Conclusively, lipid-regulating and anti-inflammatory functions mediated by YQHP with lower hepatotoxicity than simvastatin hindered the progression of HSP65 aggravated AS in ApoE<sup>-/-</sup> mice, indicating the effectiveness of Yangyin Qingre Huoxue Method in the treatment of AS.
Circulating levels of Hsp60 due to mitochondrial stress in diabetes patients could therefore be an important modulator of inflammation in endothelial cells and thus contribute to the increased incidences of atherosclerosis in diabetes mellitus.
We determined the effect of multi-antigenic construct expressing three peptides AHC (ApoB100, HSP60 and outer membrane protein of chlamydia pneumonia) in stabilizing advanced atherosclerosis in Apob<sup>tm2Sgy</sup>/Ldlr<sup>tm1Her/J</sup> mice.
We have previously shown that expression of heat shock protein 60 (HSP60) on the surface of endothelial cells is the main cause of initiating the disease as it acts as a T cell auto-antigen and can be triggered by classical atherosclerosis risk factors, such as infection (e.g.
In silico analyses of heat shock protein 60 and calreticulin to designing a novel vaccine shifting immune response toward T helper 2 in atherosclerosis.
These results suggest Pep19 from Pg HSP60 has a distinct ability to induce native-LDL oxidation as a plausible mechanism by which this peptide may drive epitope spreading to the neoantigen, i.e., oxidized LDL, in the pathogenesis of atherosclerosis.
Surprisingly, the binding molecule of Aa bacteria to the Aa_Mab was Aa chaperonin 60 or HSP60, a protein that is not only responsible for maintaining cellular proteins conformation, but also functions as a potent virulence factor prompting bone resorption in periodontitis and as a putative pathogenic factor in atherosclerosis.
It is more intriguing that the binding molecule of Aa to Aa_Mab IgM was found to be Aa chaperonin 60 or HSP60, a member of heat-shock protein family, behaving not only as a chaperone for correct protein folding but also as a powerful virulence factor of the bacteria for inducing bone resorption and as a putative pathogenic factor in atherosclerosis.
Low-density lipoprotein modified either by oxidation (oxLDL) or by human group X-secreted phospholipase A2 (LDLx) and heat shock proteins (HSP), especially HSP60 and 90, have been implicated in atherosclerosis.
In the present study, we found that HSP60 mRNA and protein expression levels in the thoracic aorta are enhanced not only in a mouse model of AS but also in high-fat diet (HFD) mice.
To elucidate the functional roles of anti-HSP60 autoantibodies in atherosclerosis and the potential use of these Fabs to treat atherosclerosis, further investigation is worthy to be performed.
Chlamydia pneumoniae infection acts as an endothelial stressor with the potential to initiate the earliest heat shock protein 60-dependent inflammatory stage of atherosclerosis.
Increased circulating level of HSP60 and HSP70 might play a role in initiation and/or progression of atherosclerosis in CKD subjects through perturbation of CD4(+)CD28(null) cells.
This is the first functional study of T-cells derived from early human atherosclerotic lesions that supports the previously proposed concept that HSP60-reactive T-cells initiate atherosclerosis by recognition of atherogenic HSP60 epitopes.
Immunization with a combination of ApoB and HSP60 peptide antigens significantly reduced early atherosclerotic lesions in the Apobtm2SgyLdlrtm1Her/J mouse model of atherosclerosis.
Thus, oral infection with H. pylori accelerates atherosclerosis in mice and the active immunisation with Hp-HSP60 or the eradication of H. pylori with antibiotics can moderate/prevent cellular immunity, resulting in a reduction of atherosclerosis.
In this study, experiments were specifically designed to investigate the effect of a HSP65-specifc Th1 to Th2 immune shift accompanied with high-titer antibodies on atherosclerosis and explore the proatherogenic cytotoxicity of Th2-deviated anti-HSP65 antibodies to endothelial cells.
We have recently presented evidence, extending this statistical association to that of causality, by showing that anti-HSP60 antibodies purified from sera of patients with documented atherosclerosis when injected into tail vein of apoE deficient mice resulted in accelerated atherosclerosis in them.
These features provide the prerequisites for a cellular immune reaction against Hsp60 expressed by stressed EC in the initial stages of atherosclerosis.