The Expression and Down Stream Effect of Lectin Like-oxidized Low Density Lipoprotein 1 (LOX-1) in Hyperglycemic State  

Oleh:

Rudijanto, Achmad

Jenis: Article from Journal - ilmiah nasional - terakreditasi DIKTI
Dalam koleksi: Acta Medica Indonesiana vol. 39 no. 01 (Jan. 2007), page 36.
Topik: hyperglycemia; LOX-i.

Ketersediaan

Perpustakaan FK Nomor Panggil: A02.K.2004.01 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

ABSTRACT The lesions of atherosclerosis represent a series of highly specific cellular and molecular responses. Low density lipoprotein (LDL), which may be modified by oxidation, glycation, aggregation, association with proteoglycans, or incorporation into immune complexes, is a major cause of injury to the endothelium and vascular smooth muscle cells (VSMC). The major cell types involved in atherogenesis, macroph¬ages and VSMC, are activated by pro-inflammatory stimuli including modified LDL Modified LDL induces inflammatory responses in macrophages, migration and proliferation of VSMC, and triggers foam cell formation. Scavenger receptors, including LOX-l, playa key role in foam cell formation by mediating the uptake of modified LDL LOX-l expression is detected in endothelial cells of early atherosclerosis lesions of human carotid arteries. Advanced lesions showed LOX-l expression not only in endothelial cells but also in macrophages and more frequently in VSMC, and may be involved in foam cell transformation in macrophages and VSMC. The metabolic abnormalities that characterize diabetes, particularly hyperglycemia, free fatty acids, and insulin resistance, provoke molecular mechanisms that alter the function and structure of blood vessels. These include increased oxidative stress, intracellular signal transduction disturbances, and activation of the receptor for advanced glycation end products (R-AGE). Data showed that LOX-l expression is enhanced by proatherogenic factors relevant to human diabetes, including high glucose, oxLDL, advance glycation end prpducts, and C-reactive protein. LOX-l expression increased also through oxygen species (ROS), endothelin-l (ET-i), tumor necrosis factor-a (TNF-a), shear stress, activation of protein kinase-C (PKC), angiotensin-ll (ANG-l/), and through inflammatory pathways. INTRODUCTION , The prevalence, incidence, and mortality from all forms of cardiovascular disease are increased in patients' with diabetes. Among the cardiovascular risk factors documented in diabetes, hyperglycemia appears as an independent risk factor for diabetic macrovascu\ar complications. I Some studies have explicitly examined the association between glycemic control, carotid intimamedia thickness, and risk factors for cardiovascular disease. Impairment of endothelium and muscle function in hyperglycemic condition contributes to abnormalities of vasodilation. 2 Endothelial dysfunction is a key, early, and potentially reversible event in atherogenesis that is commonly present in human diabetes,2.3 and plays a key role in the pathogenesis of diabetic vasculopathies.Several mechanisms may cause or contribute to endothelial dysfunction in diabetes. These include hyperglycemia, oxidative stress, oxidized LDL (oxLDL), insulin resistance, advanced glycation end products (AGEs), activation of protein kinase C (PKC), and disli pidemia. 5.6.7.8.9 Scavenger receptors (SRs) on macrophages were first described as alternative receptors to the LDL receptors in the uptake of excessive cholesterol and lipid, which leads to the development of foam cells. The members of scavenger receptors are classified into: Class A, B, C, D, E, and EIO Class A consists of SR-AI, SR¬All, SR-AIII, and the macrophage receptor with collagenous structure (MARCO). The ligands of SR-AI and II are acetylated LDL (AcLDL), AGEs, lipopolysacharide (LPS), whole bacteria, polynosinic acid, metylated BSA (M-BSA), and polyguanosinic acid. II The ligands of MARCO are AcLDL, LPS and whole bacteria. Class B consists of SR-Bi and CD36. High density lipoprotein (HDL), modified lipoproteins, anionic

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