Hypoxia induces heat shock protein expression in human coronary artery bypass grafts

Hammerer-Lercher, Angelika; Mair, Johannes; Bonatti, Johannes; Watzka, Stefan B.; Puschendorf, Bernd; Dirnhofer, Stephan

doi:10.1016/s0008-6363(01)00198-5

Cited by 65 publications

(45 citation statements)

References 34 publications

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“…7 The elevated expression of these proteins in atheromatous lesions, correlating with the severity of atherosclerosis, is consistent with a focal role that HSPs may play in the pathogenesis of the disease. 19,20 This, combined with a growing body of evidence that suggests that risk factors commonly associated with atherosclerosis, such as infectious agents and ox-LDL, are capable of inducing HSPs, points to a link between atherogenic agents and these proteins. [21][22][23][24][25][26] The finding of CD4 ϩ CD28 null cells reactive to hHSP60 during the acute phase of coronary artery disease and their absence in stable CSA and healthy individuals is of critical importance and suggests that an autoimmune T cell-mediated response may hold the balance.…”

Section: Discussionmentioning

confidence: 99%

Heat-Shock Protein 60-Reactive CD4 ⁺ CD28 ^null T Cells in Patients With Acute Coronary Syndromes

et al. 2004

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Background-CD4ϩ CD28 null T cells are present in increased numbers in the peripheral blood of patients with acute coronary syndrome (ACS) compared with patients with chronic stable angina (CSA). The triggers of activation and expansion of these cells to date remain unclear. Methods and Results-Twenty-one patients with ACS and 12 CSA patients with angiographically confirmed coronary artery disease and 9 healthy volunteers were investigated. Peripheral blood leukocytes were stimulated with human cytomegalovirus (HCMV), Chlamydia pneumoniae, human heat-shock protein 60 (hHSP60), or oxidized LDL (ox-LDL). CD4 ϩ CD28 null cells were separated by flow cytometry and assessed for antigen recognition using upregulation of interferon-␥ and perforin mRNA transcription as criteria for activation. CD4ϩ CD28 null cells from 12 of 21 patients with ACS reacted with hHSP60. No response was detected to HCMV, C pneumoniae, or ox-LDL. Incubation of the cells with anti-MHC class II and anti-CD4 antibodies but not anti-class I antibodies blocked antigen presentation, confirming recognition of the hHSP60 to be via the MHC class II pathway. Patients with CSA had low numbers of CD4 ϩ CD28 null cells. These cells were nonreactive to any of the antigens used. Circulating CD4 ϩ CD28 null cells were present in 5 of the 9 healthy controls. None reacted with hHSP60. Conclusions-We have shown that hHSP60 is an antigen recognized by CD4ϩ CD28 null T cells of ACS patients. Endothelial cells express hHSP60 either constitutively or under stress conditions. Circulating hHSP60-specific CD4 ϩ CD28 null cells may, along other inflammatory mechanisms, contribute to vascular damage in these patients.

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Section: Discussionmentioning

confidence: 99%

Heat-Shock Protein 60-Reactive CD4 ⁺ CD28 ^null T Cells in Patients With Acute Coronary Syndromes

et al. 2004

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“…It is noteworthy that many proteins expressed more highly in LSK ϩ cells are regulated by hypoxia, such as several glycolytic enzymes, 21 Hsp60, 22 and nucleophosmin. 23 Hypoxia also decreases levels of some proteins, and we see several of these reduced in the LSK ϩ cells, for example, gamma actin, 24 RhoA, 25,26 and vimentin.…”

Section: Lsk ؉ Cells Express Relatively High Levels Of Glycolytic Andmentioning

confidence: 99%

Quantitative proteomics reveals posttranslational control as a regulatory factor in primary hematopoietic stem cells

Unwin

Smith

Blinco

et al. 2006

Blood

163

146

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The proteome is determined by rates of transcription, translation, and protein turnover. Definition of stem cell populations therefore requires a stem cell proteome signature. However, the limit to the number of primary cells available has restricted extensive proteomic analysis. We present a mass spectrometric method using an isobaric covalent modification of peptides for relative quantification (iTRAQ) , IntroductionDefinition of cell form and function is derived from the transcription of specific sets of genes, followed by their translation and post-translational regulation. Cellular development alters phenotype via such changes in transcription and translation, and in this respect post-translational control of protein levels is key in many cell regulatory pathways, such as cell cycling. 1 Stem cell commitment to differentiation is a critical step in development, where proteomic changes will be observed as a cell undergoes successive commitment and developmental steps. The precise nature of the elements of gene expression that contribute to stem cell characteristics have been assessed by transcriptional profiling and the elements of a stem cell signature refined via comparative expression analyses. [2][3][4] Alternatively, the critical stem cell characteristics can be defined by analysis of the function of specific genes (in the hematopoietic system, SCL, HOX-B4, and BMI-1 5-7 ). Many key regulators are transcriptional activators or suppressors that will inevitably affect the transcriptomic profile of a cell. However, this process is known to be subject to further regulation via post-translational mechanisms. 8,9 Lin Ϫ Sca ϩ Kit ϩ (LSK ϩ ) cells and Lin Ϫ Sca ϩ Kit Ϫ (LSK Ϫ ) cells display differential abilities to reconstitute hematopoiesis, and the latter is a more mature cell type than the former, only able to support hematopoiesis in the short term. 10,11 Comparison of these 2 cell populations can help us derive knowledge of the intracellular systems that regulate the ability to maintain pluripotency and long-term self-renewal. Transcriptomic analysis, previously used to define a stem cell "signature," will not detail the true differences between stem cells and their progeny at the proteome level because of the importance of post-translational regulation of protein levels. 9 We therefore sought to establish a method for defining the proteome of stem cell populations where only limited sample is available. Furthermore, the method should not rely on transcriptome data to infer changes at the protein level. Given the limited material (approximately 1 million LSK ϩ and LSK Ϫ cells, respectively, per experiment), we developed a procedure employing isobaric tags for relative quantification (iTRAQ). This allows 4 samples to be analyzed simultaneously, giving relative quantification 12,13 on hundreds of proteins at any one time. Samples are separately proteolytically digested, and 4 isotope-coded, isobaric reagents (using differential stable isotope distribution between reporter group and balance group moieties) ...

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“…Because heat shock proteins (Hsps) offer this type of protection, the study of the expression and induction of these proteins is of particular interest, especially after hypoxia at birth. These proteins are induced as a result of a variety of stresses including elevated temperatures (Arrigo and Landry 1994;Kiang and Tsokos 1998) and hypoxia (Hammerer-Larcher et al 2001). HSPs are classified into large families according to their molecular weights (Arrigo and Landry 1994;Kiang and Tsokos 1998) as Hsp110, Hsp90, Hsp70, Hsp60, and small Hsps (sHsps) between 20 and 30 kDa.…”

Section: Introductionmentioning

confidence: 99%

Effects of hypoxia on stress proteins in the piglet heart at birth

Louapre

Grongnet²,

Tanguay

et al. 2005

Cell Stress Chaper

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Hypoxia at birth represents a very stressful event that can result in severe lifelong consequences in different tissues, including those of the heart. Heat shock and other associated stress proteins are involved in cellular protection, but their roles are not clearly defined at the time of birth. Newborn piglets were subjected to 5% oxygen and 95% nitrogen for either 1 or 4 hours. They were allowed to recover over periods of 1 to 68 hours. The relative levels of ␣B-crystallin, HspB8, Hsp20, Hsp27, Hsp60, and Hsp70 as well as nitric oxide synthases (NOS) (endothelial NOS, inducible NOS, neuronal NOS) were examined by Western blot analysis. Surprisingly, ␣B-crystallin expression was drastically increased in animals submitted to hypoxia. The hypoxia-associated factor HIFI␣ was also strongly and rapidly overexpressed. Heme oxygenase 1 was also increased. To a lesser extent, neuronal NOS was also increased in the left ventricle of animals submitted to hypoxia. This work clearly shows that the Hsp chaperone ␣B-crystallin is strongly overexpressed in the left ventricle of animals submitted to hypoxia. This observation dissociates the response to low oxygenation of ␣B-crystallin and other stress-associated proteins including Hsp27, and it indicates that heme oxygenase is not alone among HSPs in its oxygen-related gene expression.

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Hypoxia induces heat shock protein expression in human coronary artery bypass grafts

Abstract: These findings demonstrate the common cellular defense mechanism of HSP expression in response to stress in coronary artery bypass grafts. Hypoxia and heat treatment strongly induce Hsp72 and Hsp73 expression in human coronary artery bypass grafts.

Cited by 65 publications

References 34 publications

Heat-Shock Protein 60-Reactive CD4 ⁺ CD28 ^null T Cells in Patients With Acute Coronary Syndromes

Heat-Shock Protein 60-Reactive CD4 ⁺ CD28 ^null T Cells in Patients With Acute Coronary Syndromes

Quantitative proteomics reveals posttranslational control as a regulatory factor in primary hematopoietic stem cells

Effects of hypoxia on stress proteins in the piglet heart at birth

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Hypoxia induces heat shock protein expression in human coronary artery bypass grafts

Abstract: These findings demonstrate the common cellular defense mechanism of HSP expression in response to stress in coronary artery bypass grafts. Hypoxia and heat treatment strongly induce Hsp72 and Hsp73 expression in human coronary artery bypass grafts.

Cited by 65 publications

References 34 publications

Heat-Shock Protein 60-Reactive CD4 + CD28 null T Cells in Patients With Acute Coronary Syndromes

Heat-Shock Protein 60-Reactive CD4 + CD28 null T Cells in Patients With Acute Coronary Syndromes

Quantitative proteomics reveals posttranslational control as a regulatory factor in primary hematopoietic stem cells

Effects of hypoxia on stress proteins in the piglet heart at birth

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Heat-Shock Protein 60-Reactive CD4 ⁺ CD28 ^null T Cells in Patients With Acute Coronary Syndromes

Heat-Shock Protein 60-Reactive CD4 ⁺ CD28 ^null T Cells in Patients With Acute Coronary Syndromes