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The construction of a root locus involves several key steps to analyze and visualize the behavior of a system's poles with varying gain. The number of branches in the root locus equals the number of closed-loop poles and is symmetrical about the real axis.
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Fundus Photography as a Convenient Tool to Study Microvascular Responses to Cardiovascular Disease Risk Factors in Epidemiological Studies
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Unveiling the Role of the Most Impactful Cardiovascular Risk Locus through Haplotype Editing.

Valentina Lo Sardo1, Pavel Chubukov1, William Ferguson1

  • 1Department of Neuroscience, The Scripps Research Institute, La Jolla, CA 92037, USA.

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|December 12, 2018
PubMed
Summary

The 9p21.3 genetic locus significantly increases coronary artery disease (CAD) risk. This study reveals that a specific DNA segment, the risk haplotype, alters vascular smooth muscle cell (VSMC) function, contributing to CAD development.

Keywords:
arterial wallcardiovascular diseasecoronary arterydisease modelinggenome editingiPSCslncRNAstem cellsvascular smooth muscle cells

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Area of Science:

  • Genetics
  • Cardiovascular Biology
  • Stem Cell Biology

Background:

  • The 9p21.3 locus is a major genetic risk factor for coronary artery disease (CAD), particularly in non-African populations.
  • This risk is associated with a non-coding DNA segment (haplotype) of approximately 60 kb, whose function remains unclear.
  • Understanding the mechanism by which this locus influences CAD is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the functional role of the 9p21.3 risk haplotype in vascular smooth muscle cells (VSMCs).
  • To elucidate the cellular and molecular mechanisms underlying the association between the 9p21.3 locus and coronary artery disease.
  • To establish a cellular model for functional annotation of the human genome.

Main Methods:

  • Generation of induced pluripotent stem cells (iPSCs) from individuals with and without the 9p21.3 CAD risk haplotype.
  • Genome editing to delete the risk haplotype in iPSCs.
  • Differentiation of iPSCs into vascular smooth muscle cells (VSMCs).
  • Transcriptional profiling and functional assays (adhesion, contraction, proliferation) of VSMCs.

Main Results:

  • VSMCs derived from the risk haplotype exhibited widespread alterations in transcriptional networks, impacting known CAD risk genes and pathways.
  • These risk VSMCs displayed aberrant adhesion, contraction, and proliferation.
  • Deletion of the risk haplotype restored VSMC stability, while expression of the long non-coding RNA ANRIL induced risk phenotypes in non-risk VSMCs.

Conclusions:

  • The 9p21.3 risk haplotype predisposes VSMCs to a cell state associated with CAD phenotypes.
  • This study identifies novel VSMC-based gene networks involved in CAD risk.
  • Haplotype-edited iPSCs serve as a valuable tool for functional genomic annotation and understanding complex disease genetics.