 24 h, 3 and 7 days post I/R.ConclusionsOur results suggest that the cardioprotective effects of ticagrelor might partly be mediated by downregulating galectin‐3 expression in infarct area in this rat model of myocardial I/R injury.

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Section: Introductionmentioning

confidence: 92%

Ticagrelor attenuates myocardial ischaemia–reperfusion injury possibly through downregulating galectin‐3 expression in the infarct area of rats

Liu

et al. 2018

Brit J Clinical Pharma

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“…Indeed, Gal-3 could be part of a survival mechanism of the injured myocardium to cope with the ischemic insult [14]. Several evidences have pointed out Gal-3 is not a simple bystander but it represents an important player in the cardiac remodeling process following MI.…”

Section: Gal 3 In Acsmentioning

confidence: 99%

“…Noteworthy, it has a different and controversial role in early and late phases. In vivo model of MI have revealed that Gal-3 is expressed by cardiomyocytes and endothelial cells within the first hours of ischemia and regulates survival in cardiomyocytes probably through its anti-apoptotic activity [14]. Moreover, in early phases it contributes actively to the reparative processes in the infarcted area, which are essential for the maintenance of ventricular function after MI.…”

Section: Gal 3 In Acsmentioning

confidence: 99%

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Galectin-3 in acute coronary syndrome

Agnello

Bivona

Sasso

et al. 2017

Clinical Biochemistry

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“…GAL-3 is expressed in a variety of cells, e.g., endothelial and epithelial cells, activated macrophages, microglial cells, basophils, mast cells, neutrophils, neurons and cardiomyocytes [10][11][12][13][14][15][16]. So far we know that GAL-3 is closely associated with myocardial infarction in the early post MI period and later with myocardial fibrosis and heart failure [15,17]. Our aim is to further investigate if GAL-3 has any role in IR injury of the myocardium.…”

Section: Introductionmentioning

confidence: 99%

Myocardial Ischemia Reperfusion Injury: Apoptotic, Inflammatory and Oxidative Stress Role of Galectin-3

Al-Salam

Hashmi

2018

Cell Physiol Biochem

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Background/Aims: Myocardial reperfusion has the potential to salvage the ischemic myocardium after a period of coronary occlusion. Reperfusion, however, can cause a wide spectrum of deleterious effects. Galectin-3 (GAL-3), a beta galactoside binding lectin, is closely associated with myocardial infarction (MI), myocardial fibrosis and heart failure. In our study, we investigated its role in ischemia-reperfusion injuries (IR) as this phenomenon is extremely relevant to the early intervention after acute MI. Methods: C57B6/J wild type (WT) mice and GAL-3 knockout (KO) mice were used for murine model of IR injury in the heart where a period of 30 minutes ischemia was followed by 24 hours of reperfusion. Heart samples were processed for immunohistochemical and immunofluorescent labeling, morphometric analysis, western blot and enzyme-linked immunosorbent assay to identify the apoptotic, inflammatory and oxidative stress role of GAL-3. Results: Our results show that there was a significant increase in GAL-3 levels in the heart which shows GAL-3 is playing a role in the ischemia reperfusion injury. Troponin I was also significantly higher in GAL-3-KO group than wild type. Our study shows that GAL-3 is associated with an increase in the antioxidant activity in the IR injured myocardium. Antioxidant enzymes superoxide dismutase, glutathione and catalase were found to be significantly raised in the GAL-3 wild type IR as compared to the GAL-3 KO IR group. A significant increase in apoptotic activity is seen in GAL-3 KO IR group as compared with GAL-3 wild IR group. Conclusion: Our study shows that GAL-3 can affect the redox pathways, controlling cell survival and death, and plays a protective role on the myocardium following IR injury.

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Galectin-3 is expressed in the myocardium very early post–myocardial infarction

Cited by 49 publications

References 72 publications

Ticagrelor attenuates myocardial ischaemia–reperfusion injury possibly through downregulating galectin‐3 expression in the infarct area of rats

Ticagrelor attenuates myocardial ischaemia–reperfusion injury possibly through downregulating galectin‐3 expression in the infarct area of rats

Galectin-3 in acute coronary syndrome

Myocardial Ischemia Reperfusion Injury: Apoptotic, Inflammatory and Oxidative Stress Role of Galectin-3

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