Heat Shock Proteins and the Cardiovascular System


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Because it is hypothesized that amyloid oligomers can permeabilize cellular membranes and lipid bilayers, which may represent the primary toxic mechanism of amyloid pathogenesis 14 , 25 , cellular toxicity induced by the amyloid oligomers is associated with mitochondrial function as well as induction of apoptotic cell death by cytochrome c release from mitochondria 12 , Although the physiological significance of the protein interaction between mutant small HSPs and VDAC protein remains unclear, and the molecular mechanisms of mitochondrial dysfunction induced by mutant small HSPs are currently unknown, the association of mutant small HSPs with mitochondria may play an important role in cellular toxicity as well as the formation of diseases such as cardiomyopathy, cataracts, HMN, and CMT disease.

Thus, it is possible that interaction between HSPB8 and STAT3 or VDAC plays an important role in the regulation of transcription and in mitochondrial oxidative phosphorylation ability and that these protein interactions can be altered by missense mutation such as KN. These in vivo and in vitro results indicate that the immunoreactivity against the anti-oligomer antibody is somewhat dissociated from the cellular toxicity.

Thus, anti-oligomer antibody immunoreactivity can be present in native proteins, particularly HSPs. Missense mutations from arginine or lysine a positive-charged amino acid , to glycine or cysteine can markedly alter protein structure, because it is known that a positive charge must be preserved at this position for the structural and functional integrity of small HSPs 26 , Thus, higher immunoreactivity against an anti-oligomer antibody in mutant small HSPs may result from altered protein structure because of the loss of charge and changes in overall surface hydrophobicity of the protein The reason for the higher cellular toxicity of the mutant CryAB compared with that of the mutant HSPB8 remains uncertain in this study.

One possible explanation is that the cellular toxicity of the mutant CryAB RG protein may be induced by multiple factors. Previous studies showed that CryAB can bind to many contractile proteins, such as desmin, actin 28 , and titin Thus, the CryAB RG protein may retain the ability to interact with contractile proteins, and this interaction may be enhanced relative to the normal affinity of the protein, as is the case with FBX4, a member of the F-box family of proteins In addition, CryAB negatively regulates apoptosis by inhibiting caspase-3 activation CryAB RG, which is defective in chaperone activity, binds tightly to nascent contractile proteins, preventing them from folding correctly and integrating into productive sarcomeres 5.

The presence of contractile protein fragments within the aggregates suggests that mutant CryAB binding may directly disturb contractile protein function, rendering muscle tissue particularly sensitive to the action of CryAB RG Thus, the pathogenesis of mutant CryAB probably reflects a synergistic combination of these mechanisms.

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Further study will be needed to address these structure-function relationships in mutated small HSPs. In contrast, our previous study 12 , as well as the present study, showed that no obvious phenotype is observed by overexpression of HSPB8 in the heart.


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The reasons for the different findings between the previous study by another group and our results are uncertain. The aggresomal and amyloidal formation in cardiomyocytes can induce mechanical deficits in passive cytoskeletal stiffness in the heart and can observed cardiac wall stress An increase in wall stress, which can cause relatively hypoxic conditions particularly at the apex and subendocardial region of the heart, may be associated with cardiac fibrosis.

Further study on the observed in wall stress and cardiac fibrosis is required. Thus, HSPB8 may modify its own gene expression. Overexpressing HSPB8 KN resulted in increased perinuclear HSPB8-positive aggregates containing amyloid oligomer and mild cellular toxicity, whereas no aggregates or cellular toxicity were observed in myocytes overexpressing wild-type HSPB8 in vitro and in vivo.

Heat shock protein

You'll be in good company. Journal of Lipid Research. Previous Section Next Section. Immunohistochemistry Immunohistochemical analyses were performed as described previously 12 , Isolation of Mitochondrial and Cytosolic Fractions Isolation of mitochondrial and cytosolic fractions was performed as described previously Immunoprecipitation Assay Immunoprecipitation assay was performed as described previously 13 , Preparation of Isolated Mitochondria and Measurement of Mitochondrial Respiratory Function Preparation of cardiac mitochondria was performed using the method described previously Miscellaneous Methods Sample preparation for Western blotting, gel preparation, and electrophoretic conditions were carried out as described previously 12 , View this table: In this window In a new window.

Summary Overexpressing HSPB8 KN resulted in increased perinuclear HSPB8-positive aggregates containing amyloid oligomer and mild cellular toxicity, whereas no aggregates or cellular toxicity were observed in myocytes overexpressing wild-type HSPB8 in vitro and in vivo. Previous Section. Taylor R.

A new classification scheme in mammals. CrossRef Medline Google Scholar. Sun Y. Molecular structure and chaperone function. Cell Mol. Life Sci.

Background

Lee J. Muchowski P. Sanbe A. A cardiac amyloidosis. Hsu C.


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  6. Irobi J. Tang B. Qiu H. Circulation , — Protein kinase-related HspB8 and testis-specific HspB9. Acta , 1 — 6. Medline Google Scholar. PLoS One 4 , e PLoS One 6 , e Yamauchi J. Cell Res. Maloyan A. In addition, the expressions of the two HSPs appeared to increase from the very early phase at 3 days in response to isoproterenol. The findings gave us a clue: the change in HSPs expressions may be developed as an effective index for early diagnosis of heart failure if it appears similar profile in patients.

    Thus, we then evaluated patients with cardiovascular clinical or cardiographic findings. Except for control group, they were divided into three groups: 1 those at risk for development of clinical HF such as coronary heart disease or high risk factor of coronary heart disease ; 2 patients with cardiac structural abnormalities resulting from cardiac pathology such as a previous myocardial infarction and left ventricular hypertrophy ; and 3 patients with clinically identifiable HF.

    HSPs, known as a family of intracellular proteins with cytoprotective function, were considered as molecular chaperones essential for cell survival both in physiological and stress conditions [14] , [15]. Recently, HSP70 has got much attention as a clinical marker in heart failure when it was reported that increased circulating levels of HSP were associated with disease severity [16]. Diagnosis is frequently made only after progression to later stages, at which point the deteriorating pathological prosess limits effective treatment.

    Therefore, the development of sensitive and specific methods for early detection has been a task of top priority for improving the treatment of this disease. This suggested that HSP70 concentrations may have potential clinical value in screening patients who do not have specific current clinical findings or history but may be progressing silently toward future HF.

    HF is a progressive condition. In animal models overexpression of HSP70 protects the heart against damaging effects of ischemia [17]. Furthermore, it has been shown that stretch and decreased myocyte shortening results in an increased expression of HSP in the isolated perfused rabbit heart [15]. It is conceivable that HSP70 represents a protective mechanism not only in acute settings, e. It is reported that a reduction in the production of HSP70 may play a significant role in the decrease in contractile function during the development of heart failure in a rat model [19].


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    Increased expression of HSP70 could represent an innate protective mechanism which helped to restore physiological conditions [15]. It is known the activation of endogenous neurohormonal systems play an important role in cardiac remodeling and development into HF.

    Heat shock proteins

    It has been demonstrated in animal models that angiotensin II,isoporterenol and norepinephrine can induce production of HSP [20] — [22]. Plasma levels of epinephrine and norepinephrine are known to be significantly elevated in patients with CHF. Activation of the sympatho-adrenergic system in CHF could therefore explain the elevated levels of HSP70 seen in this condition.

    The relationship suggests that short-term cytokine activation is protective but during chronic activation, such as in CHF, it becomes detrimental even in patients with angiographically normal coronary arteries [24]. The source of circulating HSP in CHF is still unknown, but potentially it could be produced by white blood cells via activation of the CD14 receptor [18] , the myocardium itself [25] or by the endothelium [26].

    It was reported that intracellular and extracellular HSP70 have different roles in the regulation of cardiac remodeling and function in response to hypertension in pressure overload mice [27]. Thus, HSP70 participates in the whole pathophysiological progression of HF, and may acts as a clinical marker for early diagnosis.

    In contrast, although NT-proBNP has been used as a diagnostic and prognostic biomarker for a long time, when it was evaluated prospectively as a screening tool for stage B, the results were not promising [10] , [11] , and the guidelines did not define the use of NT-proBNP as a screening tool. In conclusion, based on our previous proteomic results, we have revealed that HSP27 and HSP70 were increased with the progression of cardiac hypertrophy and that HSP90 was not altered at the same time in animal cardiac hypertrophy model.

    Analyzed the data: Zongshi Li YS. Browse Subject Areas?

    Phenotype of Cardiomyopathy in Cardiac-specific Heat Shock Protein B8 KN Transgenic Mouse

    Click through the PLOS taxonomy to find articles in your field. Abstract Early identification for heart failure HF may be useful for disease modifying treatment in order to reduce heart disease progression or even to reverse it. Introduction Cardiovascular diseases CVDs are major causes of mortality in the world. Biochemical Analysis Fasting blood samples were drawn from antecubital vein of the patients and collected into evacuated EDTA tubes in the morning.

    Echocardiography Each patient underwent echocardiography lying in the left decubitus position at the time of study, entry using a GE-VingMedVechocardiographic machine Vivid 7 with a 3. Statistical Analysis The Kolmogorov—Smirnov test was used to test for normal distribution of continuous variables.

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    Results Isoproterenol Induced Cardiac Hypertrophy Mice receiving isoproterenol ISO infusion exhibited a significant increase in end-diastolic left ventricular posterior wall thickness LVPW;d compared with sham at 3 days 0. Download: PPT. Figure 1. Isoproterenol induced cardiac hypertrophy and dysfunction in mice. Figure 2. Isoproterenol induced cardiac hypertrophy as detected by HE staining.

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    Heat Shock Proteins and the Cardiovascular System Heat Shock Proteins and the Cardiovascular System
    Heat Shock Proteins and the Cardiovascular System Heat Shock Proteins and the Cardiovascular System
    Heat Shock Proteins and the Cardiovascular System Heat Shock Proteins and the Cardiovascular System
    Heat Shock Proteins and the Cardiovascular System Heat Shock Proteins and the Cardiovascular System
    Heat Shock Proteins and the Cardiovascular System Heat Shock Proteins and the Cardiovascular System
    Heat Shock Proteins and the Cardiovascular System Heat Shock Proteins and the Cardiovascular System
    Heat Shock Proteins and the Cardiovascular System Heat Shock Proteins and the Cardiovascular System

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