Mouse strain dependence of lung tissue mechanics: Role of specific extracellular matrix composition

The dynamic mechanical properties of lung tissue and its contents of collagen and elastic fibers were studied in strips prepared from mice instilled intratracheally with saline (C) or silica [15 (S15) and 30 days (S30) after instillation]. Resistance, elastance, and hysteresivity were studied during oscillations at different frequencies on S15 and S30. Elastance increased from C to silica groups but was similar between S15 and S30. Resistance was augmented from C to S15 and S30 and was greater in S30 than in S15 at higher frequencies. Hysteresivity was higher in S30 than in C and S15. Silica groups presented a greater amount of collagen than did C. Elastic fiber content increased progressively along time. This increment was related to the higher amount of oxytalan fibers at 15 and 30 days, whereas elaunin and fully developed elastic fibers were augmented only at 30 days. Silicosis led not only to pulmonary fibrosis but also to fibroelastosis, thus assigning a major role to the elastic system in the silicotic lung.

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Role of extracellular matrix structural components and tissue mechanics in the development of postoperative pancreatic fistula

Journal of Biomechanics ◽

10.1016/j.jbiomech.2021.110714 ◽

2021 ◽

Vol 128 ◽

pp. 110714

Author(s):

Rosa B. Schmuck ◽

Evi Lippens ◽

Dag Wulsten ◽

Daniela S. Garske ◽

Annika Strönisch ◽

...

Keyword(s):

Extracellular Matrix ◽

Pancreatic Fistula ◽

Tissue Mechanics ◽

Postoperative Pancreatic Fistula ◽

Structural Components

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Influence of obesity on remodeling of lung tissue and organization of extracellular matrix after blunt thorax trauma

Respiratory Research ◽

10.1186/s12931-020-01502-0 ◽

2020 ◽

Vol 21 (1) ◽

Author(s):

Pengfei Xu ◽

Fabian Gärtner ◽

Adrian Gihring ◽

Congxing Liu ◽

Timo Burster ◽

...

Keyword(s):

Extracellular Matrix ◽

Lung Tissue ◽

Protein Level ◽

Morphological Changes ◽

Matrix Composition ◽

Collagen Deposition ◽

Obese Mice ◽

Time Points ◽

Extracellular Matrix Components ◽

Thorax Trauma

Abstract Background Previously, it has been shown that obesity is a risk factor for recovery, regeneration, and tissue repair after blunt trauma and can affect the rate of muscle recovery and collagen deposition after trauma. To date, lung tissue regeneration and extracellular matrix regulation in obese mice after injury has not been investigated in detail yet. Methods This study uses an established blunt thorax trauma model to analyze morphological changes and alterations on gene and protein level in lean or obese (diet-induced obesity for 16 ± 1 week) male C57BL/6 J mice at various time-points after trauma induction (1 h, 6 h, 24 h, 72 h and 192 h). Results Morphological analysis after injury showed lung parenchyma damage at early time-points in both lean and obese mice. At later time-points a better regenerative capacity of lean mice was observed, since obese animals still exhibited alveoli collapse, wall thickness as well as remaining filled alveoli structures. Although lean mice showed significantly increased collagen and fibronectin gene levels, analysis of collagen deposition showed no difference based on colorimetric quantification of collagen and visual assessment of Sirius red staining. When investigating the organization of the ECM on gene level, a decreased response of obese mice after trauma regarding extracellular matrix composition and organization was detectable. Differences in the lung tissue between the diets regarding early responding MMPs (MMP8/9) and late responding MMPs (MMP2) could be observed on gene and protein level. Obese mice show differences in regulation of extracellular matrix components compared to normal weight mice, which results in a decreased total MMP activity in obese animals during the whole regeneration phase. Starting at 6 h post traumatic injury, lean mice show a 50% increase in total MMP activity compared to control animals, while MMP activity in obese mice drops to 50%. Conclusions In conclusion, abnormal regulation of the levels of extracellular matrix genes in the lung may contribute to an aberrant regeneration after trauma induction with a delay of repair and pathological changes of the lung tissue in obese mice.

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Lung tissue mechanics: from extracellular matrix to alveolar network behavior

Journal of Biomechanics ◽

10.1016/s0021-9290(06)84021-2 ◽

2006 ◽

Vol 39 ◽

pp. S267

Author(s):

B. Suki ◽

H. Parameswaran ◽

A. Majumdar

Keyword(s):

Extracellular Matrix ◽

Lung Tissue ◽

Tissue Mechanics ◽

Network Behavior

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Effects of chronic l-NAME treatment lung tissue mechanics, eosinophilic and extracellular matrix responses induced by chronic pulmonary inflammation

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00199.2007 ◽

2008 ◽

Vol 294 (6) ◽

pp. L1197-L1205 ◽

Cited By ~ 29

Author(s):

Patrícia Angeli ◽

Carla M. Prado ◽

Débora G. Xisto ◽

Pedro L. Silva ◽

Caroline P. Pássaro ◽

...

Keyword(s):

Nitric Oxide ◽

Extracellular Matrix ◽

Smooth Muscle ◽

Lung Tissue ◽

Pulmonary Inflammation ◽

Elastic Fiber ◽

Tissue Mechanics ◽

Elastic Fibers ◽

Distal Lung ◽

Alveolar Septa

The importance of lung tissue in asthma pathophysiology has been recently recognized. Although nitric oxide mediates smooth muscle tonus control in airways, its effects on lung tissue responsiveness have not been investigated previously. We hypothesized that chronic nitric oxide synthase (NOS) inhibition by Nω-nitro-l-arginine methyl ester (l-NAME) may modulate lung tissue mechanics and eosinophil and extracellular matrix remodeling in guinea pigs with chronic pulmonary inflammation. Animals were submitted to seven saline or ovalbumin exposures with increasing doses (1∼5 mg/ml for 4 wk) and treated or not with l-NAME in drinking water. After the seventh inhalation (72 h), animals were anesthetized and exsanguinated, and oscillatory mechanics of lung tissue strips were performed in baseline condition and after ovalbumin challenge (0.1%). Using morphometry, we assessed the density of eosinophils, neuronal NOS (nNOS)- and inducible NOS (iNOS)-positive distal lung cells, smooth muscle cells, as well as collagen and elastic fibers in lung tissue. Ovalbumin-exposed animals had an increase in baseline and maximal tissue resistance and elastance, eosinophil density, nNOS- and iNOS-positive cells, the amount of collagen and elastic fibers, and isoprostane-8-PGF2α expression in the alveolar septa compared with controls ( P < 0.05). l-NAME treatment in ovalbumin-exposed animals attenuated lung tissue mechanical responses ( P < 0.01), nNOS- and iNOS-positive cells, elastic fiber content ( P < 0.001), and isoprostane-8-PGF2α in the alveolar septa ( P < 0.001). However, this treatment did not affect the total number of eosinophils and collagen deposition. These data suggest that NO contributes to distal lung parenchyma constriction and to elastic fiber deposition in this model. One possibility may be related to the effects of NO activating the oxidative stress pathway.

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Pathophysiological Mechanisms Destruction of the Lung Connective Tissue in Tuberculosis

Infusion & Chemotherapy ◽

10.32902/2663-0338-2019-2-14-20 ◽

2019 ◽

pp. 14-20

Author(s):

O. S. Shevchenko ◽

I. A. Ovcharenko ◽

L. D. Todoriko

Keyword(s):

Extracellular Matrix ◽

Lung Tissue ◽

Collagen Fibers ◽

Tissue Inhibitors Of Metalloproteinases ◽

Blood Monocytes ◽

Pulmonary Tissue ◽

Α2 Macroglobulin ◽

The Family ◽

Pathological Event

Background. The restructuring of the lung tissue stroma during destructive tuberculosis is one of the most important pathological events in the formation of residual changes in the lung tissue during tuberculosis inflammation. Most patients with tuberculosis have destructive forms of this disease. Therefore, studies of pathomorphological changes in the pulmonary tissue of tuberculosispatients are very relevant. It is known that the formation of decavities in volves the destruction of the extracellular matrix, which includes collagen fibers that support the structure of the lungs. The destruction of this matrix leads to the destruction of lung tissue and is a consequence of the activity of proteinase enzymes. One of the products of the destruction of collagen fibers of the lung tissue is oxyproline and its fractions. It has been proventhatin the lungs collagen fibers break down matrix metalloproteinases (MMPs), which belong to the family of proteinases, and are able to affectall component soft he extracellular matrix. The process of MMP synthesis is regulated at the transcription level, and the irproteolytic activity is controlled by proenzymes, as well as inhibition of active enzymes by endogenous inhibitors, α2-macroglobulin and tissue inhibitors of metalloproteinases (TIMP), which play an important role in fibrosis processes. However, it is important not only the level of MMP, but also their ratio with TIMP. An increase in the level of TIMP over MMP leads to the degradation of capillaries of the interalveolar septa, while the predominance of MMP over TIMP leads to the destruction of the component soft he extracellular matrix. Recent studies indicate the role of aldosterone in the processes of fibrosis. It is able to activate blood monocytes, induce in flammation, lead to impaired fibrinolysis. Also aldosterone is able to enhance the synthesis and accumulation of collagen. Elevated levels of aldosterone, stimulating the growth of smooth muscle fibers, contribute to the development of fibrosis in the lungs. There is evidence that aldosterone is able to enhance the degradation of the extracellular matrix through the activation of MMP. Conclusions. Thus, the destruction of the extracellular matrixis one of the most important pathological event sin the formation of residual changes in the lung tissue with tuberculous inflammation.

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Lung Tissue Mechanics and Extracellular Matrix Remodeling in Acute Lung Injury

American Journal of Respiratory and Critical Care Medicine ◽

10.1164/ajrccm.164.6.2007062 ◽

2001 ◽

Vol 164 (6) ◽

pp. 1067-1071 ◽

Cited By ~ 112

Author(s):

PATRICIA R. M. ROCCO ◽

ELNARA M. NEGRI ◽

PEDRO M. KURTZ ◽

FERNANDA P. VASCONCELLOS ◽

GABRIELA H. SILVA ◽

...

Keyword(s):

Extracellular Matrix ◽

Acute Lung Injury ◽

Lung Injury ◽

Lung Tissue ◽

Tissue Mechanics ◽

Extracellular Matrix Remodeling ◽

Matrix Remodeling

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Changes in proteoglycans and lung tissue mechanics during excessive mechanical ventilation in rats

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.2001.281.5.l1078 ◽

2001 ◽

Vol 281 (5) ◽

pp. L1078-L1087 ◽

Cited By ~ 35

Author(s):

Rehab Al-Jamal ◽

Mara S. Ludwig

Keyword(s):

Extracellular Matrix ◽

Mechanical Ventilation ◽

Heparan Sulfate ◽

Lung Tissue ◽

Tissue Mechanics ◽

Alveolar Wall ◽

Matrix Component ◽

Tissue Properties ◽

Tissue Elastance

Excessive mechanical ventilation results in changes in lung tissue mechanics. We hypothesized that changes in tissue properties might be related to changes in the extracellular matrix component proteoglycans (PGs). The effect of different ventilation regimens on lung tissue mechanics and PGs was examined in an in vivo rat model. Animals were anesthetized, tracheostomized, and ventilated at a tidal volume of 8 (Vt 8), 20, or 30 (Vt 30) ml/kg, positive end-expiratory pressure of 0 (PEEP0) or 1.5 (PEEP1.5) cmH2O, and frequency of 1.5 Hz for 2 h. The constant-phase model was used to derive airway resistance, tissue elastance, and tissue damping. After physiological measurements, one lung was frozen for immunohistochemistry and the other was reserved for PG extraction and Western blotting. After 2 h of mechanical ventilation, tissue elastance and damping were significantly increased in rats ventilated at Vt 30PEEP0 compared with control rats (ventilated at Vt 8PEEP1.5). Versican, basement membrane heparan sulfate PG, and biglycan were all increased in rat lungs ventilated at Vt 30PEEP0 compared with control rats. At Vt 30PEEP0, heparan sulfate PG and versican staining became prominent in the alveolar wall and airspace; biglycan was mostly localized in the airway wall. These data demonstrate that alterations in lung tissue mechanics with excessive mechanical ventilation are accompanied by changes in all classes of extracellular matrix PG.

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