Expression of Lumican in Human Lungs

Dolhnikoff, Marisa; Morin, Jean Paul; Roughley, Peter J.; Ludwig, Mara S.

doi:10.1165/ajrcmb.19.4.2979

Cited by 70 publications

(55 citation statements)

References 34 publications

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“…Immunoblotting for lumican (Fig. 5C) revealed multiple diffuse bands predominantly from 50 -100 kDa, indicative of a proteoglycan form of lumican (33)(34)(35)(36). Consistent with the analysis of the MS signal intensities, there was significantly (p Ͻ 0.01) more lumican present in the intima of the atherosclerosis-prone internal carotid artery than in the atherosclerosis-resistant internal thoracic artery, with the mean value elevated by ϳ3-fold.…”

Section: Fig 2 Removal Of Thickened Intima For Proteomic Analysissupporting

confidence: 72%

Analysis of Intimal Proteoglycans in Atherosclerosis-prone and Atherosclerosis-resistant Human Arteries by Mass Spectrometry

Talusan

Bedri

Yang

et al. 2005

Molecular & Cellular Proteomics

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The propensity to develop atherosclerosis varies markedly among different sites in the human vasculature. To determine a possible cause for such differences in atherosclerosis susceptibility, a proteomics-based approach was used to assess the extracellular proteoglycan core protein composition of intimal hyperplasia from both the atherosclerosis-prone internal carotid artery and the atherosclerosis-resistant internal thoracic artery. The intimal proteoglycan composition in these preatherosclerotic lesions was found to be more complex than previously appreciated with up to eight distinct core proteins present, including the large extracellular proteoglycans versican and aggrecan, the basement membrane proteoglycan perlecan, the class I small leucine-rich proteoglycans biglycan and decorin, and the class II small leucine-rich proteoglycans lumican, fibromodulin, and prolargin/ PRELP (proline arginine-rich end leucine-rich repeat protein). Although most of these proteoglycans seem to be present in similar amounts at the two locations, there was a selective enhanced deposition of lumican in the intima of the atherosclerosis-prone internal carotid artery compared with the intima of the atherosclerosis-resistant internal thoracic artery. The enhanced deposition of lumican in the intima of an atherosclerosis prone artery has important implications for the pathogenesis of atherosclerosis.

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Section: Fig 2 Removal Of Thickened Intima For Proteomic Analysissupporting

confidence: 72%

Analysis of Intimal Proteoglycans in Atherosclerosis-prone and Atherosclerosis-resistant Human Arteries by Mass Spectrometry

Talusan

Bedri

Yang

et al. 2005

Molecular & Cellular Proteomics

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“…Decorin, biglycan and lumican are small proteoglycans which interact with fibrillar collagens, participating in the maintenance of the extracellular milieu [39][40][41]. In vitro studies have indicated that fibroblasts from COPD patients present abnormal production of proteoglycans and altered expression of the transforming growth factor (TGF)-b Smad pathway when exposed to cigarette smoke or different cytokines [42,43].…”

Section: Discussionmentioning

confidence: 99%

Extracellular matrix composition in COPD

et al. 2012

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Extracellular matrix (ECM) composition has an important role in determining airway structure. We postulated that ECM lung composition of chronic obstructive pulmonary disease (COPD) patients differs from that observed in smoking and nonsmoking subjects without airflow obstruction.We determined the fractional areas of elastic fibres, type-I, -III and -IV collagen, versican, decorin, biglycan, lumican, fibronectin and tenascin in different compartments of the large and small airways and lung parenchyma in 26 COPD patients, 26 smokers without COPD and 16 nonsmoking control subjects.The fractional area of elastic fibres was higher in non-obstructed smokers than in COPD and nonsmoking controls, in all lung compartments. Type-I collagen fractional area was lower in the large and small airways of COPD patients and in the small airways of non-obstructed smokers than in nonsmokers. Compared with nonsmokers, COPD patients had lower versican fractional area in the parenchyma, higher fibronectin fractional area in small airways and higher tenascin fractional area in large and small airways compartments. In COPD patients, significant correlations were found between elastic fibres and fibronectin and lung function parameters.Alterations of the major ECM components are widespread in all lung compartments of patients with COPD and may contribute to persistent airflow obstruction.

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“…10 Lumican belongs to the family of small leucine-rich repeat keratan sulfate proteoglycans (SLRPs) and is one of 10 members of SLRPs found in the lungs. 11 Many members of SLRPs (eg, decorin, lumican, biglycan) play roles in tissue morphogenesis during embryonic development and in adults through their matricellular functions as regulator of collagen fi brillogenesis. [12][13][14] A previous study has shown that lumican increased human corneal epithelial cell migration through the extracellular signal-regulated kinase (ERK) 1/2 pathway.…”

Section: Reduction Of Vili In Lumican-defi Cient Micementioning

confidence: 99%

Lumican Regulates Ventilation-Induced Epithelial-Mesenchymal Transition Through Extracelluar Signal-Regulated Kinase Pathway

Chu

Hung

et al. 2013

Chest

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A cute lung injury (ALI) and its most severe manifestation, ARDS, are characterized by an initial inhomogeneous infl ammatory reaction or epithelial injury that is followed by fi broblast proliferation and extracellular matrix (ECM) accumulation. 1,2 Mechanical ventilation is required for life support in patients with ARDS; however, the potential for overdistension of the healthy parts of the lungs is great. Ventilatorinduced lung injury (VILI) is characterized by noncardiogenic pulmonary edema; release of infl ammatory cytokines; infl ux of neutrophils; and increased message for the ECM proteins , including proteoglycans. 3,4 High tidal volume (V t ) mechanical ventilation can lead to the production of infl ammatory cytokines, including tumor necrosis factor-a , IL-1 b , macrophage infl ammatory protein (MIP)-2, and transforming growth factor-b 1 (TGF-b 1 ). 5,6 Chemokines are expressed in both the acute infl ammatory response and the subsequent wound remodeling after lung injury. Previous studies demonstrated that MIP-2 induces neovascularization and promotes angiogenesis during VILI. 5,7 As a major profi brogenic Methods: Male C57BL/6 mice (either wild type or lumican null) aged 3 months and weighing between 25 and 30 g were exposed to low V T (6 mL/kg) or high V T (30 mL/kg) mechanical ventilation with room air for 2 to 8 h. Nonventilated mice were used as control subjects. Results: We found that high V T mechanical ventilation increased microvascular permeability, neutrophil infl ux, production of free radicals, MIP-2 and TGF-b 1 proteins, positive staining of a -smooth muscle actin and S100A4/fi broblast-specifi c protein-1, Masson trichrome staining and extracellular collagen, and activation of lumican and ERK1/2 in wild-type mice. Decreased staining of the epithelial marker E-cadherin was also observed. Mechanical stretch-augmented EMT was attenuated with lumican-defi cient mice and pharmacologic inhibition of ERK1/2 activity by PD98059. Conclusions: The data suggest that lumican promotes high V T mechanical ventilation-induced lung injury and EMT through the activation of the ERK1/2 pathway.

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Expression of Lumican in Human Lungs

Cited by 70 publications

References 34 publications

Analysis of Intimal Proteoglycans in Atherosclerosis-prone and Atherosclerosis-resistant Human Arteries by Mass Spectrometry

Analysis of Intimal Proteoglycans in Atherosclerosis-prone and Atherosclerosis-resistant Human Arteries by Mass Spectrometry

Extracellular matrix composition in COPD

Lumican Regulates Ventilation-Induced Epithelial-Mesenchymal Transition Through Extracelluar Signal-Regulated Kinase Pathway

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