Phosphatidylinositol 3‐kinase and ERK1/2 are not involved in adenosine A1, A2A or A3 receptor‐mediated preconditioning in rat ventricle strips

Button, Laura; Mireylees, Stewart E.; Germack, Renée; Dickenson, John M.

doi:10.1113/expphysiol.2005.030635

Cited by 7 publications

(2 citation statements)

References 36 publications

(55 reference statements)

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“…The role of ERK1/2 as a potential mediator of protection in the setting of PC has been controversial, with some studies supporting its role (7,11,25) and several studies failing to demonstrate a role for ERK1/2 (6,27,28). We observed that ERK1/2 is markedly activated immediately after H 2 O 2 PC and that this activation occurred also with not cytoprotective H 2 O 2 concentrations.…”

Section: Discussionmentioning

confidence: 60%

H₂O₂preconditioning modulates phase II enzymes through p38 MAPK and PI3K/Akt activation

Angeloni

Motori

Fabbri

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Ischemic preconditioning is a complex cardioprotective phenomenon that involves adaptive changes in cells and molecules and occurs in a biphasic pattern: an early phase after 1-2 h and a late phase after 12-24 h. While it is widely accepted that reactive oxygen species are strongly involved in triggering ischemic preconditiong, it is not clear if they play a major role in the early or late phase of preconditioning and which are the mechanisms involved. The present study was designed to investigate the mechanisms behind H(2)O(2)-induced cardioprotection in rat neonatal cardiomyocytes. We focused on antioxidant and phase II enzymes and their modulation by protein kinase signaling pathways and nuclear-factor-E(2)-related factor-1 (Nrf1) and Nrf2. H(2)O(2) preconditioning was able to counteract oxidative stress more effectively in the late than in the early phase of adaptation. In particular, H(2)O(2) preconditioning counteracted oxidative stress-induced apoptosis by decreasing caspase-3 activity, increasing Bcl2 expression and selectively increasing the expression and activity of antioxidant and phase II enzymes through Nrf1 and Nrf2 translocation to the nucleus. The downregulation of Nrf1 and Nrf2 by small interfering RNA reduced the expression level of phase II enzymes. Specific inhibitors of phosphatidylinositol 3-kinase/Akt and p38 MAPK activation partially reduced the cardioprotection elicited by H(2)O(2) preconditioning and the induction and activity of phase II enzymes. These findings demonstrate, for the first time, a key role for Nrf1, and not only for Nrf2, in the induction of phase II enzymes triggered by H(2)O(2) preconditioning.

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Section: Discussionmentioning

confidence: 60%

H₂O₂preconditioning modulates phase II enzymes through p38 MAPK and PI3K/Akt activation

Angeloni

Motori

Fabbri

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…In addition, hypoxic PC [102, 103] as well as delayed hypoxic PC [104, 105], adenosine-induced PC [106] as well as adenosine-induced delayed PC [107], isoflurane/desflurane-induced PC [83, 108], metabolic PC [109], and opioid-induced delayed PC are associated with increased ERK1/2 activation [110]. Moreover, mitochondrial K ATP channel openers activate ERK1/2 by an oxidant-dependent mechanism [111].…”

Section: Ischemic Preconditioning (Ipc)mentioning

confidence: 99%

Role of Mitogen-Activated Protein Kinases in Myocardial Ischemia-Reperfusion Injury during Heart Transplantation

Vassalli

Milano

Moccetti

2012

Journal of Transplantation

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In solid organ transplantation, ischemia/reperfusion (IR) injury during organ procurement, storage and reperfusion is an unavoidable detrimental event for the graft, as it amplifies graft inflammation and rejection. Intracellular mitogen-activated protein kinase (MAPK) signaling pathways regulate inflammation and cell survival during IR injury. The four best-characterized MAPK subfamilies are the c-Jun NH2-terminal kinase (JNK), extracellular signal- regulated kinase-1/2 (ERK1/2), p38 MAPK, and big MAPK-1 (BMK1/ERK5). Here, we review the role of MAPK activation during myocardial IR injury as it occurs during heart transplantation. Most of our current knowledge regarding MAPK activation and cardioprotection comes from studies of preconditioning and postconditioning in nontransplanted hearts. JNK and p38 MAPK activation contributes to myocardial IR injury after prolonged hypothermic storage. p38 MAPK inhibition improves cardiac function after cold storage, rewarming and reperfusion. Small-molecule p38 MAPK inhibitors have been tested clinically in patients with chronic inflammatory diseases, but not in transplanted patients, so far. Organ transplantation offers the opportunity of starting a preconditioning treatment before organ procurement or during cold storage, thus modulating early events in IR injury. Future studies will need to evaluate combined strategies including p38 MAPK and/or JNK inhibition, ERK1/2 activation, pre- or postconditioning protocols, new storage solutions, and gentle reperfusion.

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Cardiovascular Biology of the A3 Adenosine Receptor

Headrick

Peart

Wan

et al. 2009

A3 Adenosine Receptors From Cell Biology to Pharmacology and Therapeutics

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Phosphatidylinositol 3‐kinase and ERK1/2 are not involved in adenosine A₁, A_2A or A₃ receptor‐mediated preconditioning in rat ventricle strips

Cited by 7 publications

References 36 publications

H₂O₂preconditioning modulates phase II enzymes through p38 MAPK and PI3K/Akt activation

H₂O₂preconditioning modulates phase II enzymes through p38 MAPK and PI3K/Akt activation

Role of Mitogen-Activated Protein Kinases in Myocardial Ischemia-Reperfusion Injury during Heart Transplantation

Cardiovascular Biology of the A3 Adenosine Receptor

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Phosphatidylinositol 3‐kinase and ERK1/2 are not involved in adenosine A1, A2A or A3 receptor‐mediated preconditioning in rat ventricle strips

Cited by 7 publications

References 36 publications

H2O2preconditioning modulates phase II enzymes through p38 MAPK and PI3K/Akt activation

H2O2preconditioning modulates phase II enzymes through p38 MAPK and PI3K/Akt activation

Role of Mitogen-Activated Protein Kinases in Myocardial Ischemia-Reperfusion Injury during Heart Transplantation

Cardiovascular Biology of the A3 Adenosine Receptor

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Product

Resources

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Phosphatidylinositol 3‐kinase and ERK1/2 are not involved in adenosine A₁, A_2A or A₃ receptor‐mediated preconditioning in rat ventricle strips

H₂O₂preconditioning modulates phase II enzymes through p38 MAPK and PI3K/Akt activation

H₂O₂preconditioning modulates phase II enzymes through p38 MAPK and PI3K/Akt activation