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apoptosis suppress autophagy AND (mycaridal OR heart)

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https://read.qxmd.com/read/30787203/-malat1-mir-15b-5p-mapk1-mediates-endothelial-progenitor-cells-autophagy-and-affects-coronary-atherosclerotic-heart-disease-via-mtor-signaling-pathway
#1
Ying Zhu, Tianrui Yang, Jinlan Duan, Ninghui Mu, Tong Zhang
Objective: Present study focused on the influence of lncRNA MALAT1 on coronary atherosclerotic heart disease (CAD) by regulating miR-15b-5p/ MAPK1 and mTOR signaling pathway. Method: Differentially expressed genes and activated pathway were investigated through bioinformatics analysis. QRT-PCR was conducted to verify expression of MALAT1 , miR-15b-5p and MAPK1 in CAD blood samples and endothelial progenitor cells (EPCs). In addition, the interactions among MALAT1 , miR-15b-5p and MAPK1 were revealed by Luciferase reporter assay...
February 21, 2019: Aging
https://read.qxmd.com/read/30621510/endothelial-leptin-receptor-deletion-promotes-cardiac-autophagy-and-angiogenesis-following-pressure-overload-by-suppressing-akt-mtor-signaling
#2
Rajinikanth Gogiraju, Astrid Hubert, Jörg Fahrer, Beate K Straub, Moritz Brandt, Philip Wenzel, Thomas Münzel, Stavros Konstantinides, Gerd Hasenfuss, Katrin Schäfer
BACKGROUND: Cardiac remodeling is modulated by overnutrition or starvation. The adipokine leptin mediates energy balance between adipose tissue and brain. Leptin and its receptors are expressed in the heart. METHODS AND RESULTS: To examine the importance of endothelial leptin signaling in cardiac hypertrophy, transverse aortic constriction was used in mice with inducible endothelium-specific deletion of leptin receptors (End.LepR-KO) or littermate controls (End...
January 2019: Circulation. Heart Failure
https://read.qxmd.com/read/30618070/mtor-and-beclin1-two-key-autophagy-related-molecules-and-their-roles-in-myocardial-ischemia-reperfusion-injury
#3
REVIEW
Binhao Shi, Mengqing Ma, Yitian Zheng, Yanyan Pan, Xianhe Lin
Autophagy is the general term of lysosomal degradation of substances in cells, which is considered the key to maintaining the normal structure and function of the heart. It also has a correlation with several heart diseases, in particular, myocardial ischemia/reperfusion (I/R) injury. At the stage of myocardial ischemia, autophagy degrades nonfunctional cytoplasmic proteins providing the critical nutrients for the critical life activities, thereby suppressing cell apoptosis and necrosis. However, autophagy is likely to affect the heart negatively in the reperfusion stage...
January 7, 2019: Journal of Cellular Physiology
https://read.qxmd.com/read/30556888/overexpression-of-mir-638-attenuated-the-effects-of-hypoxia-reoxygenation-treatment-on-cell-viability-cell-apoptosis-and-autophagy-by-targeting-atg5-in-the-human-cardiomyocytes
#4
P Zhao, B-L Zhang, K Liu, B Qin, Z-H Li
OBJECTIVE: Myocardial ischemia/reperfusion (I/R) injury largely contributed to the damage of myocardial tissues in patients with coronary disease, which may subsequently lead to heart failure. MicroRNAs (miRNAs) are considered to be involved in the process of myocardial I/R injury. The present study aimed to investigate the in vitro functional role of miR-638 in the myocardial I/R injury in the human cardiomyocytes (HCMs). PATIENTS AND METHODS: MTT assay and flow cytometry assay were performed to determine cell viability and apoptosis of HCMs...
December 2018: European Review for Medical and Pharmacological Sciences
https://read.qxmd.com/read/30536615/lncrna-malat1-protects-cardiomyocytes-from-isoproterenol-induced-apoptosis-through-sponging-mir-558-to-enhance-ulk1-mediated-protective-autophagy
#5
Xiaoyan Guo, Xiaoguang Wu, Yan Han, Erhu Tian, Jiangtao Cheng
Investigating the molecular mechanisms of myocardial infarction (MI) and subsequent heart failure have gained considerable attention worldwide. Long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been previously demonstrated to regulate the proliferation and metastasis of several tumors. However, little is known about the effects of MALAT1 in MI and in regulating the cell date after MI. In our study, first, it was shown that the expression levels of MALAT1 were increased in the MI samples compared with normal tissues using quantitative reverse-transcription polymerase chain reaction...
December 7, 2018: Journal of Cellular Physiology
https://read.qxmd.com/read/30367996/soluble-receptor-for-advance-glycation-end-products-inhibits-ischemia-reperfusion-induced-myocardial-autophagy-via-the-stat3-pathway
#6
Mengqiu Dang, Xiangjun Zeng, Buxing Chen, Hongxia Wang, Huihua Li, Yu Liu, Xiuling Zhang, Xianxian Cao, Fenghe Du, Caixia Guo
The pathogenesis of myocardial ischemia/reperfusion (I/R) is poorly understood, but recent evidence suggests that autophagy plays crucial roles in I/R injuries. Soluble receptor for advanced glycation end-products (sRAGE) exerts protective effects during I/R by decreasing cardiac apoptosis, which is mediated via increasing the ubiquitin proteasome system (UPS) and signal transducer and activator of transcription 3 (STAT3). The present study examined the effects and mechanisms of sRAGE on I/R-triggered cardiac autophagy...
October 25, 2018: Free Radical Biology & Medicine
https://read.qxmd.com/read/30336249/the-involvement-of-autophagic-flux-in-the-development-and-recovery-of-doxorubicin-induced-neurotoxicity
#7
Xueyuan Zhou, Pengfei Xu, Ruili Dang, Yujin Guo, Gongying Li, Yi Qiao, Ruining Xie, Yuanyuan Liu, Pei Jiang
Doxorubicin (Dox) is an effective anti-cancer agent, whose clinical use is limited by the cytotoxicity in non-target tissues, especially the heart and brain. The drug-induced neuronal damage is primarily mediated by oxidative stress, in which autophagy plays a central role. Although numerous studies indicate the involvement of autophagy in neurodegenerative diseases and brain injury, the evidence concerning autophagic process in Dox-induced neuronal death is limited. We found that repeated Dox administration induced the protein expression of LC3II and P62 and impaired autophagic flux with enhanced autophagasome accumulation in rat hippocampus, whereas two weeks after the cessation of Dox treatment, the autophagic process was restored, even stimulated, with normalized protein levels of LC3II and P62 and enhanced expression of Becline-1, indicating a compensatory response in the recovery state...
October 15, 2018: Free Radical Biology & Medicine
https://read.qxmd.com/read/30292723/curcumin-protects-against-diabetic-cardiomyopathy-by-promoting-autophagy-and-alleviating-apoptosis
#8
Qing Yao, Zhi-Qiang Ke, Shuang Guo, Xiao-Song Yang, Fei-Xue Zhang, Xiu-Fen Liu, Xiao Chen, Hong-Guang Chen, Huan-Ya Ke, Chao Liu
The effects of curcumin on regulating cardiac apoptosis and autophagy were analyzed in diabetic models both in vivo and in vitro. In vivo, experimental diabetes was induced in mice by low-dose STZ injection combined with a high-fat diet. In vitro, cultured H9c2 cardiomyoblasts were exposed to high d-glucose concentrations combined with palmitate. Our results showed that apoptosis was increased and autophagy was suppressed in the hearts of diabetic mice, which was ameliorated by curcumin treatment, ultimately improving cardiac function...
October 4, 2018: Journal of Molecular and Cellular Cardiology
https://read.qxmd.com/read/30031611/recombinant-human-brain-natriuretic-peptide-regulates-pi3k-akt-mtor-pathway-through-lncrna-egot-to-attenuate-hypoxia-induced-injury-in-h9c2-cardiomyocytes
#9
Chengxi Zhang, Sinian Pan, Ayipaxa Aisha, Minawaer Abudoukelimu, Leile Tang, Yesheng Ling
This study aimed to investigate whether recombinant human brain natriuretic peptide (rhBNP) regulated hypoxia-induced injury in H9c2 cardiomyocytes through lncRNA EGOT. H9c2 cardiomyocytes were cultured under normoxia and hypoxia (21% and 3% O2 ) conditions, and whether hypoxia induced injury by assessing cell viability, apoptosis and autophagy. H9c2 cells were then treated with different doses of exogenous rhBNP (200, 600 and 900 nmol/L, respectively) and the effects of rhBNP on hypoxia-induced injury in H9c2 cells as well as the expression of EGOT were studied...
September 10, 2018: Biochemical and Biophysical Research Communications
https://read.qxmd.com/read/30022684/hydrogen-sulfide-protects-human-cardiac-fibroblasts-against-h-2-o-2-induced-injury-through-regulating-autophagy-related-proteins
#10
Ao Feng, Chen Ling, Lin Xin-Duo, Wu Bing, Wu San-Wu, Zhan Yu, Huang Yu-Lan, Zhang You-En
Autophagy, an intracellular bulk degradation process of proteins and organelles, can be induced by myocardial ischemia in the heart. However, the causative role of autophagy in the survival of human cardiac fibroblasts and the underlying mechanisms are incompletely understood. Oxidative stress can induce autophagy in cultured cells upon hydrogen peroxide (H2 O2 ) exposure. Because hydrogen sulfide (H2 S) regulates reactive oxygen species (ROS) and apoptosis, we hypothesize that H2 S may have a cardioprotective function...
August 2018: Cell Transplantation
https://read.qxmd.com/read/29956395/concurrence-of-autophagy-with-apoptosis-in-alveolar-epithelial-cells-contributes-to-chronic-pulmonary-toxicity-induced-by-methamphetamine
#11
Yun Wang, Yu-Han Gu, Li-Ye Liang, Ming Liu, Bin Jiang, Mei-Jia Zhu, Xin Wang, Lin Shi
OBJECTIVES: Methamphetamine (MA) abuse evokes pulmonary toxicity. The aim of our study is to investigate if autophagy is induced by MA and if autophagy-initiated apoptosis in alveolar epithelial cells is involved in MA-induced chronic pulmonary toxicity. MATERIALS AND METHODS: The rats in Control group and MA group were tested by Doppler and HE staining. The alveolar epithelial cells were treated with MA, following by western blot, RT-PCR and immunofluorescence assay...
October 2018: Cell Proliferation
https://read.qxmd.com/read/29932232/the-cardioprotective-effect-of-thymoquinone-on-ischemia-reperfusion-injury-in-isolated-rat-heart-via-regulation-of-apoptosis-and-autophagy
#12
Junhui Xiao, Zun-Ping Ke, Yan Shi, Qiutang Zeng, Zhe Cao
Thymoquinone (TQ), as the active constituents of black cumin (Nigella sativa) seed oil, has been reported to have potential protective effects on the cardiovascular system. This study aimed to investigate the effects and the underlying mechanisms of TQ on myocardial ischemia-reperfusion (I/R) injury in Langendorff-perfused rat hearts. Wister rat hearts were subjected to I/R and the experimental group were pretreated with TQ prior to I/R. Hemodynamic parameters, myocardial infarct size, cardiac marker enzymes, superoxide dismutase (SOD), malondialdehyde (MDA) content, and cardiomyocyte apoptosis were assayed...
June 22, 2018: Journal of Cellular Biochemistry
https://read.qxmd.com/read/29719509/mangiferin-enhanced-autophagy-via-inhibiting-mtorc1-pathway-to-prevent-high-glucose-induced-cardiomyocyte-injury
#13
Jun Hou, Dezhi Zheng, Wenjing Xiao, Dandan Li, Jie Ma, Yonghe Hu
Mangiferin functions as a perfect anti-oxidative compound in the diabetic heart, however, the exact mechanism remains to be elucidated. Here, we show the cardioprotective effect of mangiferin under high glucose-induced cardiotoxic condition mainly contributed to enhanced autophagy via suppressing mTORC1 downstream signal transduction. Primary neonatal rat cardiomyocytes were cultured to detect myocytes injury, autophagy, and related signal transduction under different doses of glucose and mangiferin treatment...
2018: Frontiers in Pharmacology
https://read.qxmd.com/read/29701696/estrogen-and-or-estrogen-receptor-%C3%AE-inhibits-bnip3-induced-apoptosis-and-autophagy-in-h9c2-cardiomyoblast-cells
#14
Bih-Cheng Chen, Yi-Jiun Weng, Marthandam Asokan Shibu, Chien-Kuo Han, Yueh-Sheng Chen, Chia-Yao Shen, Yueh-Min Lin, Vijaya Padma Viswanadha, Hsin-Yueh Liang, Chih-Yang Huang
The process of autophagy in heart cells maintains homeostasis during cellular stress such as hypoxia by removing aggregated proteins and damaged organelles and thereby protects the heart during the times of starvation and ischemia. However, autophagy can lead to substantial cell death under certain circumstances. BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3), a hypoxia-induced marker, has been shown to induce both autophagy and apoptosis. A BNIP3-docked organelle, e.g., mitochondria, also determines whether autophagy or apoptosis will take place...
April 26, 2018: International Journal of Molecular Sciences
https://read.qxmd.com/read/29577900/protective-effects-of-kenpaullone-on-cardiomyocytes-following-h-2-o-2-induced-oxidative-stress-are-attributed-to-inhibition-of-connexin-43-degradation-by-sgsm3
#15
Hyun-Chel Joo, Jung-Won Choi, Hanbyeol Moon, Chang Youn Lee, Kyung-Jong Yoo, Sang Woo Kim, Ki-Chul Hwang
A previous study showed that small G protein signaling modulator 3 (SGSM3) was highly correlated with Cx43 in heart functions and that high levels of SGSM3 may induce Cx43 turnover through lysosomal degradation in infarcted rat hearts. Here, we investigated the protective effects of kenpaullone on cardiomyocytes following H2 O2 -induced oxidative stress mediated by the interaction of SGSM3 with Cx43. We found that the gap junction protein Cx43 was significantly down-regulated in an H2 O2 concentration-dependent manner, whereas expression of SGSM3 was up-regulated upon H2 O2 exposure in H9c2 cells...
May 5, 2018: Biochemical and Biophysical Research Communications
https://read.qxmd.com/read/29554809/does-p53-inhibition-suppress-myocardial-ischemia-reperfusion-injury
#16
Toshiyuki Yano, Koki Abe, Masaya Tanno, Takayuki Miki, Atsushi Kuno, Tetsuji Miura, Charles Steenbergen
p53 is well known as a regulator of apoptosis and autophagy. In addition, a recent study showed that p53 is a modulator of the opening of the mitochondrial permeability transition pore (mPTP), a trigger event of necrosis, but the role of p53 in necrosis induced by myocardial ischemia-reperfusion (I/R) remains unclear. The aim of this study was to determine the role of p53 in acute myocardial I/R injury in perfused mouse hearts. In male C57BL6 mice between 12 and 15 weeks of age, 2 types of p53 inhibitors were used to suppress p53 function during I/R: pifithrin-α, an inhibitor of transcriptional functions of p53, and pifithrin-μ, an inhibitor of p53 translocation from the cytosol to mitochondria...
July 2018: Journal of Cardiovascular Pharmacology and Therapeutics
https://read.qxmd.com/read/29505745/cardioprotective-effect-of-paeonol-against-epirubicin-induced-heart-injury-via-regulating-mir-1-and-pi3k-akt-pathway
#17
Jing Wu, Chao Sun, Ruoyi Wang, Juan Li, Meng Zhou, Mi Yan, Xia Xue, Chuanxin Wang
Cardiotoxicity is a dose-dependent side effect of epirubicin that restricts its clinical utility in cancer chemotherapy. Paeonol is an active constituent with various biological activities, including the protection of antineoplastic-induced toxicities. In the present study, we investigated the protective effect of paeonol on epirubicin-induced cardiotoxicity and explored the underlying mechanism. A series of methods were used including a MTT assay, flow cytometry, echocardiography, TUNEL staining, a dual-luciferase reporter assay, immunofluorescence, RT-PCR and Western blotting...
April 25, 2018: Chemico-biological Interactions
https://read.qxmd.com/read/29476905/tax1bp1-overexpression-attenuates-cardiac-dysfunction-and-remodeling-in-stz-induced-diabetic-cardiomyopathy-in-mice-by-regulating-autophagy
#18
Yang Xiao, Qing Qing Wu, Ming Xia Duan, Chen Liu, Yuan Yuan, Zheng Yang, Hai Han Liao, Di Fan, Qi Zhu Tang
Diabetic cardiomyopathy is associated with suppressed autophagy and augmented inflammation in the heart. The effects of Tax1 binding protein 1 (TAX1BP1) on both autophagy and inflammation suggest that it may participate in the progression of diabetic cardiomyopathy. Mice were injected with streptozotocin (STZ) to induce experimental diabetes. An adenovirus system was used to induce heart specific TAX1BP1 overexpression 12 weeks after STZ injection. TAX1BP1 expression was significantly decreased in STZ-induced diabetic mouse hearts...
May 2018: Biochimica et Biophysica Acta. Molecular Basis of Disease
https://read.qxmd.com/read/29284690/ampk%C3%AE-2-protects-against-the-development-of-heart-failure-by-enhancing-mitophagy-via-pink1-phosphorylation
#19
Bei Wang, Jiali Nie, Lujin Wu, Yangyang Hu, Zheng Wen, Lingli Dong, Ming-Hui Zou, Chen Chen, Dao Wen Wang
RATIONALE: Mitochondrial dysfunction plays an important role in heart failure (HF). However, the molecular mechanisms regulating mitochondrial functions via selective mitochondrial autophagy (mitophagy) are poorly understood. OBJECTIVE: We sought to determine the role of AMPK (AMP-activated protein kinase) in selective mitophagy during HF. METHODS AND RESULTS: An isoform shift from AMPKα2 to AMPKα1 was observed in failing heart samples from HF patients and transverse aortic constriction-induced mice, accompanied by decreased mitophagy and mitochondrial function...
March 2, 2018: Circulation Research
https://read.qxmd.com/read/29157081/regulation-of-becn1-mediated-autophagy-by-hspb6-insights-from-a-human-hspb6-s10f-mutant
#20
Guan-Sheng Liu, Hongyan Zhu, Wen-Feng Cai, Xiaohong Wang, Min Jiang, Kobina Essandoh, Elizabeth Vafiadaki, Kobra Haghighi, Chi Keung Lam, George Gardner, George Adly, Persoulla Nicolaou, Despina Sanoudou, Qiangrong Liang, Jack Rubinstein, Guo-Chang Fan, Evangelia G Kranias
HSPB6/Hsp20 (heat shock protein family B [small] member 6) has emerged as a novel cardioprotector against stress-induced injury. We identified a human mutant of HSPB6 (HSPB6S10F ) exclusively present in dilated cardiomyopathy (DCM) patients. Cardiac expression of this mutant in mouse hearts resulted in remodeling and dysfunction, which progressed to heart failure and early death. These detrimental effects were associated with reduced interaction of mutant HSPB6S10F with BECN1/Beclin 1, leading to BECN1 ubiquitination and its proteosomal degradation...
2018: Autophagy
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