Remote renal preconditioning-induced cardioprotection: a key role of hypoxia inducible factor-prolyl 4-hydroxylases

Kant, Ravi; Diwan, Vishal; Jaggi, Amteshwar Singh; Singh, Nirmal; Singh, Devinder

doi:10.1007/s11010-008-9717-5

Cited by 46 publications

(31 citation statements)

References 28 publications

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“…Other investigators demonstrated that preconditioning at a remote organ such as renal ischemia-reperfusion can also induce cardioprotection [35] . Interestingly, a recent study suggested a role for HIF-1 activation in the remote renal preconditioning of rat hearts, since the authors were able to abolish the remote preconditioning by a putative activator of PHDs, alpha-ketoglutarate (200 mg/kg, ip) [36] . On the other hand, a few conflicting results have been published on the role of HIF-1α in ischemic preconditioning.…”

Section: Involvement Of Hif-1 In Ischemic Preconditioning and Post Comentioning

confidence: 99%

Hypoxia inducible factor 1 (HIF-1) and cardioprotection

2010

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Since its discovery in early 1990s, hypoxia inducible factor 1 (HIF-1) has been increasingly recognized for its key role in transcriptional control of more than a hundred genes that regulate a wide-spectrum of cellular functional events, including angiogenesis, vasomotor control, glucose and energy metabolism, erythropoiesis, iron homeostasis, pH regulation, cell proliferation and viability. Evidence accumulated during the past 7 years suggests a critical role for HIF-1α in mediating cardioprotection. The purpose of our present article is to provide an updated overview on this important regulator of gene expression in the cellular stress-responsive and adaptive process. We have particularly emphasized the involvement of HIF-1 in the induction of cardioprotective molecules, such as inducible nitric oxide synthase (iNOS), hemeoxygenase 1 (HO-1), and erythropoietin (EPO), which in turn alleviate myocardial damages caused by harmful events such as ischemia-reperfusion injury. Despite these advances, further in-depth studies are needed to elucidate the possible coordination or interaction between HIF-1α and other key transcription factors in regulating protein expression that leads to cardioprotection.

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Section: Involvement Of Hif-1 In Ischemic Preconditioning and Post Comentioning

confidence: 99%

Hypoxia inducible factor 1 (HIF-1) and cardioprotection

2010

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“…For example, remote ischemic preconditioning (remote IPC) is a powerful innate mechanism which prevents lethal ischemic injury by prior sub-lethal ischemia at an anatomically distant site [1] and has been exploited in a number of clinical settings [2]. Remote IPC and its associated applications may rely upon release of endocrine factors from ischemic cells that initiate adaptive gene programs in recipient tissue [3], and a number of these factors may be directly regulated by the master transcription factor of hypoxia, HIF-α [4–6]. However, the full complement of such HIF-dependent molecular effectors remains undefined.…”

Section: Introductionmentioning

confidence: 99%

An Argonaute 2 switch regulates circulating miR-210 to coordinate hypoxic adaptation across cells

Hale

Lee

Annis

et al. 2014

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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Complex organisms may coordinate molecular responses to hypoxia by specialized avenues of communication across multiple tissues, but these mechanisms are poorly understood. Plasma-based, extracellular microRNAs have been described, yet, their regulation and biological functions in hypoxia remain enigmatic. We found a unique pattern of release of the hypoxia-inducible microRNA-210 (miR-210) from hypoxic and reoxygenated cells. This microRNA is also elevated in human plasma in physiologic and pathologic conditions of altered oxygen demand and delivery. Released miR-210 can be delivered to recipient cells, and its direct suppression of its direct target ISCU and mitochondrial metabolism is primarily evident in hypoxia. To regulate these hypoxia-specific actions, prolyl-hydroxylation of Argonaute 2 acts as a molecular switch that reciprocally modulates miR-210 release and intracellular activity in source cells as well as regulates intracellular activity in recipient cells after miR-210 delivery. Therefore, Argonaute 2-dependent control of released miR-210 represents a unique communication system that integrates the hypoxic response across anatomically distinct cells, preventing unnecessary activity of delivered miR-210 in normoxia while still preparing recipient tissues for incipient hypoxic stress and accelerating adaptation.

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“…The infarct size was expressed as percentage of total left ventricular volume (% LVV) and total left ventricular weight (% LVW) respectively. [15][16][17] Estimation of Lactate Dehydrogenase (LDH) LDH was estimated in samples of coronary effluent collected after stabilization (basal), immediately and 30 min after reperfusion using 2,4-DNPH method as described by King.…”

Section: Methodsmentioning

confidence: 99%

Possible Mechanism of Rottlerin Induced Modulation of Ischemia Reperfusion Injury in Isolated Rat Hearts

Kaur

Singh

et al. 2008

Biological & Pharmaceutical Bulletin

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Coronary artery diseases represent a global burden on health care resources and poised to become the leading cause of morbidity and mortality in the world by 2020. Early reperfusion is essential to salvage ischemic myocardium; however reperfusion of ischemic region is not devoid of deleterious effects. Reperfusion of ischemic myocardium is noted to produce detrimental morphological and functional changes in the form of reperfusion injury manifested as reperfusion arrhythmias, myocardial stunning, micro-vascular and endothelial dysfunction leading to impairment of reflow. 1,2)Myocardial ischemia and reperfusion lead to activation of two novel PKC iso-forms (PKCd and PKCe) which are reported to play opposing roles during myocardial ischemia and reperfusion (I/R).3,4) PKCd has been reported to mediate I/R induced myocardial injury through activation of mitochondrial pathway, 5,6) whereas PKCe has been reported to provide cardioprotection through preconditioning. 7) PKCd has been implicated in I/R induced myocardial injury by producing apoptotic and necrotic cell death. 4,5) A selective peptide inhibitor of PKCd i.e. dV1-1, has been reported to reduce I/R induced myocardial injury by inhibiting apoptotic as well as necrotic cell death. 6)Ischemia and reperfusion has also been reported to activate protein kinases such as p-38 mitogen activated protein kinase (p-38 MAPK); which further increases transcription of pro-inflammatory cytokines such as tumor necrosis factora (TNF-a).8,9) Administration of SB 203580, a selective p-38 MAPK inhibitor, has been reported to attenuate the apoptotic and necrotic cell death of cardiomyocytes.10) Rottlerin is a specific non-peptide inhibitor of PKCd,11,12) which is also reported to activate p-38 MAPK.13) Therefore, the present study was designed to investigate the modulatory effects of rottlerin, an inhibitor of PKCd and activator of p-38 MAPK on ischemia reperfusion induced myocardial injury. MATERIAL AND METHODSWistar albino, rats of either sex weighing 150-200 g maintained at standard animal diet (Kisan Feeds Ltd., Chandigarh, India) and tap water ad libitum were employed in the present study. The animals were procured from 'disease free small animal house' Chaudary Charn Singh, Haryana Agriculture University, Hisar (Haryana), India. They were exposed to 12 h cycle of light and dark. The protocol of the study was duly approved by Institutional Animal Ethics Committee and care of the animals was taken as per guidelines of the Committee for the Purpose of Control and Supervision of Experiments on Animals (CPCSEA), Ministry of Environment and Forest, Govt. of India (Reg. No. 107/CPCSEA 1999).Drugs and Chemicals Rottlerin (Sigma Aldrich, St. Louis, U.S.A.) and FR-167653 (Fujisawa Pharmaceutical Co., Ltd., Osaka, Japan) were dissolved in 1 : 5 mixtures of ethanol with normal saline and saline respectively. All other reagents used in the study were of analytic grade.Isolated Rat Heart Preparation Rats were heparinised (500 I.U., i.p.) about 20 min before sacrificing the animal by cerv...

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Remote renal preconditioning-induced cardioprotection: a key role of hypoxia inducible factor-prolyl 4-hydroxylases

Cited by 46 publications

References 28 publications

Hypoxia inducible factor 1 (HIF-1) and cardioprotection

Hypoxia inducible factor 1 (HIF-1) and cardioprotection

An Argonaute 2 switch regulates circulating miR-210 to coordinate hypoxic adaptation across cells

Possible Mechanism of Rottlerin Induced Modulation of Ischemia Reperfusion Injury in Isolated Rat Hearts

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