Second harmonic generation imaging of collagen scaffolds within the alveolar ducts of healthy and emphysematous mouse lungs

Mostaço-Guidolin, Leila B.; Loube, Jeffrey; Barlow, Aaron; Osei, Emmanuel T.; Vasilescu, Dragoș șM; Fouadi, M.; Young, C. D.; Scott, Alan L.; Mitzner, Wayne; Hackett, Tillie L.

doi:10.1007/s00418-020-01959-6

Cited by 13 publications

(9 citation statements)

References 38 publications

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“…ECM remodelling in asthma involves the airway epithelial basement membrane, laminar propria, bronchial and pulmonary vasculature [ 89 , 92 , 93 ]. The compositions of the airway smooth muscle (ASM) ECM, epithelial basement membrane and interstitial ECM have also been shown to be altered in asthma, with a predominant deposition of fibronectin, collagen I and III [ 94 ]. Most recently, the topography of fibrillar collagen fibers has also been assessed and shown to be more disorganized and fragmented in the airway laminar propria and pulmonary vasculature [ 89 , 95 ].…”

Section: The Ecm In Lung Remodeling and Diseasementioning

confidence: 99%

The Role of miRNAs in Extracellular Matrix Repair and Chronic Fibrotic Lung Diseases

Usman

Hackett

2021

Cells

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The lung extracellular matrix (ECM) plays a key role in the normal architecture of the lung, from embryonic lung development to mechanical stability and elastic recoil of the breathing adult lung. The lung ECM can modulate the biophysical environment of cells through ECM stiffness, porosity, topography and insolubility. In a reciprocal interaction, lung ECM dynamics result from the synthesis, degradation and organization of ECM components by the surrounding structural and immune cells. Repeated lung injury and repair can trigger a vicious cycle of aberrant ECM protein deposition, accompanied by elevated ECM stiffness, which has a lasting effect on cell and tissue function. The processes governing the resolution of injury repair are regulated by several pathways; however, in chronic lung diseases such as asthma, chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary disease (IPF) these processes are compromised, resulting in impaired cell function and ECM remodeling. Current estimates show that more than 60% of the human coding transcripts are regulated by miRNAs. miRNAs are small non-coding RNAs that regulate gene expressions and modulate cellular functions. This review is focused on the current knowledge of miRNAs in regulating ECM synthesis, degradation and topography by cells and their dysregulation in asthma, COPD and IPF.

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Section: The Ecm In Lung Remodeling and Diseasementioning

confidence: 99%

The Role of miRNAs in Extracellular Matrix Repair and Chronic Fibrotic Lung Diseases

Usman

Hackett

2021

Cells

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“…This fiber system determines the micromechanical properties of the interalveolar septa ( Bou Jawde et al, 2020 ) and contributes to mechanical stabilization of the gas-exchanging surface area. In addition, the thick side accommodates excess interstitial fluid, thus preserving the gas exchange function of the thin side ( Weibel, 2009 ; Beretta et al, 2021 ; Mostaco-Guidolin et al, 2021 ).…”

Section: An Overview Of the Functional Design Of The Lungmentioning

confidence: 99%

“…The latter equals alveolar pressure minus pleural pressure and is known as the elastic recoil pressure because it is countered by inwardly-directed stresses due to fiber elasticity and interfacial surface tension. The fiber network of the lungs comprises three distinct systems ( Wagner et al, 2015 ; Weibel, 2017 ; Mostaco-Guidolin et al, 2021 ). Located most centrally is the axial system , which enters the lung at the pulmonary hilum and follows the run of the dichotomous branching of the conducting airways.…”

Section: Stabilization Of the Pulmonary Acinus: Balance Between Diste...mentioning

confidence: 99%

Acinar micromechanics in health and lung injury: what we have learned from quantitative morphology

et al. 2023

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Within the pulmonary acini ventilation and blood perfusion are brought together on a huge surface area separated by a very thin blood-gas barrier of tissue components to allow efficient gas exchange. During ventilation pulmonary acini are cyclically subjected to deformations which become manifest in changes of the dimensions of both alveolar and ductal airspaces as well as the interalveolar septa, composed of a dense capillary network and the delicate tissue layer forming the blood-gas barrier. These ventilation-related changes are referred to as micromechanics. In lung diseases, abnormalities in acinar micromechanics can be linked with injurious stresses and strains acting on the blood-gas barrier. The mechanisms by which interalveolar septa and the blood-gas barrier adapt to an increase in alveolar volume have been suggested to include unfolding, stretching, or changes in shape other than stretching and unfolding. Folding results in the formation of pleats in which alveolar epithelium is not exposed to air and parts of the blood-gas barrier are folded on each other. The opening of a collapsed alveolus (recruitment) can be considered as an extreme variant of septal wall unfolding. Alveolar recruitment can be detected with imaging techniques which achieve light microscopic resolution. Unfolding of pleats and stretching of the blood-gas barrier, however, require electron microscopic resolution to identify the basement membrane. While stretching results in an increase of the area of the basement membrane, unfolding of pleats and shape changes do not. Real time visualization of these processes, however, is currently not possible. In this review we provide an overview of septal wall micromechanics with focus on unfolding/folding as well as stretching. At the same time we provide a state-of-the-art design-based stereology methodology to quantify microarchitecture of alveoli and interalveolar septa based on different imaging techniques and design-based stereology.

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“…While there is no increase in ECM surrounding airway smooth muscle (ASM), the increased proportion of fibronectin, elastin fibers and matrix metalloproteinase (MMP)-9 and MMP-12 [31] are related to disease severity (bronchoconstriction and bronchodilation) [32]. The ECM in the bronchial and, more recently, distal pulmonary vasculature, has also been shown to involve the deposition of disorganized fibrillar collagen in children and adults with mild and fatal asthma [33][34][35][36][37]. It was previously proposed that chronic inflammation involving mast cells, eosinophils, neutrophils, and CD4 + T cells lead to a chronic cycle of injury resulting in airway remodeling over the lifetime of an individual with asthma [38][39][40].…”

Section: Asthmamentioning

confidence: 99%

Modeling Extracellular Matrix-Cell Interactions in Lung Repair and Chronic Disease

Hackett

Osei

2021

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Second harmonic generation imaging of collagen scaffolds within the alveolar ducts of healthy and emphysematous mouse lungs

Cited by 13 publications

References 38 publications

The Role of miRNAs in Extracellular Matrix Repair and Chronic Fibrotic Lung Diseases

The Role of miRNAs in Extracellular Matrix Repair and Chronic Fibrotic Lung Diseases

Acinar micromechanics in health and lung injury: what we have learned from quantitative morphology

Modeling Extracellular Matrix-Cell Interactions in Lung Repair and Chronic Disease

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