Differential bradykinin B1 and B2 receptor regulation in cell death induced by hepatic ischaemia/reperfusion injury

2014 ◽  
Vol 127 (6) ◽  
pp. 405-413 ◽  
Author(s):  
Mayra A. Paio ◽  
Maria Kouyoumdjian ◽  
Durval R. Borges ◽  
Marcia R. Nagaoka
Keyword(s):  
Cell Death ◽  
Reperfusion Injury ◽  
Apoptotic Cell ◽  
Receptor Regulation ◽  
Necrotic Cell Death ◽  
Necrotic Cell ◽  
Ischaemia Reperfusion Injury ◽  
B1 Receptor ◽  
Ischaemia Reperfusion ◽  
Kinin B1 Receptor

In the present study, we have demonstrated that the kinin B1 receptor may participate in apoptotic cell death signalling, whereas the B2 receptor may be involved in necrotic cell death during IRI.

Urocortin inhibits Beclin1-mediated autophagic cell death in cardiac myocytes exposed to ischaemia/reperfusion injury

2006 ◽  
Vol 40 (6) ◽  
pp. 846-852 ◽  
Author(s):  
Lauren Valentim ◽  
Kevin M. Laurence ◽  
Paul A. Townsend ◽  
Christopher J. Carroll ◽  
Surinder Soond ◽  
...  
Keyword(s):  
Cell Death ◽  
Reperfusion Injury ◽  
Cardiac Myocytes ◽  
Autophagic Cell Death ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion

Mitochondrial protein kinase Cϵ (PKCϵ): emerging role in cardiac protection from ischaemic damage

2007 ◽  
Vol 35 (5) ◽  
pp. 1052-1054 ◽  
Author(s):  
G.R. Budas ◽  
D. Mochly-Rosen
Keyword(s):  
Protein Kinase ◽  
Reperfusion Injury ◽  
Mitochondrial Permeability Transition ◽  
Apoptotic Cell ◽  
Critical Role ◽  
Mitochondrial Protein ◽  
Permeability Transition ◽  
K Channel ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion

Mitochondria mediate diverse cellular functions including energy generation and ROS (reactive oxygen species) production and contribute to signal transduction. Mitochondria are also key regulators of cell viability and play a central role in necrotic and apoptotic cell death pathways induced by cardiac ischaemia/reperfusion injury. PKC (protein kinase C) ϵ plays a critical role in cardioprotective signalling pathways that protect the heart from ischaemia/reperfusion. Emerging evidence suggests that the cardioprotective target of PKCϵ resides at the mitochondria. Proposed mitochondrial targets of PKCϵ include mitoKATP (mitochondrial ATP-sensitive K+ channel), components of the MPTP (mitochondrial permeability transition pore) and components of the electron transport chain. This review highlights mitochondrial targets of PKCϵ and their possible role in cardioprotective signalling in the setting of ischaemia/reperfusion injury.

Polydatin post-treatment alleviates myocardial ischaemia/reperfusion injury by promoting autophagic flux

2016 ◽  
Vol 130 (18) ◽  
pp. 1641-1653 ◽  
Author(s):  
Yuanna Ling ◽  
Guiming Chen ◽  
Yi Deng ◽  
Huixiong Tang ◽  
Long Ling ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Reperfusion Injury ◽  
Myocardial Ischaemia ◽  
Reactive Oxygen ◽  
Post Treatment ◽  
Autophagic Flux ◽  
Oxygen Species ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion

The present paper provides evidence that polydatin (PD) post-treatment alleviates myocardial ischaemia/reperfusion (I/R) injury by promoting autophagic flux to clear damaged mitochondria to reduce reactive oxygen species (ROS) and cell death.

scholarly journals Concurrent Assessment of Calpain and Caspase-3 Activation after Oxygen–Glucose Deprivation in Primary Septo-Hippocampal Cultures

2001 ◽  
Vol 21 (11) ◽  
pp. 1281-1294 ◽  
Author(s):  
Jennifer K. Newcomb-Fernandez ◽  
Xiurong Zhao ◽  
Brian R. Pike ◽  
Kevin K. W. Wang ◽  
Andreas Kampfl ◽  
...  
Keyword(s):  
Cell Death ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Glucose Deprivation ◽  
Apoptotic Cell Death ◽  
Oxygen Glucose Deprivation ◽  
Necrotic Cell Death ◽  
Necrotic Cell ◽  
Lactate Dehydrogenase Release ◽  
Hippocampal Cultures

The contributions of calpain and caspase-3 to apoptosis and necrosis after central nervous system (CNS) trauma are relatively unexplored. No study has examined concurrent activation of calpain and caspase-3 in necrotic or apoptotic cell death after any CNS insult. Experiments used a model of oxygen–glucose deprivation (OGD) in primary septo-hippocampal cultures and assessed cell viability, occurrence of apoptotic and necrotic cell death phenotypes, and protease activation. Immunoblots using an antibody detecting calpain and caspase-3 proteolysis of α-spectrin showed greater accumulation of calpain-mediated breakdown products (BDPs) compared with caspase-3–mediated BDPs. Administration of calpain and caspase-3 inhibitors confirmed that activation of these proteases contributed to cell death, as inferred by lactate dehydrogenase release. Oxygen–glucose deprivation resulted in expression of apoptotic and necrotic cell death phenotypes, especially in neurons. Immunocytochemical studies of calpain and caspase-3 activation in apoptotic cells indicated that these proteases are almost always concurrently activated during apoptosis. These data demonstrate that calpain and caspase-3 activation is associated with expression of apoptotic cell death phenotypes after OGD, and that calpain activation, in combination with caspase-3 activation, could contribute to the expression of apoptotic cell death by assisting in the degradation of important cellular proteins.

scholarly journals Participation of Caspase-3-Like Protease in Necrotic Cell Death of Myocardium During Ischemia -Reperfusion Injury in Rat Hearts

2003 ◽  
Vol 67 (3) ◽  
pp. 248-252 ◽  
Author(s):  
Yoshihisa Naka ◽  
Yoshiki Sawa ◽  
Motonobu Nishimura ◽  
Nobuaki Hirata ◽  
Hideki Ueda ◽  
...  
Keyword(s):  
Cell Death ◽  
Reperfusion Injury ◽  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Necrotic Cell Death ◽  
Necrotic Cell ◽  
Rat Hearts

Why is it worth testing the ability of zinc to protect against ischaemia reperfusion injury for human application

Metallomics ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1330-1343 ◽  
Author(s):  
Joseph Ischia ◽  
Damien M. Bolton ◽  
Oneel Patel
Keyword(s):  
Cell Death ◽  
Reperfusion Injury ◽  
Organ Dysfunction ◽  
Oxygen Supply ◽  
Tissue Injury ◽  
Blood Oxygen ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion

Ischaemia (interruption in the blood/oxygen supply) and subsequent damage induced by reperfusion (restoration of blood/oxygen supply) ultimately leads to cell death, tissue injury and permanent organ dysfunction.

Sign in / Sign up

Export Citation Format

Share Document