Complement activating antibodies against the 60 kD heat shock proteins as a new and independent family risk factor of coronary heart disease

Heat shock proteins (HSPs) are molecular chaperones involved in a variety of life activities. HSPs function in the refolding of misfolded proteins, thereby contributing to the maintenance of cellular homeostasis. Heat shock factor (HSF) is activated in response to environmental stresses and binds to heat shock elements (HSEs), promoting HSP translation and thus the production of high levels of HSPs to prevent damage to the organism. Here, we summarize the role of molecular chaperones as anti-heat stress molecules and their involvement in immune responses and the modulation of apoptosis. In addition, we review the potential application of HSPs to cancer therapy, general medicine, and the treatment of heart disease.

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The model homologue of the partially defective human 5,10-methylenetetrahydrofolate reductase, considered as a risk factor for stroke due to increased homocysteine level, can be protected and reactivated by heat shock proteins

Metabolic Brain Disease ◽

10.1007/s11011-016-9844-8 ◽

2016 ◽

Vol 31 (5) ◽

pp. 1041-1045 ◽

Cited By ~ 1

Author(s):

Michał Grabowski ◽

Bogdan Banecki ◽

Leszek Kadziński ◽

Joanna Jakóbkiewicz-Banecka ◽

Magdalena Gabig-Cimińska ◽

...

Keyword(s):

Risk Factor ◽

Heat Shock ◽

Heat Shock Proteins ◽

Methylenetetrahydrofolate Reductase ◽

Homocysteine Level ◽

Shock Proteins

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Hyperhomocysteinemia and Heat Shock Proteins. Epidemiological Study in a General Population.

Blood ◽

10.1182/blood.v106.11.4107.4107 ◽

2005 ◽

Vol 106 (11) ◽

pp. 4107-4107

Author(s):

Elena Dulin ◽

Maria Concepcion Guisasola ◽

Mª Mar Desco ◽

Antonio Suarez ◽

Pedro Garcia-Barreno

Keyword(s):

Risk Factor ◽

Heat Shock ◽

Heat Shock Proteins ◽

Task Force ◽

Biochemical Study ◽

Vascular Risk Factor ◽

Molecular Study ◽

Vascular Risk ◽

Population Classification ◽

Shock Proteins

Abstract Records and objectives: This study is planned with the objective of identifying new efficacious risk vascular markers. For this work the hyperhomocysteinemia as independent thrombotic vascular risk factor, atherosclerosis as inflammatory illness and Heat Shock Proteins (HSP70i) as molecules likely involved in the vascular damage are considered. Subjects and methods: Workers of the HGGM have volunteered and given their consent. 53 male (M) and 54 female (F) were studied randomly. Anamnesis and epidemiological questionnaire were performed. Arterial pressure was measured and blood samples were taken for neutrophils leukocytes isolation by gradient, biochemical study and DNA extraction. We performed quantification of homocysteine (tHcy) by HPLC; Reactive-C-Protein (RCP), serum and intraleukocitary HSP70i, and HSP70i antibodies by ELISA; molecular study of the polymorphism of C677T of the enzyme metilentetrahidropholatereductase (MTHFR) by PCR-RFLP. Task force of coronary risk was applied for the population classification. Results: The studied population present [tHcy] ≥ 11 umol/L in the 12% of the cases. The mutation C677T appears in heterozygote subjects (CT) in the 45% of the cases and in homozygote subjects in the 17%. Subjects were classified into 3 groups: G-0, without vascular risk factors, n=77 (32M and 45F); G-1, with a moderated risk factor (>10%) but without illness n=26 (18M and 8F) and G-2, with an evident atherosclerotic illness n=4 (3M and 1F) Conclusions: The following correlations have been proved: Inverse (p<0.05) between [tHcy] and [HSP70i] in neutrophils in females G-0 and males G1 wild type (CC) Inverse (p<0.05) between [tHcy] and serum [HSP70i] in males G-1 homozygotes (TT) Direct (p<0.05) between [tHcy] and [RCP] in females G-0 heterozygotes (CT) Direct (p<0.05) between [tHcy] and cholesterol in females G-0 homozygotes (TT) Direct (p<0.01) between [tHcy] and HTA in males G-0 heterozygotes (CT) This study has been partially financed by FIS 03/1308

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