Isolation, culturing and gene expression profiling of inner mass cells from stable and vulnerable carotid atherosclerotic plaques

PLoS One. 2019 Jun 26;14(6):e0218892. doi: 10.1371/journal.pone.0218892. eCollection 2019.

Abstract

The connective tissue components that form the atherosclerotic plaque body are produced by the plaque inner mass cells (PIMC), located inside the plaque. We report an approach to isolate and culture cells from the connective tissue of stable and vulnerable human atherosclerotic plaques based on elimination of non-connective tissue cells such as blood and non-plaque intima cells with a lysis buffer. The resulting plaque cells were characterized by growth capacity, morphology, transcriptome profiling and specific protein expression. Plaque cells slowly proliferated for up to three passages unaffected by the use of proliferation stimulants or changes of culture media composition. Stable plaques yielded more cells than vulnerable ones. Plaque cell cultures also contained several morphological cellular types. RNA-seq profiles of plaque cells were different from any of the cell types known to be involved in atherogenesis. The expression of the following proteins was observed in cultured plaque cells: smooth muscle cells marker α-SMA, macrophage marker CD14, extracellular matrix proteins aggrecan, fibronectin, neovascularisation markers VEGF-A, CD105, cellular adhesion receptor CD31 and progenitor/dedifferentiation receptor CD34. Differential expression of several notable transcripts in cells from stable and vulnerable plaques suggests the value of plaque cell culture studies for the search of plaque vulnerability markers.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Aged
  • Antigens, CD / metabolism
  • Atherosclerosis / genetics
  • Atherosclerosis / metabolism
  • Biomarkers / metabolism
  • Carotid Arteries / metabolism*
  • Cell Proliferation / genetics
  • Female
  • Gene Expression Profiling / methods
  • Humans
  • Macrophages / metabolism
  • Male
  • Myocytes, Smooth Muscle / metabolism
  • Plaque, Atherosclerotic / genetics*
  • Plaque, Atherosclerotic / metabolism*
  • Transcriptome / genetics*
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • Actins
  • Antigens, CD
  • Biomarkers
  • Vascular Endothelial Growth Factor A

Grants and funding

This work was supported by the Russian Science Foundation (http://rscf.ru/en/) grant number 18-15-00080 to PPL and partially by Russian State funded budget project of ICBFM SB RAS # АААА-А17-117020210026-2 to EAP. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.