Effect of Ischemic Postconditioning on Cell Apoptosis and Expression of Relevant Genes in Non-Culprit Coronary Arteries

Wang, Jian; He, Songyuan

doi:10.1136/jim-2020-001328

Cited by 6 publications

(5 citation statements)

References 14 publications

(18 reference statements)

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“…Our previous studies have shown that IP could significantly affect the expression of mRNA angiotensin II receptor type 1 (AT1), connexin 43 (Cx43), and β-tubulin, which are key factors in regulating the state of blood vessels and play an important role in nonculprit lesions in the patients with MI [ 13 ]. Consistently, western blot assay showed that IR obviously upregulated the level of AT1, Cx43 and β-tubulin in nonculprit coronary arterial tissues; however, these increases of AT1 and Cx43 were notably alleviated by IP.…”

Section: Resultsmentioning

confidence: 99%

“…The acute myocardial ischemia animal model was constructed according to our previous published literature [ 13 ].…”

Section: Methodsmentioning

confidence: 99%

“…In addition, IP can reduce tissue reperfusion injury by mobilizing endogenous repair mechanism [ 12 ]. Our previous research found that IP could inhibit the progression of nonculprit lesions [ 13 ]. However, the mechanism by which IP regulated the occurrence and development of nonculprit lesions remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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Ischemic postconditioning protects nonculprit coronary arteries against ischemia-reperfusion injury via downregulating miR-92a, miR-328 and miR-494

Wang

Yan

et al. 2022

Aging

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Background: Nonculprit lesions are closely related to the prognosis of patients with ST-segment elevation myocardial infarction (STEMI). Our previous research found that ischemic postconditioning (IP) could inhibit the progression of nonculprit lesions. However, the mechanism by which IP regulates the occurrence and development of nonculprit lesions remains unclear. Methods: Firstly, a rabbit ischemia-reperfusion (IR) model was constructed. Next, the morphological characteristics of the coronary arterial tissues and myocardial tissues of the rabbits were observed using hematoxylin-eosin (H&E) staining. Then, western blot was performed to detect the expressions of AT1, Cx43, β-tubulin, Bax, Bcl-2 and cleaved caspase 3. Finally, to further confirm the effect of IP on nonculprit coronary arterial tissues, an in vitro model of oxygen and glucose deprivation/reperfusion (OGD/R) was established. Results: IR notably induced the cells apoptosis in nonculprit coronary arterial tissues and in myocardial tissues, while IR-induced cell apoptosis was significantly inhibited by IP. In addition, IP protected nonculprit coronary arterial tissues against IR via downregulating miR-92a, miR-328 and miR-494 and mRNA AT1, Cx43 and β-tubulin. Consistently, OGD/R-induced injury of Human umbilical vein endothelial cells (HUVECs) was reversed by IP. Conclusions: In this study, IP could protect nonculprit coronary arteries against IR injury via downregulating miR-92a, miR-328 and miR-494. Our findings may provide new directions for the treatment of nonculprit lesions.

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Section: Resultsmentioning

confidence: 99%

“…The acute myocardial ischemia animal model was constructed according to our previous published literature [ 13 ].…”

Section: Methodsmentioning

confidence: 99%

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Ischemic postconditioning protects nonculprit coronary arteries against ischemia-reperfusion injury via downregulating miR-92a, miR-328 and miR-494

Wang

Yan

et al. 2022

Aging

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“…The effectiveness of the stimulation of AT1R may depend on the accessibility of the AT1R-associated protein (ATRAP), which is able to enhance the internalization of AT1R from the cell surface to cytoplasm and reduce the action of Ang II [74]. More recently, studies performed on non-culprit arteries harvested from the rabbit model of myocardial ischemia-reperfusion provided evidence that the expression of AT1R was higher in the ischemia-reperfusion group than in the sham group, but expressions of AT1R, connexin 43, and β-tubulin were lower in the ischemic postconditioning group than in the ischemia reperfusion group [75].…”

Section: Experimental Evidence For the Negative Role Of Ang II In The...mentioning

confidence: 99%

Interplay of Angiotensin Peptides, Vasopressin, and Insulin in the Heart: Experimental and Clinical Evidence of Altered Interactions in Obesity and Diabetes Mellitus

Szczepanska-Sadowska

2024

IJMS

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The present review draws attention to the specific role of angiotensin peptides [angiotensin II (Ang II), angiotensin-(1-7) (Ang-(1-7)], vasopressin (AVP), and insulin in the regulation of the coronary blood flow and cardiac contractions. The interactions of angiotensin peptides, AVP, and insulin in the heart and in the brain are also discussed. The intracardiac production and the supply of angiotensin peptides and AVP from the systemic circulation enable their easy access to the coronary vessels and the cardiomyocytes. Coronary vessels and cardiomyocytes are furnished with AT1 receptors, AT2 receptors, Ang (1-7) receptors, vasopressin V1 receptors, and insulin receptor substrates. The presence of some of these molecules in the same cells creates good conditions for their interaction at the signaling level. The broad spectrum of actions allows for the engagement of angiotensin peptides, AVP, and insulin in the regulation of the most vital cardiac processes, including (1) cardiac tissue oxygenation, energy production, and metabolism; (2) the generation of the other cardiovascular compounds, such as nitric oxide, bradykinin (Bk), and endothelin; and (3) the regulation of cardiac work by the autonomic nervous system and the cardiovascular neurons of the brain. Multiple experimental studies and clinical observations show that the interactions of Ang II, Ang(1-7), AVP, and insulin in the heart and in the brain are markedly altered during heart failure, hypertension, obesity, and diabetes mellitus, especially when these diseases coexist. A survey of the literature presented in the review provides evidence for the belief that very individualized treatment, including interactions of angiotensins and vasopressin with insulin, should be applied in patients suffering from both the cardiovascular and metabolic diseases.

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“…Postconditioning activates several cellular signalling pathways, such as those involved in apoptosis, oxidative stress, inflammatory responses, and mitochondrial function [ 9 ]. For example, extensive studies have reported that apoptosis induced by IRI can be attenuated by post-conditioning [ 10 ]. This may be beneficial for cardiomyocyte preservation and infarct size reduction.…”

Section: Introductionmentioning

confidence: 99%

A Novel Postconditioning Approach Attenuates Myocardial Ischaemia-Reperfusion Injury in Rats

Zhao,

Liu,

Chen

et al. 2024

Rev. Cardiovasc. Med.

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Background: Ischaemia-reperfusion injury (IRI) is the damage that occurs when blood flow is restored to a tissue or organ after a period of ischaemia. Postconditioning is a therapeutic strategy aimed at reducing the tissue damage caused by IRI. Postconditioning in rodents is a useful tool to investigate the potential mechanisms of postconditioning. Currently, there is no convenient approach for postconditioning rodents. Methods: Rats were subjected to a balloon postconditioning procedure. A balloon was used to control the flow in the vessel. This allowed for easy and precise manipulation of perfusion. Evans blue and triphenyltetrazolium chloride (TTC) double staining were used to determine the infarct size. Apoptosis in the myocardium was visualised and quantified by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). Western blotting was performed to assess the expression of key apoptotic proteins, i.e. , B-cell lymphoma 2 (Bcl-2), Bcl-2 Associated X (Bax), and cleaved caspase-3. Results: The balloon control approach to postconditioning provided accurate control of coronary blood flow and simplified the postconditioning manipulation. Infarct size reduction was observed in IRI rats after post-conditioning. There was a decrease in cardiac apoptosis in IRI rats after conditioning, as detected by TUNEL staining. IRI rats showed increased Bcl-2 levels and decreased Bax and cleaved caspase-3 levels in the myocardium. Conclusions: Postconditioning was successfully applied in rats using this novel approach. Postconditioning with this approach reduced infarct size and apoptosis in the area at risk.

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Effect of Ischemic Postconditioning on Cell Apoptosis and Expression of Relevant Genes in Non-Culprit Coronary Arteries

Cited by 6 publications

References 14 publications

Ischemic postconditioning protects nonculprit coronary arteries against ischemia-reperfusion injury via downregulating miR-92a, miR-328 and miR-494

Ischemic postconditioning protects nonculprit coronary arteries against ischemia-reperfusion injury via downregulating miR-92a, miR-328 and miR-494

Interplay of Angiotensin Peptides, Vasopressin, and Insulin in the Heart: Experimental and Clinical Evidence of Altered Interactions in Obesity and Diabetes Mellitus

A Novel Postconditioning Approach Attenuates Myocardial Ischaemia-Reperfusion Injury in Rats

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