Lung tissue destruction by proteinase 3 and cathepsin G mediated elastin degradation is elevated in chronic obstructive pulmonary disease

Biochemical and Biophysical Research Communications
Natasja Stæhr GudmannDiana Julie Leeming

Abstract

Chronic obstructive pulmonary disease (COPD) is characterized by high levels of protease activity leading to degradation of elastin followed by loss of elasticity of the lung and the development of emphysema. Elastin is an essential structural component of the lung parenchyma to support the expansion and recoil of the alveoli during breathing. The lung extracellular matrix is vulnerable to pathological structural changes upon upregulation of serine proteases, including cathepsin G (CG) and proteinase 3 (PR3). In this study, we explored the diagnostic features of elastin neo-epitopes generated by CG and PR3. Two novel competitive enzyme-linked immunosorbent assays (ELISA) measuring CG and PR3 generated elastin fragments (EL-CG and ELP-3 respectively) were developed for assessment in serum. Both assays were technically robust and biologically validated in serum from patients with COPD. Serological levels of both elastin fragments were significantly elevated in patients with COPD compared to healthy controls. These data suggest that EL-CG and ELP-3 may serve as plausible biologic markers of destructive changes in COPD.

Citations

Nov 24, 2018·Journal of Cancer Research and Clinical Oncology·Jeppe Thorlacius-UssingNicholas Willumsen
Apr 25, 2020·Cells·Valeria De PasqualeLuigi Michele Pavone
Mar 13, 2019·Scientific Reports·Sarah Rank RønnowJørgen Vestbo
Nov 17, 2020·Frontiers in Veterinary Science·Ana AmaralGraça Ferreira-Dias
Feb 11, 2021·International Journal of Molecular Sciences·Stefanie A I WeissDieter E Jenne
Feb 3, 2020·Biochimica Et Biophysica Acta. General Subjects·Preety PanwarDieter Brömme
May 27, 2021·International Reviews of Immunology·Abraham U Morales-PrimoJaime Zamora-Chimal

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