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Galectin-3 expression in human atherosclerotic lesions
M Nachtigal1, Z Al-Assaad, E P Mayer
1Department of Pathology, University of South Carolina, School of Medicine, and Pathology, Columbia 29208, USA. maurice@med.sc.edu
The American Journal of Pathology
|May 20, 1998
Summary
Galectin-3 is elevated in atherosclerotic lesions, particularly in foam cells and macrophages within carotid arteries. This suggests galectin-3 plays a role in the development of atherosclerosis.
Area of Science:
- Cardiovascular Biology
- Immunology
- Molecular Biology
Background:
- Atherosclerosis is a chronic inflammatory disease characterized by plaque buildup in arteries.
- Galectin-3, a beta-galactoside-binding lectin, has been implicated in various inflammatory processes.
Purpose of the Study:
- To investigate the expression and localization of galectin-3 in human atherosclerotic lesions.
- To determine the cellular sources of galectin-3 within these lesions.
Main Methods:
- Immunohistochemistry using monoclonal antibodies (M3/38 for galectin-3, 1A4 for smooth muscle alpha-actin, HAM56 for macrophages).
- Reverse transcription polymerase chain reaction (RT-PCR) to quantify galectin-3 mRNA levels.
- Western blot analysis to assess galectin-3 protein levels.
Main Results:
- Galectin-3 was detected in advanced atherosclerotic lesions from carotid endarterectomies and lower limb amputations, but not in normal arteries or umbilical cords.
- Galectin-3 was primarily localized to foam cells and macrophages within atherosclerotic plaques.
- Higher galectin-3 expression was observed in carotid lesions compared to lower limb lesions.
- RT-PCR and Western blot confirmed significantly higher galectin-3 transcripts and protein levels in atherosclerotic arteries versus umbilical cord arteries.
Conclusions:
- Increased expression of galectin-3 in atherosclerotic lesions indicates its involvement in atherogenesis.
- Galectin-3's localization in foam cells and macrophages suggests a role in plaque inflammation and development.