Insulin-like Growth Factor-1-mediated Neuroprotection against Oxidative Stress Is Associated with Activation of Nuclear Factor κB

Heck, Stefanie; Lezoualc’h, Frank; Engert, Stefanie; Behl, Christian

doi:10.1074/jbc.274.14.9828

Cited by 193 publications

(127 citation statements)

References 52 publications

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“…Previous reports have shown that IGF-1, its receptors, and binding proteins are all upregulated in response to ischemia and other neurodegenerative conditions (Schwab et al, 1997;Beilharz et al, 1998;Fernandez et al, 1998). This upregulation appears to provide neuroprotection, because exogenous IGF-1 both in vivo and in vitro protects neurons from different types of injury (Tagami et al, 1997;Heck et al, 1999;Guan et al, 2000;Wang et al, 2000;Yamaguchi et al, 2000).…”

Section: Discussionmentioning

confidence: 97%

“…The expression of IGF-1 and its binding proteins are altered in response to brain ischemia (Lee et al, 1996;Schwab et al, 1997;Beilharz et al, 1998), and exogenous administration of IGF-1 significantly reduces neuronal loss in different models of cerebral ischemia (Johnston et al, 1996;Tagami et al, 1997;Guan et al, 2000;Wang et al, 2000). Furthermore, it has been shown that IGF-1 protects cultured neurons against diverse forms of injury, including hypoxia and oxidative stress (Heck et al, 1999;Yamaguchi et al, 2001).…”

Section: Abstract: Global Cerebral Ischemia; Hypoxia-inducible Factomentioning

confidence: 99%

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Activation of Hypoxia-Inducible Factor-1 in the Rat Cerebral Cortex after Transient Global Ischemia: Potential Role of Insulin-Like Growth Factor-1

Chávez¹,

2002

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Hypoxia-inducible factor-1 (HIF-1) is a transcription factor that regulates the adaptive response to hypoxia in mammalian cells. It consists of a regulatory subunit HIF-1␣, which accumulates under hypoxic conditions, and a constitutively expressed subunit HIF-1␤.In this study we analyzed HIF-1␣ expression in the rat cerebral cortex after transient global ischemia induced by cardiac arrest and resuscitation. Our results showed that HIF-1␣ accumulates as early as 1 hr of recovery and persists for at least 7 d.In addition, the expression of HIF-1 target genes, erythropoietin and Glut-1, were induced at 12 hr to 7d of recovery. A logical explanation for HIF-1␣ accumulation might be that the brain remained hypoxic for prolonged periods after resuscitation. By using the hypoxic marker 2-(2-nitroimidazole-1[H]-y1)-N- (2,2,3,3,3-pentafluoropropyl)-acetamide (EF5), we showed that the brain is hypoxic during the first hours of recovery from cardiac arrest, but the tissue is no longer hypoxic at 2 d. Thus, the initial ischemic episode must have activated other nonhypoxic mechanisms that maintain prolonged HIF-1␣ accumulation. One such mechanism might be initiated by insulin-like growth factor-1 (IGF-1). Our results showed that IGF-1 expression was upregulated after cardiac arrest and resuscitation. In addition, we showed that IGF-1 was able to induce HIF-1␣ in pheochromocytoma cells and cultured neurons as well as in the brain of rats that received intracerebroventricular and systemic IGF-1 infusion. Moreover, infusion of a selective IGF-1 receptor antagonist abrogates HIF-1␣ accumulation after cardiac arrest and resuscitation. Our study suggest that activation of HIF-1 might be part of the mechanism by which IGF-1 promotes cell survival after cerebral ischemia.

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Section: Discussionmentioning

confidence: 97%

Section: Abstract: Global Cerebral Ischemia; Hypoxia-inducible Factomentioning

confidence: 99%

Activation of Hypoxia-Inducible Factor-1 in the Rat Cerebral Cortex after Transient Global Ischemia: Potential Role of Insulin-Like Growth Factor-1

Chávez¹,

2002

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“…178 Thus PKB/Akt appears to function in parallel with NIK to activate IKK. Similarly, the PI3K-PKB/Akt pathway ( Figure 2) is involved in the activation of NF-B by PDGF, 179 insulin, 180 IGF-1 181 and NGF. 182 Activation of NF-B has a role in the anti-apoptotic signaling of these cytokines.…”

Section: Role Of the Rel/nf-b Transcription Factors In The Control Ofmentioning

confidence: 99%

Suppression of apoptosis: role in cell growth and neoplasia

White

McCubrey

2001

Leukemia

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A cell is a potentially dangerous thing. In unicellular organisms, cells divide and multiply in a manner that is chiefly determined by the availability of nutritional substrates. In a multicellular organism, each cell has a distinct growth potential that is designed to subsume a role in the function of the whole body. Departure from this path to one of uncontrolled cellular proliferation leads to cancer. For this reason, evolution has endowed cells with an elaborate set of systems that cause errant cells to self-destruct. This process of cell suicide is known as apoptosis or programmed cell death and it plays a crucial role in the growth of both normal and malignant cells. In this review, we describe the mechanisms whereby programmed cell death is induced and executed. In particular, we concentrate on how anti-apoptotic signals generated by cytokines promote cell survival and how these signal transduction pathways may be involved in the pathogenesis of neoplasia. Understanding how these processes contribute to tumorigenesis may suggest new therapeutic options. Leukemia (2001) 15, 1011-1021.

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“…(Heck et al, 1999). In unstressed cells, NF-kB is retained in the cytoplasm as a heterodimer with IkB.…”

Section: Nf-kbmentioning

confidence: 99%

Regulated nuclear localization of stress-responsive factors: how the nuclear trafficking of protein kinases and transcription factors contributes to cell survival

Ferrigno

Silver

1999

Oncogene

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The details of nuclear transport mechanisms are emerging rapidly, largely through work with model organisms. Here, we brie¯y describe these advances, with an emphasis on the remaining challenges. We then address the nuclear transport of some high pro®le cellular regulators, including p53 and the proto-oncogene PKB/Akt. We discuss the mechanisms that contribute to the di erential subcellular localization of these proteins. Finally, we analyse the provocative patterns that emerge from our overview.

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Insulin-like Growth Factor-1-mediated Neuroprotection against Oxidative Stress Is Associated with Activation of Nuclear Factor κB

Cited by 193 publications

References 52 publications

Activation of Hypoxia-Inducible Factor-1 in the Rat Cerebral Cortex after Transient Global Ischemia: Potential Role of Insulin-Like Growth Factor-1

Activation of Hypoxia-Inducible Factor-1 in the Rat Cerebral Cortex after Transient Global Ischemia: Potential Role of Insulin-Like Growth Factor-1

Suppression of apoptosis: role in cell growth and neoplasia

Regulated nuclear localization of stress-responsive factors: how the nuclear trafficking of protein kinases and transcription factors contributes to cell survival

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