Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02749 (beta2-glycoprotein I)
 836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence in animal models that beta2-glycoprotein I (beta2GPI), the principal target of autoimmune antiphospholipid antibodies, is involved in the initiation and progression of atherosclerosis, prompted us to investigate the possible role of this self protein as a target autoantigen of immune reactions in patients with carotid atherosclerosis. Plaque-infiltrating T lymphocytes from patients, and circulating T lymphocytes from patients and healthy subjects were tested by cell proliferation assay and by flow cytometry for intracellular cytokine expression in response to beta2GPI. ELISA was used to detect cytokine production in culture supernatants and anti-beta2GPI/anti-cardiolipin antibodies in serum samples. Eight of 35 PBMC samples and 1 of 5 plaque-infiltrating T lymphocyte samples from patients proliferated in response to beta2GPI, whereas PBMC from healthy subjects did not. Patients PBMC samples that proliferated in response to beta2GPI produced significantly higher IFN-gamma and TNF-alpha than non-proliferating PBMC. beta2GPI-specific plaque-derived T lymphocytes expressed IFN-gamma, TNF-alpha and IL-4, suggesting concomitant Th1 and Th2 activation. Only one patients serum was positive for anti-beta2GPI and anti-cardiolipin IgM antibodies. These new findings indicate that beta2GPI induces a cellular immune response in a subpopulation of patients with carotid atherosclerosis thus contributing to the inflammatory responses involved in carotid atherosclerotic disease.
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PMID:Beta2-glycoprotein I is a target of T cell reactivity in patients with advanced carotid atherosclerotic plaques. 2037 96

High levels of cholesterol, especially as low-density lipoprotein (LDL), are a well-known risk factor for atherosclerotic-related diseases. The key atherogenic property of LDL is its ability to form atherosclerotic plaque. Proprotein convertase subtilisin/kexin-9 (PCSK9) is an indirect regulator of plasma LDL levels by controlling the number of LDL receptor molecules expressed at the plasma membrane, especially in the liver. Herein, we performed a combination of affinity chromatography, mass spectrometry analysis and identification, and gene expression studies to identify proteins that interact with PCSK9. Through these studies, we identified three proteins, alpha-1-antitrypsin (A1AT), alpha-1-microglobulin/bikunin precursor (AMBP), and apolipoprotein H (APOH) expressed by C3A cells that interact with PCSK9. The expression levels of A1AT and APOH increased in cells treated with MITO+ medium, a condition previously shown to affect the function of PCSK9, as compared to treating with Regular (control) medium. However, AMBP expression did not change in response to the treatments. Additional studies are required to determine which of these proteins can modulate the expression/function of PCSK9. The identification of endogenous modulators of PCSK9's function could lead to the development of novel diagnostic tests or treatment options for patients suffering hypercholesterolemia in combination with other chronic metabolic diseases.
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PMID:Identification of Novel Proteins Interacting with Proprotein Convertase Subtilisin/Kexin 9. 3258 53


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