Protective Effect of Adeno-Mediated Human Bcl-xL Gene Transfer to the Mouse Liver in a Partial Ischemia/Reperfusion Model

Honda, Kazuo; Tohyama, Taiji; Kotegawa, Hiroshi; Kojima, Yoh; Kushihata, Fumiki; Watanabe, Jun; Kobayashi, Nobuaki

doi:10.1016/j.jss.2008.10.019

Cited by 5 publications

(4 citation statements)

References 22 publications

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“…CHOP regulates the intrinsic apoptosis pathway via BCL2 family proteins, and these proteins, including BCL2, BCL-x L , and BAX, are involved in liver IRI. (35)(36)(37) Our results show that liver IRI was attenuated in CHOP-deficient mice through the inhibition of BAX expression and the attenuation of apoptosis. The proapoptotic molecule BAX, which stimulates cytochrome c release from mitochondria and increases caspase 3 activity, occurs downstream of CHOP and plays an important role in CHOPmediated apoptosis.…”

Section: Discussionmentioning

confidence: 57%

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CAAT/enhancer binding protein–homologous protein deficiency attenuates liver ischemia/reperfusion injury in mice

et al. 2018

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Ischemia/reperfusion injury (IRI) is one of the main causes of liver dysfunction after liver surgery. Involvement of endoplasmic reticulum (ER) stress in various diseases has been demonstrated, and CAAT/enhancer binding protein-homologous protein (CHOP) is a transcriptional regulator that is induced by ER stress. It is also a key regulator of ER stress-mediated apoptosis. The aim of this study was to investigate the role of CHOP in liver IRI. Wild type (WT) and CAAT/enhancer binding protein-homologous protein knockout (CHOP-/-) mice were subjected to 70% liver warm ischemia/reperfusion for 60 minutes. At different times after reperfusion, liver tissues and blood samples were collected for evaluation. Induction of ER stress including CHOP expression was ascertained. Liver damage was evaluated based on serum liver enzymes, liver histology, and neutrophil infiltration. Hepatocyte death including apoptosis was assessed. Liver warm IRI induced ER stress in both WT and CHOP-/- mice. In addition, CHOP expression was up-regulated in WT mice. At 6 hours after reperfusion, liver damage was attenuated in CHOP-/- mice. On the basis of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling staining, apoptotic and necrotic cells were significantly reduced in CHOP-/- mice. CHOP deficiency also reduced the cleavage of caspase 3 and expression of the proapoptotic protein B cell lymphoma 2-associated X protein. Liver IRI induces CHOP expression, and CHOP deficiency attenuates liver IRI by inhibiting apoptosis. Elucidation of the function of CHOP in liver IRI may contribute to further investigation for a therapy against liver IRI associated with the ER stress pathway. Liver Transplantation 24 645-654 2018 AASLD.

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Section: Discussionmentioning

confidence: 57%

“…CHOP regulates the intrinsic apoptosis pathway via BCL2 family proteins, and these proteins, including BCL2, BCL‐x L , and BAX, are involved in liver IRI . Our results show that liver IRI was attenuated in CHOP‐deficient mice through the inhibition of BAX expression and the attenuation of apoptosis.…”

Section: Discussionmentioning

confidence: 64%

CAAT/enhancer binding protein–homologous protein deficiency attenuates liver ischemia/reperfusion injury in mice

et al. 2018

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“…The inflammatory response that follows IR and leads to organ dysfunction is caused by hepatocyte necrosis and apoptosis [1]. While necrosis has classically been considered to be the sole mode of cell death induced by IR, there is increasing evidence that apoptosis, or programmed cell death, also plays a critical role [1][2][3][4][5]. Apoptosis can be triggered by various extracellular (extrinsic apoptosis) or intracellular (intrinsic apoptosis) stimuli, such as binding to cell surface receptors or treatment with cytotoxic drugs, respectively [6].…”

Section: Introductionmentioning

confidence: 99%

Anti-Apoptotic Pro-Survival Effect of Clotrimazole in a Normothermic Ischemia Reperfusion Injury Animal Model

Iannelli¹,

Sousa²,

Zucchini³

et al. 2011

Journal of Surgical Research

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“…Sin embargo, el trasplante de hígado resulta ser un procedimiento urgente que no permite la realización de complejas maniobras previas. En el caso del trasplante con donante vivo, podría ser de utilidad limitada debido a factores éticos(189)(190)(191) .En conclusión, de las diversas estrategias farmacológicas enunciadas, solamente un número limitado resultan de aplicación clínica, siendo las estrategias quirúrgicas las de mayor utilización. La terapia génica, al menos en la actualidad, se encuentra lejana de poder ser una realidad en la práctica diaria.…”

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Estudio experimental de la isquemia-reperfusión hepática

Pozo¹

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Objetivos del trabajo: 1) Conocer el efecto de la isquemia-reperfusión sobre la concentración de diferentes marcadores de injuria hepática. 2) Establecer el efecto de la isquemia-reperfusión sobre las diferentes poblaciones celulares del hígado de rata. 3) Investigar el efecto de la Lidocaína administrándola a los animales en estudio, evaluar si su efecto protector frente a la isquemia-reperfusión planteado por diferentes equipos de trabajo a nivel miocárdico y cerebral, se cumple en el hígado de rata.

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Protective Effect of Adeno-Mediated Human Bcl-xL Gene Transfer to the Mouse Liver in a Partial Ischemia/Reperfusion Model

Cited by 5 publications

References 22 publications

CAAT/enhancer binding protein–homologous protein deficiency attenuates liver ischemia/reperfusion injury in mice

CAAT/enhancer binding protein–homologous protein deficiency attenuates liver ischemia/reperfusion injury in mice

Anti-Apoptotic Pro-Survival Effect of Clotrimazole in a Normothermic Ischemia Reperfusion Injury Animal Model

Estudio experimental de la isquemia-reperfusión hepática

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