Identification of potential target genes of cardioprotection against ischemia–reperfusion injury by express sequence tags analysis in rat hearts

Kim, Hyoung Kyu; Kang, Se Won; Jeong, Sang Hoon; Kim, Nari; Ko, Jae Hong; Bang, Hyoweon; Park, Won Sun; Choi, Tae-Hoon; Ha, Young-Ran; Lee, Yong Seok; Youm, Jae Boum; Ko, Kyung Soo; Rhee, Byoung Doo; Han, Jin

doi:10.1016/j.jjcc.2012.02.004

Cited by 22 publications

(19 citation statements)

References 41 publications

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“…Recently, a few in vitro studies have shown that TRAP1 overexpression protects isolated rat cardiomyocytes from hypoxia-induced mitochondrial damage and cell death [12,13]. In the present study, we found that TRAP1 overexpression also protects HL-1 cells, a cardiac muscle cell line, from hypoxic cell death.…”

Section: Discussionsupporting

confidence: 76%

“…Further, overexpression of TRAP1 in rat brain improves mitochondrial function and reduces focal ischemia-induced cerebral infarction and neurological impairments [12]. Other studies have found that TRAP1 expression is induced in rat hearts following I/R treatment in vivo [13] and in isolated rat cardiomyocytes following hypoxia treatment in vitro [14]. Further, TRAP1 overexpression prevents hypoxia-induced mitochondrial damage and cell death in isolated rat cardiomyocytes [14,15].…”

Section: Introductionmentioning

confidence: 99%

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TRAP1 Provides Protection Against Myocardial Ischemia-Reperfusion Injury by Ameliorating Mitochondrial Dysfunction

Peng

Dong

et al. 2015

Cell Physiol Biochem

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Background: Tumor necrosis factor receptor-associated protein 1 (TRAP1), an essential mitochondrial chaperone is induced in rat hearts following ischemia/reperfusion (I/R), but its role in myocardial I/R injury is unclear. The present study examined the function of TRAP1 in cardiomyocyte hypoxia/reoxygenation injury in vitro and myocardial I/R injury in vivo. Methods: HL-1 cardiomyocytes transfected with TRAP1 or vector were subjected to simulated I/R (SI/R) in vitro. Cell death and mitochondrial function were assessed. Wild type (WT) and TRAP1 knockout (TRAP1 KO) mice were subjected to cardiac I/R in vivo. The infarct size and myocardial apoptosis were determined. WT and TRAP1 KO cardiomyocytes were subjected to SI/R in vitro. Mitochondrial function was assessed. Results: TRAP1 overexpression protects HL-1 cardiomyocytes from SI/R-induced cell death in vitro. The reduced cell death was associated with decreased ROS generation, better-preserved mitochondrial ETC complex activity, membrane potential, and ATP production, as well as delayed mPTP opening. Loss of TRAP1 aggravates SI/R-induced mitochondrial damage in cardiomyocytes in vitro and myocardial I/R injury and apoptosis in vivo. Conclusion: The results of the present study show that TRAP1 provides cardioprotection against myocardial I/R by ameliorating mitochondrial dysfunction.

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Section: Discussionsupporting

confidence: 76%

Section: Introductionmentioning

confidence: 99%

TRAP1 Provides Protection Against Myocardial Ischemia-Reperfusion Injury by Ameliorating Mitochondrial Dysfunction

Peng

Dong

et al. 2015

Cell Physiol Biochem

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“…Tu et al found that I/R induced rupture of myocardial fibers and degradation of F-actin as well as MLC-2 phosphorylation in the myocardial tissue [24]. Kim et al observed that I/R increased expression of genes encoding MLC-2 in rat hearts, which compensated for disorganization of sarcomeric myofibrillar proteins [29,30]. In this study, we found that H/R down-regulated MR-1 expression and induced disruption of F-actin and α-actinin disorganization with cardiomyocyte injury, as well as the up-regulation of MLC-2 expression and phosphorylation.…”

Section: Discussionmentioning

confidence: 99%

Myofibrillogenesis regulator-1 attenuates hypoxia/reoxygenation-induced injury by repairing microfilaments in neonatal rat cardiomyocytes

Tao

Wang

Liu

et al. 2015

Experimental Cell Research

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“…Riskli miyokarttaki infarkt boyutunun küçülmesinde ve ST-segment elevasyonlu hastaların iyileştirilmesinde en etkili tedavi reperfüzyon terapisi olmasına rağmen, koroner kan akımının restorasyonunun paradoksal biçimde ek bir miyokart hasarını indükleyebilme ihtimali reperfüzyon terapisini iki ucu keskin bir bıçağa çevirmektedir 70 . Oksidatif stres, intraselüler kalsiyum birikimi, hızlı pH restorasyonu ve inflamasyon gibi birçok faktörün rol oynadığı kompleks bir olgu olan reperfüzyon hasarımitokondriyal geçirgenlik geçiş gözeneklerinin (MPTP, mitochondrial permeability transition pore) en azından kısmen açılmasına neden olur 71,72 .…”

Section: İskemi-reperfüzyon Hasarlarında Netrin-1unclassified

Role of Netrin-1 in Cardiovascular Diseases

Görür¹,

Ünal²,

Tamer³

2018

Arşiv Kaynak Tarama Dergisi

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Netrins which are a family of laminin-like proteins, first described for their role in embryonic axonal guidance. These chemotropic molecules act as a bifunctional regulator of neuron migration. Researchers have proven the roles of netrin-1 in the development and formation of non-neural tissue apart from its role in the central nervous system .In cardiovascular area, netrin-1 is involved in angiogenesis, promotes atherosclerosis, protects the heart against ischemia-reperfusion injury, and reduces the infarct size. These findings make netrin-1 an important therapeutic target especially with its contradicted effects in physiological and pathophysiological processes. The aim of this review is to highlight the diverse and opposite effects and the functions of netrin-1 signalling during the cardiovascular diseases. ÖZLaminin benzeri proteinlerin bir ailesi olan netrinler, başlangıçta embriyonik aksonal rehberlikteki rolleri ile tanımlanmıştır. Kemotropik özellik gösteren bu moleküller nöron göçünün iki fonksiyonlu bir düzenleyicisi gibi davranırlar. Araştırmacılar, merkezi sinir sistemindeki rolünden bağımsız olarak netrin-1'in sinir haricindeki dokuların gelişiminde ve oluşumunda rol oynadığını kanıtlamıştırKardiyovasküler alanla ilgili olarak, netrin-1 anjiyogenezi teşvik eder ve aterosklerozu hızlandırır, kalbi iskemireperfüzyon hasarına karşı korur ve infarktüs boyutunu azaltır.Bu bulgular, özellikle birçok fizyolojik ve patofizyolojik süreçte birbiriyle çelişebilen etkileri olduğu için netrin-1'i önemli bir terapötik hedef haline getirmektedir. Bu derlemede ateroskleroz, anjiyojenez ve iskemi reperfüzyon onarımı da dahil olmak üzere kardiyovasküler hastalıklar sırasında netrin-1 sinyallerinin işlevleri gözden geçirilmiştir.

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Identification of potential target genes of cardioprotection against ischemia–reperfusion injury by express sequence tags analysis in rat hearts

Abstract: The global profiling of cardiac ischemia-related genes provides the possible mechanisms of IR and IPC and ways of treating IR injury.

Cited by 22 publications

References 41 publications

TRAP1 Provides Protection Against Myocardial Ischemia-Reperfusion Injury by Ameliorating Mitochondrial Dysfunction

TRAP1 Provides Protection Against Myocardial Ischemia-Reperfusion Injury by Ameliorating Mitochondrial Dysfunction

Myofibrillogenesis regulator-1 attenuates hypoxia/reoxygenation-induced injury by repairing microfilaments in neonatal rat cardiomyocytes

Role of Netrin-1 in Cardiovascular Diseases

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