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Author Chellan, Bijoy ♦ Narayani, Jayakumari ♦ Appukuttan, P. S.
Source Sree Chitra Tirunal Institute for Medical Sciences & Technology
Content type Text
Publisher Experimental and Molecular Pathology
File Format PDF
Language English
Subject Domain (in DDC) Natural sciences & mathematics ♦ Life sciences; biology ♦ Physiology & related subjects ♦ Biochemistry ♦ Technology ♦ Medicine & health
Subject Domain (in MeSH) Amino Acids, Peptides, and Proteins ♦ Chemicals and Drugs ♦ Circulatory and Respiratory Physiological Phenomena ♦ Biological Sciences
Subject Keyword Biochemistry
Abstract Lipoprotein(a) [Lp(a)], a modified LDL molecule, is implicated in atherogenesis. Mechanisms of the accumulation of [Lp(a)] in atherosclerotic vessels is lacking in literature. We sought to investigate the complementarities of the carbohydrate structures on Lp(a) and LDL with galectin-1 (a carbohydrate binding protein) and whether endogenous galectin-1 binds Lp(a) in situ. We investigated T-antigen structures on Lp(a) and LDL by enzyme-linked lectin assay using T-antigen specific lectins, galectin-1 and jacalin. Both jacalin and galectin-1 bound strongly to Lp(a) and to a much lesser extent, to LDL. Galectin-1 recognition of the lipoproteins was abolished when the O-linked sugars were selectively removed. Localization of endogenous galectin-1 within histological sections of human internal mammary artery and in vitro binding of Lp(a) to the tissues was analyzed by immunohistochemical staining. The Lp(a)-binding pattern was found to overlap with the localization of galectin-1. The poor Lp (a)-binding on inhibiting tissue galectin-1 with lactose, suggested the binding of Lp(a) to galectin-1. This may be suggestive of a mechanism by which Lp(a) accumulates within arterial walls in atherogenesis. (c) 2007 Elsevier Inc. All rights reserved.
Education Level UG and PG
Learning Resource Type Article
Educational Framework Medical Council of India (MCI)
Volume Number 83
Issue Number 3
Page Count 6
Starting Page 399
Ending Page 404