ARC contributes to the inhibitory effect of preconditioning on cardiomyocyte apoptosis

Li, Yu Zhen; Liu, Xiu Hua; Zhu, Xiao Mei; Cai, Li

doi:10.1007/s10495-007-0094-4

Cited by 14 publications

(8 citation statements)

References 23 publications

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“…And a similar inhibitory effect on peroxynitrite formation is also demonstrated under postconditioning conditions [7]. In addition, our previous study suggests that ARC contributes to the inhibitory effect of preconditioning on cardiomyocyte apoptosis [18]. Similarly, in the present study, our data show that postconditioning could attenuate the down-regulation of ARC induced by H/R, and inhibition of endogenous ARC attenuates the anti-apoptotic effect of postconditioning.…”

Section: Discussionsupporting

confidence: 88%

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The cardioprotective effect of postconditioning is mediated by ARC through inhibiting mitochondrial apoptotic pathway

2009

Apoptosis

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Section: Discussionsupporting

confidence: 88%

“…The preparation of primary culture of neonatal rat cardiomyocytes was performed as we previously described [18]. In brief, hearts from rats were minced and digested with trypsin.…”

Section: Neonatal Rat Cardiomyocyte Cultures and Experimental Protocolsmentioning

confidence: 99%

The cardioprotective effect of postconditioning is mediated by ARC through inhibiting mitochondrial apoptotic pathway

2009

Apoptosis

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“…Mcl-1 has been shown to be required for neural precursor survival and the regulation of injury-induced neuronal cell death (Arbour et al 2008). The other antiapoptotic gene identified in the preconditioning group in the current study was Nol3, also known as ARC, which is an apoptosis repressor with a caspase recruitment domain and has been shown to possess the ability to block hypoxiainduced cardiomyocyte apoptosis and to contribute to the inhibitory effect of preconditioning on cardiomyocyte apoptosis (Li et al 2007). Nol3 was upregulated after 3 h of reperfusion in both preconditioning and postconditioning treatment groups and after 16 h of reperfusion in the preconditioning-treated group.…”

Section: Discussionmentioning

confidence: 74%

Neuroprotection Induced In Vitro by Ischemic Preconditioning and Postconditioning: Modulation of Apoptosis and PI3K–Akt Pathways

2010

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Preconditioning and postconditioning are mild ischemic exposures before or after severe injurious ischemia, respectively, that elicit endogenous neuroprotective responses. Molecular mechanisms of neuroprotection through preconditioning and postconditioning are not completely understood. Here we optimized the in vitro oxygen and glucose deprivation (OGD) models of preconditioning and postconditioning in primary cortical neuron cultures that allow the studies of the corresponding molecular mechanisms of neuroprotection. We found that the cortical cells preconditioned with a single 45-min OGD treatment administered 24 h prior to injurious 2 h OGD were robustly protected after both 3 h and 16 h of reperfusion. For the postconditioning treatment, we found that three cycles of 15 min OGD followed by 15 min reperfusion, applied immediately after injurious 2 h OGD and prior to complete reperfusion, resulted in effective neuroprotection at both 3 h and 16 h of reperfusion. Using real-time RT-PCR arrays focused on genes of the apoptosis and PI3K-Akt pathways, we found that injurious OGD mainly induced apoptosis-related and repressed PI3K-Akt pathway-related genes after either 3 h or 16 h of reperfusion. Preconditioning treatment resulted in the activation of both pro-survival and anti-apoptotic pathways after 3 h of reperfusion and mainly anti-apoptotic pathway after 16 h of reperfusion. In contrast, the activation of PI3K-Akt pathway mainly contributed to the neuroprotective effect by the postconditioning treatment after 3 h of reperfusion, but differential gene expression likely contributed minimally, if at all, to the neuroprotection observed after 16 h of reperfusion. Among the novel markers of neuroprotection, Nol3 gene upregulation was observed after 3 h of reperfusion following either preconditioning or postconditioning treatments and after 16 h of reperfusion following preconditioning treatment.

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“…The apoptosis repressor with caspase recruitment domain (ARC) protein was originally described in normal heart [1, 2], brain [3], and muscle [4] cells. It protects these cells from apoptosis induced by various stressors.…”

Section: Introductionmentioning

confidence: 99%

Apoptosis repressor with caspase recruitment domain is regulated by MAPK/PI3K and confers drug resistance and survival advantage to AML

Mak

et al. 2013

Apoptosis

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The apoptosis repressor with caspase recruitment domain (ARC) protein is known to suppress both intrinsic and extrinsic apoptosis. We previously reported that ARC expression is a strong, independent adverse prognostic factor in acute myeloid leukemia (AML). Here, we investigated the regulation and role of ARC in AML. ARC expression is upregulated in AML cells co-cultured with bone marrow-derived mesenchymal stromal cells (MSCs) and suppressed by inhibition of MAPK and PI3K signaling. AML patient samples with RAS mutations (N = 64) expressed significantly higher levels of ARC than samples without RAS mutations (N = 371) (P = 0.016). ARC overexpression protected and ARC knockdown sensitized AML cells to cytarabine and to agents that selectively induce intrinsic (ABT-737) or extrinsic (TNF-related apoptosis inducing ligand) apoptosis. NOD-SCID mice harboring ARC-overexpressing KG-1 cells had significantly shorter survival than mice injected with control cells (median 84 versus 111 days) and significantly fewer leukemia cells were present when NOD/SCID IL2R null mice were injected with ARC knockdown as compared to control Molm13 cells (P = 0.005 and 0.03 at 2 and 3 weeks, respectively). Together, these findings demonstrate that MSCs regulate ARC in AML through activation of MAPK and PI3K signaling pathways. ARC confers drug resistance and survival advantage to AML in vitro and in vivo, suggesting ARC as a novel target in AML therapy.

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ARC contributes to the inhibitory effect of preconditioning on cardiomyocyte apoptosis

Abstract: These data indicate that ARC participates in preconditioning-triggered cardioprotection by interfering with cytochrome c release and caspase-3 activation.

Cited by 14 publications

References 23 publications

The cardioprotective effect of postconditioning is mediated by ARC through inhibiting mitochondrial apoptotic pathway

The cardioprotective effect of postconditioning is mediated by ARC through inhibiting mitochondrial apoptotic pathway

Neuroprotection Induced In Vitro by Ischemic Preconditioning and Postconditioning: Modulation of Apoptosis and PI3K–Akt Pathways

Apoptosis repressor with caspase recruitment domain is regulated by MAPK/PI3K and confers drug resistance and survival advantage to AML

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