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Gene expression in atherogenesis
H Monajemi1, E K Arkenbout, H Pannekoek
1Department of Biochemistry, Academic Medical Center, University of Amsterdam, The Netherlands.
Thrombosis and Haemostasis
|August 7, 2001
Summary
Atherosclerosis involves altered gene expression in vascular and blood cells. New high-throughput technologies reveal key transcription factors like NF-kappaB and PPARs, offering potential for novel cardiovascular disease treatments.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Genetics
Background:
- Atherosclerosis pathogenesis involves complex genetic alterations in vascular and blood cells.
- Gene-environment and gene-gene interactions contribute to differential gene expression.
- Understanding these genetic changes requires advanced high-throughput technologies.
Purpose of the Study:
- To review key observations on gene expression in atherosclerosis.
- To highlight the role of specific transcription factors in disease development.
- To discuss the potential of new technologies for cardiovascular research.
Main Methods:
- Differential gene expression analysis using technologies like DD/RT-PCR, SAGE, and DNA microarrays.
- Focus on transcription factors such as nuclear factor-kappaB (NF-kappaB) and peroxisome proliferation-activating receptors (PPARs).
- Investigation of the NGFI-B subfamily of orphan receptors and the Sp/XKLF family of transcription factors.
Main Results:
- Differential expression of dozens to hundreds of genes occurs during atherosclerosis.
- NF-kappaB and PPARs play significant roles in vascular and blood cells.
- The NGFI-B subfamily is induced in neointimal smooth muscle cells.
- Sp/XKLF family members, like LKLF, are implicated in cell communication and maintaining the atherogenic phenotype.
Conclusions:
- High-throughput technologies provide crucial insights into atherogenesis.
- Knowledge of gene expression and transcription factor roles can lead to novel therapeutic strategies.
- Future treatments may involve gene therapy or drugs targeting aberrant gene expression to reverse cellular phenotypes.