Altered gene expression during hypoxia and reoxygenation of the heart

Piacentini, Lucia; Karliner, Joel S.

doi:10.1016/s0163-7258(99)00010-8

Cited by 43 publications

(23 citation statements)

References 193 publications

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“…The signal transduction mechanism(s) by which hypoxia regulates genes has not been clearly determined [29]. Increased activity of the AP-1 complex in response to hypoxia is in substantial part due to increased abundance of its components mediated by enhanced RNA transcription [29].…”

Section: Discussionmentioning

confidence: 99%

“…Increased activity of the AP-1 complex in response to hypoxia is in substantial part due to increased abundance of its components mediated by enhanced RNA transcription [29]. Thus hypoxia induces expression of various proto-oncogenes, including those that encode Jun and Fos proteins [42][43][44][45].…”

Section: Discussionmentioning

confidence: 99%

“…As AP-1-binding activity has been ascribed to the Fos proteins, c-fos, FosB, Fra1 and Fra2, and the Jun proteins, c-jun JunB and JunD [28,29], we used antibodysupershift or depletion studies to determine the identity of the nuclear proteins that are involved. Inclusion of fibroblast nuclear extracts from cells that were cultured under normoxic conditions with the radiolabelled k1410 to k1362 bp oligonuclotide yielded a clear-cut mobility shift with consistent protein binding ( Figure 7).…”

Section: Figure 7 Emsa Of Cardiac Fibroblast Nuclear Extracts Demonstmentioning

confidence: 99%

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A functional activating protein 1 (AP-1) site regulates matrix metalloproteinase 2 (MMP-2) transcription by cardiac cells through interactions with JunB-Fra1 and JunB-FosB heterodimers

Bergman

Cheng

Honbo

et al. 2003

Biochemical Journal

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196

149

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Enhanced synthesis of a specific matrix metalloproteinase, MMP-2, has been demonstrated in experimental models of ventricular failure and in cardiac extracts from patients with ischaemic cardiomyopathy. Cultured neonatal rat cardiac fibroblasts and myocytes were used to analyse the determinants of MMP-2 synthesis, including the effects of hypoxia. Culture of rat cardiac fibroblasts for 24 h in 1 % oxygen enhanced MMP-2 synthesis by more than 5-fold and augmented the MMP-2 synthetic responses of these cells to endothelin-1, angiotensin II and interleukin 1β. A series of MMP-2 promoter-luciferase constructs were used to map the specific enhancer element(s) that drive MMP-2 transcription in cardiac cells. Deletion studies mapped a region of potent transactivating function within the 91 bp region from k1433 to k1342 bp, the activity of which was increased by hypoxia. Oligonucleotides from this region were cloned in front of a heterologous simian-virus-40 (SV40) promoter and mapped the enhancer activity to a region between k1410 and k1362 bp that included a potential activating protein 1 (AP-1)-binding sequence, C −"$*% CTGACCTCC. Site-specific mutagenesis of the core TGAC sequence (indicated in bold) eliminated the transactivating activity within the k1410 to k1362 bp sequence. Electrophoretic mobility shift assays (EMSAs) using the k1410

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Figure 7 Emsa Of Cardiac Fibroblast Nuclear Extracts Demonstmentioning

confidence: 99%

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A functional activating protein 1 (AP-1) site regulates matrix metalloproteinase 2 (MMP-2) transcription by cardiac cells through interactions with JunB-Fra1 and JunB-FosB heterodimers

Bergman

Cheng

Honbo

et al. 2003

Biochemical Journal

Self Cite

196

149

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“…During hypoxia and subsequent reoxygenation, changes in the cellular redox status occur, altering the ratio of oxidized and reduced forms of glutathione. This, in turn, can alter the redox state of cysteine residues on various cellular proteins, resulting in partial loss of tertiary structure or denaturation (Piacentini and Karliner, 1999). Although the exact nature of the trigger for Hsp70 induction is not established, it is thought that under unstressed conditions Hsp70 members are complexed with heat shock factor (HSF) monomers.…”

Section: Correlation Between Hsp73 and Hsp72 Expressionmentioning

confidence: 99%

Tissue-specific expression of inducible and constitutive Hsp70 isoforms in the western painted turtle

Scott

Locke

Buck

2003

Journal of Experimental Biology

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Expression of Hsp73 and Hsp72 in four tissues of the naturally anoxia-tolerant western painted turtle (Chrysemys picta) was investigated in response to a 24 h forced dive and following 1 h recovery. Of the tissues examined, brain and liver displayed approximately threefold and sevenfold higher basal Hsp73 expression than heart and skeletal muscle. Basal Hsp72 expression was relatively low in all tissues examined. After the 24 h forced dive and 1 h recovery, Hsp73 expression did not differ significantly from basal expression with the exception of liver, where expression decreased significantly after 1 h recovery. Hsp72 expression was unchanged in liver following a 24 h dive; however, it increased twofold in brain and threefold in heart and skeletal muscle. Dive-induced Hsp72 expression was found to correlate inversely with basal Hsp73 expression. Following 1 h recovery, Hsp72 expression was significantly elevated in all tissues above levels in dived animals. These data indicate a tissue-specific pattern of Hsp73 and Hsp72 expression in the western painted turtle during both unstressed and stressed conditions.

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“…Hypoxia and oxidative stress induce biochemical and functional changes, despite which the heart attempts to maintain its function to counteract oxygen tension changes (AnayaPrado et al 2002). Hypoxia and reoxygenation alter the pattern of cardiac proteins through changes in their gene expression, mRNA stability, translation rate, posttranslational modifications, and protein degradation (Piacentini and Karliner 1999). This results in an attempt by ischemic myocardiocytes to protect themselves from ischemia-reperfusion, by up-regulating the levels of stress proteins (Cornelussen et al 2003) and antioxidants (Becker 2004).…”

Section: Discussionmentioning

confidence: 99%

Heat shock proteins, end effectors of myocardium ischemic preconditioning?

et al. 2006

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The purpose of this study was to investigate (1) whether ischemia-reperfusion increased the content of heat shock protein 72 (Hsp72) transcripts and (2) whether myocardial content of Hsp72 is increased by ischemic preconditioning so that they can be considered as end effectors of preconditioning. Twelve male minipigs (8 protocol, 4 sham) were used, with the following ischemic preconditioning protocol: 3 ischemia and reperfusion 5-minute alternative cycles and last reperfusion cycle of 3 hours. Initial and final transmural biopsies (both in healthy and ischemic areas) were taken in all animals. Heat shock protein 72 messenger ribonucleic acid (mRNA) expression was measured by a semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) method using complementary DNA normalized against the housekeeping gene cyclophilin. The identification of heat shock protein 72 was performed by immunoblot. In our ''classic'' preconditioning model, we found no changes in mRNA hsp72 levels or heat shock protein 72 content in the myocardium after 3 hours of reperfusion. Our experimental model is valid and the experimental techniques are appropriate, but the induction of heat shock proteins 72 as end effectors of cardioprotection in ischemic preconditioning does not occur in the first hours after ischemia, but probably at least 24 hours after it, in the so-called ''second protection window.''

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Altered gene expression during hypoxia and reoxygenation of the heart

Cited by 43 publications

References 193 publications

A functional activating protein 1 (AP-1) site regulates matrix metalloproteinase 2 (MMP-2) transcription by cardiac cells through interactions with JunB-Fra1 and JunB-FosB heterodimers

A functional activating protein 1 (AP-1) site regulates matrix metalloproteinase 2 (MMP-2) transcription by cardiac cells through interactions with JunB-Fra1 and JunB-FosB heterodimers

Tissue-specific expression of inducible and constitutive Hsp70 isoforms in the western painted turtle

Heat shock proteins, end effectors of myocardium ischemic preconditioning?

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