Angiogenic regulatory influence of extracellular matrix deposited by resting state asthmatic and non-asthmatic airway smooth muscle cells is similar

Alen Faiz, Louise M. Harkness, Gavin Tjin, Victor Bernal, Peter Horvatovich, Alan James, John G. Elliot, Janette K. Burgess*, Anthony W. Ashton

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

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Abstract

The extracellular matrix (ECM) is the tissue microenvironment that regulates the characteristics of stromal and systemic cells to control processes such as inflammation and angiogenesis. Despite ongoing anti-inflammatory treatment, low levels of inflammation exist in the airways in asthma, which alters ECM deposition by airway smooth muscle (ASM) cells. The altered ECM causes aberrant behaviour of cells, such as endothelial cells, in the airway tissue. We therefore sought to characterize the composition and angiogenic potential of the ECM deposited by asthmatic and non-asthmatic ASM. After 72 hours under non-stimulated conditions, the ECM deposited by primary human asthmatic ASM cells was equal in total protein, collagen I, III and fibronectin content to that from non-asthmatic ASM cells. Further, the matrices of non-asthmatic and asthmatic ASM cells were equivalent in regulating the growth, activity, attachment and migration of primary human umbilical vein endothelial cells (HUVECs). Under basal conditions, asthmatic and non-asthmatic ASM cells intrinsically deposit an ECM of equivalent composition and angiogenic potential. Previous findings indicate that dysregulation of the airway ECM is driven even by low levels of inflammatory provocation. This study suggests the need for more effective anti-inflammatory therapies in asthma to maintain the airway ECM and regulate ECM-mediated aberrant angiogenesis.

Original languageEnglish
Number of pages10
JournalJournal of cellular and molecular medicine
DOIs
Publication statusPublished - 18-Jun-2021

Keywords

  • airway smooth muscle
  • angiogenesis
  • asthma
  • extracellular matrix
  • inflammation
  • SUBEPITHELIAL FIBROSIS
  • INFLAMMATION
  • DISEASE
  • PROLIFERATION
  • HYPERPLASIA
  • DIFFERENTIATION
  • HYPERTROPHY
  • EXPRESSION
  • PROTEINS
  • COLLAGEN

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