Anti-Inflammatory Effect of Heat Shock Protein Induction Is Related to Stabilization of IκBα Through Preventing IκB Kinase Activation in Respiratory Epithelial Cells

Yoo, Chul Gyu; Lee, Seung‐Hee; Lee, Choon Taek; Kim, Youngwhan; Han, Sang Beom; Shim, Young Soo

doi:10.4049/jimmunol.164.10.5416

Cited by 246 publications

(188 citation statements)

References 43 publications

(45 reference statements)

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“…Specifically, heat shock inhibits the activation of I B kinase (IKK) activity that normally occurs in response to proinflammatory stimuli (17,121), leading to decreases in phosphorylation (17,121) and subsequent ubiquination (95) of I B␣. The net effect is an inhibition of the degradation of I B␣ that normally occurs after exposure to proinflammatory stimuli (17,93,95,112,121), which prevents NF-B translocation to the nucleus by maintaining it in an inactive, bound state in the cytoplasm. This mechanism functions in the presence of inhibitors of protein synthesis (17) and does not require increased expression of IKK (121).…”

Section: Changes In Expression Of Other Genes As a Results Of Heat Stressmentioning

confidence: 99%

“…The net effect is an inhibition of the degradation of I B␣ that normally occurs after exposure to proinflammatory stimuli (17,93,95,112,121), which prevents NF-B translocation to the nucleus by maintaining it in an inactive, bound state in the cytoplasm. This mechanism functions in the presence of inhibitors of protein synthesis (17) and does not require increased expression of IKK (121). Additionally, heat stress has been shown to increase I B␣ mRNA expression in some experimental systems (89,113), which may help prevent the pool of available I B␣ protein from diminishing after a proinflammatory stimulus (89), and it has been suggested that HSPs may also stabilize the cytoplasmic I B␣/NF-B complex (111), thus contributing to the inhibitory effect.…”

Section: Changes In Expression Of Other Genes As a Results Of Heat Stressmentioning

confidence: 99%

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Invited Review: Effects of heat and cold stress on mammalian gene expression

Sonna

Fujita

Gaffin

et al. 2002

Journal of Applied Physiology

539

409

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This review examines the effects of thermal stress on gene expression, with special emphasis on changes in the expression of genes other than heat shock proteins (HSPs). There are ∼50 genes not traditionally considered to be HSPs that have been shown, by conventional techniques, to change expression as a result of heat stress, and there are <20 genes (including HSPs) that have been shown to be affected by cold. These numbers will likely become much larger as gene chip array and proteomic technologies are applied to the study of the cell stress response. Several mechanisms have been identified by which gene expression may be altered by heat and cold stress. The similarities and differences between the cellular responses to heat and cold may yield key insights into how cells, and by extension tissues and organisms, survive and adapt to stress.

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Section: Changes In Expression Of Other Genes As a Results Of Heat Stressmentioning

confidence: 99%

Section: Changes In Expression Of Other Genes As a Results Of Heat Stressmentioning

confidence: 99%

Invited Review: Effects of heat and cold stress on mammalian gene expression

Sonna

Fujita

Gaffin

et al. 2002

Journal of Applied Physiology

539

409

View full text Add to dashboard Cite

show abstract

“…However, our data suggest that changes in intracellular glutathione do not explain the suppression of NF-B DNA-binding activity of PAEC in response to pretreatment with the NO donor, SNAP. Induction of heat shock protein, HSP70 (79), decreases the activation of NF-B DNA-binding activity in epithelial cells (79), but we have not been able to detect induction of HSP70 in response to NO treatment of PAEC (data not shown).…”

Section: Discussionmentioning

confidence: 84%

Effect of Redox Modulation on Xenogeneic Target Cells: The Combination of Nitric Oxide and Thiol Deprivation Protects Porcine Endothelial Cells from Lysis by IL-2-Activated Human NK Cells

Tsuyuki

Horvath‐Arcidiacono

Bloom

2001

The Journal of Immunology

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Evidence suggests that NK cells contribute to the pathogenesis of delayed rejection of vascularized xenografts, and NK cells have been suggested to participate in hyperacute xenograft rejection. Endothelial cells have been shown to be the primary target of the recipient’s immune responses that mediate both hyperacute and delayed xenograft rejection. Under conditions of oxidative stress induced by thiol deprivation, but not under normal conditions, pretreatment of porcine aortic endothelial cells (PAECs) with the NO donor, S-nitroso-N-acetyl-penicillamine, dramatically inhibited killing of PAEC target cells by IL-2-activated human NK cells. This same combined treatment reduced both surface expression and mRNA levels of E-selectin. Moreover, anti-E-selectin mAb, but not Ab to VCAM-1, protected PAEC from lysis by human IL-2-activated NK cells in a dose-dependent manner. These findings suggest that expression of porcine E-selectin is important for the cytotoxicity of PAEC mediated by activated human NK cells and may be involved in the redox-mediated modulation of that cytotoxicity. It is known that NF-κB activation is required for transcription of E-selectin, and the current data show that the suppression of E-selectin expression by S-nitroso-N-acetyl-penicillamine pretreatment and thiol deprivation was associated with reduced NF-κB DNA-binding activity in PAEC. These data suggest that the regulation of porcine E-selectin may be important for modulating delayed xenograft rejection and that manipulation of cellular redox systems may provide a means to protect xenogeneic endothelial cells from NK cell-mediated cytotoxicity.

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“…A inibição de vias de sinalização intracelular, tais como a da proteína quinase ativada por mitógenos (MAPK) e do fator nuclear kappa B (NF-κB), também tem sido indicada como mecanismo envolvido na proteção antiapoptótica desempenhada pelas HSPs (26,40) . Tanto a via da MAPK, quanto a do NF-κB, ao ser inibidas, reduzem a ativação de sinais de tradução e expressão de citocinas pró-inflamatórias, tais como a interleucina-1β (IL-1β) e o fator de necrose tumoral-α (TNF-α) (26) .…”

Section: Aspectos Moleculares De Ação Da Glutaminaunclassified

Glutamina: aspectos bioquímicos, metabólicos, moleculares e suplementação

Cruzat

Petry

Tirapegui

2009

Rev Bras Med Esporte

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A glutamina é o aminoácido livre mais abundante no plasma e no tecido muscular. Nutricionalmente é classificada como um aminoácido não essencial, uma vez que pode ser sintetizada pelo organismo a partir de outros aminoácidos. A glutamina está envolvida em diferentes funções, tais como a proliferação e desenvolvimento de células, o balanço acidobásico, o transporte da amônia entre os tecidos, a doação de esqueletos de carbono para a gliconeogênese, a participação no sistema antioxidante e outras. Por meio de técnicas de biologia molecular, estudos demonstram que a glutamina pode também influenciar diversas vias de sinalização celular, em especial a expressão de proteínas de choque térmico (HSPs). As HSPs contribuem para a manutenção da homeostasia da célula na presença de agentes estressores, tais como as espécies reativas de oxigênio (ERO). Em situações de elevado catabolismo muscular, como após exercícios físicos intensos e prolongados, a concentração de glutamina pode tornar-se reduzida. A menor disponibilidade desse aminoácido pode diminuir a resistência da célula a lesões, levando a processos de apoptose celular. Por essas razões, a suplementação com L-glutamina, tanto na forma livre, quanto como dipeptídeo, tem sido investigada. Alguns aspectos bioquímicos, metabólicos e mecanismos moleculares da glutamina, bem como os efeitos de sua suplementação, são abordados no presente trabalho.Palavras-chave: glutamina, exercício, HSP, suplementação, dipeptídeo. aBStRaCtGlutamine is the most frequent free amino acid in the serum and muscular tissue. Nutritionally, it is classified as a non-essential amino acid, once it can be synthesized by the body from other amino acids. Glutamine is involved in different functions, such as cell proliferation and development, basic acid balance, ammonia transportation between tissues, carbon skeleton donation to the gluconeogenesis, participation in the antioxidant system, among others. Molecular biology techniques show that it may also influence several cell signaling ways, especially the expression of heat shock proteins (HSP). The HSPs contribute to the maintenance of the cellular homeostasis in the presence of stress agents such as oxygen reactive species (ORE). In situations of high cellular catabolism, as after intense and prolonged physical exercises, the glutamine concentration may become reduced. Lower availability of this amino acid may decrease the cell resistance to injuries, leading to cellular apoptosis processes. Therefore, L-glutamine supplementation either in free form or as dipeptide has been investigated. Some biochemical and metabolic aspects, molecular mechanism of glutamine, as well as the effects of its supplementation are approached in the present article.Keywords: glutamine, exercise, HSP, supplementation, dipeptide. intRodUÇÃoEm 1873, Hlasiwetz e Habermann foram os primeiros a considerar a glutamina como sendo uma molécula com propriedades biologicamente importantes. Posteriormente, novas observações levaram os pesquisadores a pensar que a amônia encontrada...

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Anti-Inflammatory Effect of Heat Shock Protein Induction Is Related to Stabilization of IκBα Through Preventing IκB Kinase Activation in Respiratory Epithelial Cells

Cited by 246 publications

References 43 publications

Invited Review: Effects of heat and cold stress on mammalian gene expression

Invited Review: Effects of heat and cold stress on mammalian gene expression

Effect of Redox Modulation on Xenogeneic Target Cells: The Combination of Nitric Oxide and Thiol Deprivation Protects Porcine Endothelial Cells from Lysis by IL-2-Activated Human NK Cells

Glutamina: aspectos bioquímicos, metabólicos, moleculares e suplementação

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