AEBP1 exacerbates myocardial ischemia-reperfusion injury via inhibition of IκBα DOI Open Access

Wei-Na Xue

Folia Morphologica, Journal Year: 2023, Volume and Issue: unknown

Published: Oct. 31, 2023

Myocardial ischaemia/reperfusion injury (MIRI) remains a major cause of death after cardiovascular diseases. Up-regulation adipocyte enhancer binding protein 1 (AEBP1) has been found in ischaemic cardiomyopathy patients. However, its influence and detailed mechanisms MIRI are obscure. In this study, expression target molecules was determined by RT-qPCR Western blotting. Cell viability apoptosis were evaluated CCK-8 TUNEL. Inflammatory cytokine levels assessed ELISA. function pathological changes examined echocardiography HE staining. Cardiac infarct size TTC Our data indicate that oxygen-glucose deprivation/ reoxygenation (OGD/R) resulted high AEBP1 but low IκBα cardiomyocytes. vitro knockdown increased viability, inhibited inflammation H9c2 cells under OGD/R. interacted with to degradation facilitated the nuclear translocation NF-κB. Moreover, silencing attenuated siAEBP1-medaited inhibition OGD/R-treated cells, suggesting involved pro-inflammatory action AEBP1. Finally, deficiency mitigated rats through IκBα/NF-κB pathway. Taken together, exacerbated repressing trigger NF-κB-mediated inflammation.

Language: Английский

The roles of long noncoding RNA NEAT1 in cardiovascular diseases DOI
Xiaoying Jiang, Mingjuan Zhang

Hypertension Research, Journal Year: 2024, Volume and Issue: 47(3), P. 735 - 746

Published: Jan. 4, 2024

Language: Английский

Citations

4
Isoflurane pretreatment protects against myocardial ischemia/reperfusion injury via mediating lncRNA CASC15/miR-542-3p axis DOI
Xiaoyi Wang,

Yueping Wang,

Yawei Yuan

et al.

Toxicology Mechanisms and Methods, Journal Year: 2024, Volume and Issue: 34(6), P. 694 - 702

Published: April 4, 2024

The protective effect of isoflurane on cardiomyocyte ischemia/reperfusion injury (I/RI) was explored in hypoxia and reoxygenation (H/R) induced model. In terms mechanism, the participation long non-coding RNA CASC15/microR-542-3p axis further discussed. H9c2 cells received H/R treatment to mimic myocardial I/RI. RT-qPCR performed quantify mRNA levels. Cell viability apoptosis were evaluated after pretreatment cell transfection. ELISA measure concentrations inflammatory/oxidative stress-related cytokines (TNF-α, IL-6, MDA, SOD). target relationship between CASC12 miR-542-3p determined

Language: Английский

Citations

3
Mesenchymal Stem Cell-Derived Long Noncoding RNAs in Cardiac Injury and Repair DOI Creative Commons

Talan Tran,

Cláudia Ferreira da Cruz, Anthony K. N. Chan

et al.

Cells, Journal Year: 2023, Volume and Issue: 12(18), P. 2268 - 2268

Published: Sept. 13, 2023

Cardiac injury, such as myocardial infarction and heart failure, remains a significant global health burden. The limited regenerative capacity of the adult poses challenge for restoring its function after injury. Mesenchymal stem cells (MSCs) have emerged promising candidates cardiac regeneration due to their ability differentiate into various cell types secrete bioactive molecules. In recent years, attention has been given noncoding RNAs derived from MSCs, particularly long (lncRNAs), potential role in injury repair. LncRNAs are RNA molecules that do not encode proteins but play critical roles gene regulation cellular responses including repair regeneration. This review focused on MSC-derived lncRNAs implications regeneration, effects function, remodeling, cardiomyocyte angiogenesis. Understanding molecular mechanisms may contribute development novel therapeutic strategies treating cardiovascular diseases. However, further research is needed fully elucidate address challenges this field.

Language: Английский

Citations

8
MiR-125b-5p Alleviates the Damage of Myocardial Infarction by Inhibiting the NFAT2 to Reduce F2RL2 Expression DOI
Zhenhua Wu,

Jie Geng,

Yunpeng Bai

et al.

Regenerative Medicine, Journal Year: 2023, Volume and Issue: 18(7), P. 543 - 559

Published: June 21, 2023

Aim: To explore the effect of miR-125b-5p/nuclear factor activated T cells 1 (NFAT2)/F2RL2 on myocardial infarction (MI). Method: After establishment MI mouse model and oxygen glucose deprivation (OGD)-induced cell model, effects NFAT2 process were observed, miR-125b-5p/NFAT2/F2RL2 viability, apoptosis, inflammatory factors levels determined. Result: silencing relieved inhibited inflammation in mice. In OGD-induced human coronary artery endothelial cardiac microvascular cells, miR-125b-5p enhanced yet repressed apoptosis levels. overexpression reversed miR-125b-5p, while F2RL2 offset overexpression. Conclusion: MiR-125b-5p alleviates injury by inhibiting level to reduce expression.

Language: Английский

Citations

7
Myocardial infarction complexity: A multi-omics approach DOI

Xiaolan Liu,

Lulu Wang, Yan Wang

et al.

Clinica Chimica Acta, Journal Year: 2023, Volume and Issue: 552, P. 117680 - 117680

Published: Nov. 25, 2023

Language: Английский

Citations

7
Ginkgolide B Blocks Vascular Remodeling after Vascular Injury via Regulating Tgfβ1/Smad Signaling Pathway DOI Creative Commons
Quan Wang,

Shuai Ni,

Ling Li

et al.

Cardiovascular Therapeutics, Journal Year: 2023, Volume and Issue: 2023, P. 1 - 13

Published: Dec. 13, 2023

Coronary artery disease (CAD) is the most prevalent cardiovascular worldwide, resulting in myocardial infarction (MI) and even sudden death. Following percutaneous coronary intervention (PCI), restenosis caused by vascular remodeling always formed at stent implantation site. Here, we show that Ginkgolide B (GB), a naturally occurring terpene lactone, effectively suppresses subsequent wild-type mice following left carotid (LCA) injury. Additional experiments reveal GB exerts protective effect on further through modulation of Tgfβ1/Smad signaling pathway vivo human smooth muscle cells (HVSMAs) but not umbilical vein endothelial (HUVECs) vitro. Moreover, beneficial abolished after incubated with pirfenidone (PFD, drug for idiopathic pulmonary fibrosis, IPF), which can inhibit Tgfβ1. In Tgfβ1-/- mice, treatment capsules Yinxingneizhi Zhusheye (including B) fails to improve restenosis. conclusion, our data identify could be potential novel therapeutic agent block vessel injury-associated significant repression pathway.

Language: Английский

Citations

4
Construction of LncRNA-mediated CeRNA network for investigating the immune pathogenesis of myocardial infarction DOI Creative Commons
Dongmei Wei,

Yuanting Meng,

Hua Fan

et al.

Medicine, Journal Year: 2024, Volume and Issue: 103(10), P. e37413 - e37413

Published: March 8, 2024

Myocardial infarction (MI) is a cardiovascular disease that seriously threatens human health. However, an immune-related competitive endogenous RNA (ceRNA) network has not been reported in MI.

Language: Английский

Citations

1
Effect of remote ischemic preconditioning intervention on serum levels of microRNA-582–5p/HMGB1 in patients with acute cerebral infarction DOI
Ting C. Zhao, Meng Li, Qiuyue Yan

et al.

Clinical Neurology and Neurosurgery, Journal Year: 2024, Volume and Issue: 241, P. 108291 - 108291

Published: April 21, 2024

Language: Английский

Citations

1
AEBP1 exacerbates myocardial ischemia-reperfusion injury via inhibition of IκBα DOI Open Access

Wei-Na Xue

Folia Morphologica, Journal Year: 2023, Volume and Issue: unknown

Published: Oct. 31, 2023

Myocardial ischaemia/reperfusion injury (MIRI) remains a major cause of death after cardiovascular diseases. Up-regulation adipocyte enhancer binding protein 1 (AEBP1) has been found in ischaemic cardiomyopathy patients. However, its influence and detailed mechanisms MIRI are obscure. In this study, expression target molecules was determined by RT-qPCR Western blotting. Cell viability apoptosis were evaluated CCK-8 TUNEL. Inflammatory cytokine levels assessed ELISA. function pathological changes examined echocardiography HE staining. Cardiac infarct size TTC Our data indicate that oxygen-glucose deprivation/ reoxygenation (OGD/R) resulted high AEBP1 but low IκBα cardiomyocytes. vitro knockdown increased viability, inhibited inflammation H9c2 cells under OGD/R. interacted with to degradation facilitated the nuclear translocation NF-κB. Moreover, silencing attenuated siAEBP1-medaited inhibition OGD/R-treated cells, suggesting involved pro-inflammatory action AEBP1. Finally, deficiency mitigated rats through IκBα/NF-κB pathway. Taken together, exacerbated repressing trigger NF-κB-mediated inflammation.

Language: Английский

Citations

2