&lt;i&gt;Egr-1&lt;/i&gt;, the Potential Target of Calcium Channel Blockers in Cardioprotection with Ischemia/Reperfusion Injury in Rats

Huang, Zhanqin; Li, Haiqing; Guo, Fuxiao; Jia, Qiang-Yong; Zhang, Yanmei; Liu, Xing‐Ping; Shi, Guo‐Ming

doi:10.1159/000227809

Cited by 28 publications

(28 citation statements)

References 27 publications

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“…And Egr-1 protein is believed to act as an intracellular "third messenger" owing to its recruiting expression of multiple downstream target genes [24][25][26] /MAPK pathway are involved in the activation and expression of Egr-1 [11,[28][29][30][31][32]. We also found that three types of classical calcium antagonists (verapamil, diltiazem and nifedipine) could down-regulate Egr-1 overexpression induced by I/R stimulation [33]. These would seem to imply that Ca 2+ and Egr-1 are two important links in the signal pathway of I/R injury.…”

Section: Introductionmentioning

confidence: 75%

Egr-1, a Central and Unifying Role in Cardioprotection from Ischemia-Reperfusion Injury?

Gao

Jia²,

Guo³

et al. 2009

Cell Physiol Biochem

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Aims: Our previous studies have shown that N-n-butyl haloperidol iodide (F₂) can antagonize myocardial ischemia/reperfusion (I/R) injury by blocking intracellular Ca²⁺ overload and suppressing Egr-1 overexpression. The present study is to investigate the relation between the reduction of Ca²⁺ overload and the inhibition of Egr-1 overexpression. Methods: The Sprague-Dawley rat myocardial I/R model and cultured cardiomyocyte hypoxia-reoxygenation (H/R) model were established. Administration of Egr-1 antisense oligodeoxyribonucleotide (AS-ODN) only or combining with F₂, Egr-1 protein expression was examined by Western-blot analyses. Hemodynamic parameters, creatine kinase (CK) and lactate dehydrogenase (LDH), superoxide dismutase (SOD) and malondialdehyde (MDA), myeloperoxidase (MPO), cardiac troponin I (cTnI), and tumor necrosis factor-α (TNF-α) were measured to assess the degree of injury and inflammation of myocardial tissues and cells. Results: Treatment with Egr-1 AS-ODN significantly reduced Egr-1 protein expression and attenuated injury and inflammation of myocardium caused by I/R or H/R evidenced by the amelioration of hemodynamics, the decrease in leakage of CK, LDH, cTnI, the increase in MDA generation, the decrease in SOD activity, the reduction of MPO activity in myocardial tissues and release of TNF-α from cultured cardiomyocytes. Treatment with F₂ combined with Egr-1 AS-ODN, the inhibition of Egr-1 protein expression and inflammation (MPO activity and TNF-α level) were not enhanced, but the protection from myocardial I/R (or H/R) injury was significantly increased in hemodynamics and cytomembrane permeability relative to the using of Egr-1 AS-ODN only. Conclusion: These data suggest that the inhibition of Egr-1 overexpression cannot involve all mechanisms of cardioprotection from I/R injury.

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Section: Introductionmentioning

confidence: 75%

Egr-1, a Central and Unifying Role in Cardioprotection from Ischemia-Reperfusion Injury?

Gao

Jia²,

Guo³

et al. 2009

Cell Physiol Biochem

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“…It was found that six hub genes identified for the control heart are differentially expressed in Sox6 KO heart (Table 4). Among these, Egr1 in cluster J4 (Table 2), which is involved in angiogenesis [86], cardiac hypertrophy [111], and cardioprotection [112], demonstrated significantly decreased expression at P7 and P14 in the Sox6 KO hearts compared to control (Fig 4A). Since expression of genes promoting angiogenesis was significantly upregulated during the juvenile stage (Tables 1 and 2), the reduced expression of Egr1 may have a functional consequence.…”

Section: Resultsmentioning

confidence: 99%

Transcriptome Dynamics and Potential Roles of Sox6 in the Postnatal Heart

Ichihashi

Peng

et al. 2016

PLoS ONE

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The postnatal heart undergoes highly coordinated developmental processes culminating in the complex physiologic properties of the adult heart. The molecular mechanisms of postnatal heart development remain largely unexplored despite their important clinical implications. To gain an integrated view of the dynamic changes in gene expression during postnatal heart development at the organ level, time-series transcriptome analyses of the postnatal hearts of neonatal through adult mice (P1, P7, P14, P30, and P60) were performed using a newly developed bioinformatics pipeline. We identified functional gene clusters by principal component analysis with self-organizing map clustering which revealed organized, discrete gene expression patterns corresponding to biological functions associated with the neonatal, juvenile and adult stages of postnatal heart development. Using weighted gene co-expression network analysis with bootstrap inference for each of these functional gene clusters, highly robust hub genes were identified which likely play key roles in regulating expression of co-expressed, functionally linked genes. Additionally, motivated by the role of the transcription factor Sox6 in the functional maturation of skeletal muscle, the role of Sox6 in the postnatal maturation of cardiac muscle was investigated. Differentially expressed transcriptome analyses between Sox6 knockout (KO) and control hearts uncovered significant upregulation of genes involved in cell proliferation at postnatal day 7 (P7) in the Sox6 KO heart. This result was validated by detecting mitotically active cells in the P7 Sox6 KO heart. The current report provides a framework for the complex molecular processes of postnatal heart development, thus enabling systematic dissection of the developmental regression observed in the stressed and failing adult heart.

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“…Third, the farnesyl-transferase inhibitor, tipirfanib induces apoptosis in AML cells by inducing calcium influx that seems to be mediated by a store operating calcium entry (SOCE)-like pathway[25]. SOCE is found to play a role in calcium homeostasis of non-excitable cells[17] and to interact with CCBs in some reports[18, 19]. …”

Section: Introductionmentioning

confidence: 99%

The effect of calcium channel blockers on the outcome of acute myeloid leukemia

Chae

Dimou

Pierce

et al. 2014

Leukemia & Lymphoma

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The effect of calcium channel blockers (CCBs), beta blockers and angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) on the prognosis of patients with acute myeloid leukemia (AML) is largely unknown. We collected data on the use of these medications on 1043 patients with AML excluding promyelocytic leukemia diagnosed and treated at MD Anderson Cancer Center between 2000 and 2012. Treatment with either amlodipine or diltiazem predicted a worse overall survival (HR 1.6 95% CI 1.22-2.06, p<0.0001). There was no difference in survival depending on whether the patients were taking beta blockers, ACE inhibitors or ARBs. The effect of CCBs on survival was independent from the NCCN risk classification, age, performance status, response to treatment, year of diagnosis and CD34 levels, assessed by flow cytometry (HR=1.39, 95% CI 1.05-1.80, p=0.02). Treatment with either amlodipine or diltiazem predicts worse survival in patients with AML independent of known prognostic factors.

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<i>Egr-1</i>, the Potential Target of Calcium Channel Blockers in Cardioprotection with Ischemia/Reperfusion Injury in Rats

Cited by 28 publications

References 27 publications

Egr-1, a Central and Unifying Role in Cardioprotection from Ischemia-Reperfusion Injury?

Egr-1, a Central and Unifying Role in Cardioprotection from Ischemia-Reperfusion Injury?

Transcriptome Dynamics and Potential Roles of Sox6 in the Postnatal Heart

The effect of calcium channel blockers on the outcome of acute myeloid leukemia

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