Relationship Between Circulating Serpina3g, Matrix Metalloproteinase-9, and Tissue Inhibitor of Metalloproteinase-1 and -2 with Chronic Obstructive Pulmonary Disease Severity

Uysal, Pelin; Uzun, Hafize

doi:10.3390/biom9020062

Cited by 27 publications

(21 citation statements)

References 41 publications

(47 reference statements)

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“…The MMP-9 concentration and the MMP-9/TIMP-1 ratio were higher in patients with emphysema than in those with other phenotypes. This and other studies have suggested that the MMP-9 concentration and the MMP-9/TIMP-1 ratio are the best predictors of emphysema in COPD patients [ 415 ].…”

Section: Mmps and Timps In Human Diseasesmentioning

confidence: 57%

“…Another example of protease−antiprotease imbalance in the development of inflammatory disease occurs in COPD, which is a group of progressive lung diseases, most commonly emphysema and chronic bronchitis [ 415 ]. In a previous study, Uysal et al classified patients with COPD by the severity of symptoms and risk of exacerbation, and they found that elevated plasma levels of MMP-9, TIMP-1, and TIMP-2 correlated with the severity of disease.…”

Section: Mmps and Timps In Human Diseasesmentioning

confidence: 99%

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The Roles of Matrix Metalloproteinases and Their Inhibitors in Human Diseases

Cabral-Pacheco

Garza‐Veloz

Rosa

et al. 2020

IJMS

692

464

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Matrix metalloproteinases (MMPs) are a family of zinc-dependent extracellular matrix (ECM) remodeling endopeptidases that have the capacity to degrade almost every component of the ECM. The degradation of the ECM is of great importance, since it is related to embryonic development and angiogenesis. It is also involved in cell repair and the remodeling of tissues. When the expression of MMPs is altered, it can generate the abnormal degradation of the ECM. This is the initial cause of the development of chronic degenerative diseases and vascular complications generated by diabetes. In addition, this process has an association with neurodegeneration and cancer progression. Within the ECM, the tissue inhibitors of MMPs (TIMPs) inhibit the proteolytic activity of MMPs. TIMPs are important regulators of ECM turnover, tissue remodeling, and cellular behavior. Therefore, TIMPs (similar to MMPs) modulate angiogenesis, cell proliferation, and apoptosis. An interruption in the balance between MMPs and TIMPs has been implicated in the pathophysiology and progression of several diseases. This review focuses on the participation of both MMPs (e.g., MMP-2 and MMP-9) and TIMPs (e.g., TIMP-1 and TIMP-3) in physiological processes and on how their abnormal regulation is associated with human diseases. The inclusion of current strategies and mechanisms of MMP inhibition in the development of new therapies targeting MMPs was also considered.

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Section: Mmps and Timps In Human Diseasesmentioning

confidence: 57%

Section: Mmps and Timps In Human Diseasesmentioning

confidence: 99%

The Roles of Matrix Metalloproteinases and Their Inhibitors in Human Diseases

Cabral-Pacheco

Garza‐Veloz

Rosa

et al. 2020

IJMS

692

464

View full text Add to dashboard Cite

show abstract

“…The levels of MMP-9 in serum and exhaled breath condensate of COPD patients signi cantly increased [39,40]. Some scholars have considered the MMP-9 concentration and the MMP-9/TIMP-1 ratio are the best predictors for emphysema in COPD patients [41,42]. In T0901317 treated 6 week-group, the level of MMP9 was lower compared to the ozone exposure group.…”

Section: Discussionmentioning

confidence: 99%

liver X receptors inhibit pulmonary inflammation and airway remodeling induced by ozone exposure in mice

Yu¹,

Zheng²,

Wang³

et al. 2020

Preprint

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Ozone (O3) exposure can lead to airway inflammation, hyperreactivity and airway remodeling. Liver X receptors (LXRs) play an important role in attenuating inflammation. The therapeutic effects of LXRs on ozone-induced pulmonary inflammation and airway remodeling were examined. C57/BL6 mice were exposed to ozone for 1 or 6 weeks. LXR agonist T0901317 was administered to mice at one hour before ozone exposure. As expected, ozone-exposed mice developed lung inflammation with augmented neutrophil, macrophage, TNF-α, IL-6, IL-8 and G-CSF in the bronchoalveolar lavage fluid and serum. The increase in MMP-9 and α-SMA expression, and collagen deposition around airway reflected the airway remodeling in ozone-exposed mice. Compared with ozone-exposed mice, LXR agonist T0901317 inhibited the ozone-induced inflammation after 1 and 6 weeks in the ozone exposure model. In addition, the treatment with the LXR agonist prevented alveolar enlargement and reduced airway remodeling in 6-week ozone-induced mice. Therefore, LXRs may repress pulmonary inflammation and attenuate the progression of airway remodeling.

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“…Mohamed et al found that MMP-9 and TIMP-1 play important roles in the pathophysiology of asthma exacerbation and airway remodeling [ 46 ]. Uysal et al found that MMP-9 concentration and the MMP-9/TIMP-1 ratio are the best predictors of emphysema in patients with COPD [ 47 ]. Overall, the results of that experiment are the same as those reported in an earlier study [ 42 ].…”

Section: Discussionmentioning

confidence: 99%

Expression of Matrix Metalloproteinase-2, Matrix Metalloproteinase-9, Tissue Inhibitor of Metalloproteinase-1, and Changes in Alveolar Septa in Patients with Chronic Obstructive Pulmonary Disease

Zhang

et al. 2020

Med Sci Monit

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Background This study investigated the relationship between the pathological alteration of alveolar septa and (1) pulmonary function and (2) matrix metalloproteinase (MMP)-2, MMP-9, and tissue inhibitor matrix metalloproteinase 1 (TIMP-1) expression in chronic obstructive pulmonary disease (COPD). Material/Methods Sixty patients with pulmonary disease were divided into control (n=20) and COPD (n=40) groups. Postoperative lung tissue specimens were examined. Hematoxylin and eosin and elastin van Gieson staining detected pathological alterations of pulmonary alveolar septa. Septa thickness was measured. MMP-2, MMP-9, and TIMP-1 expression levels were detected by immunohistochemical staining. Correlations were determined by Pearson analysis. Results Forced expiratory volume in 1 s (FEV 1 ), forced vital capacity, FEV 1 percent predicted (FEV 1 %pre), and diffusion capacity of carbon monoxide percent predicted (DLCO%pre) in COPD patients were significantly lower than in those of the control group ( P <0.05). MMP-2, MMP-9, and TIMP-1 expression levels were significantly higher in the COPD group than in control, especially the severe group ( P <0.05). Septa thickness was negatively correlated with FEV 1 %pre ( r =−0.335; P <0.05) and positively correlated with MMP-2 and TIMP-1 expression ( P <0.05). Proportion of collagenous fiber was negatively correlated with FEV 1 %pre and DLCO%pre ( P <0.01), and positively correlated with MMP-2, MMP-9, and TIMP-1 expression ( P <0.01). Proportion of elastic fibers was negatively correlated with collagenous fiber. Conclusions The pathological alteration of alveolar septa was correlated with pulmonary function and expression levels of MMP-2, MMP-9, and TIMP-1, which can play vital roles in COPD progression.

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Relationship Between Circulating Serpina3g, Matrix Metalloproteinase-9, and Tissue Inhibitor of Metalloproteinase-1 and -2 with Chronic Obstructive Pulmonary Disease Severity

Cited by 27 publications

References 41 publications

The Roles of Matrix Metalloproteinases and Their Inhibitors in Human Diseases

The Roles of Matrix Metalloproteinases and Their Inhibitors in Human Diseases

liver X receptors inhibit pulmonary inflammation and airway remodeling induced by ozone exposure in mice

Expression of Matrix Metalloproteinase-2, Matrix Metalloproteinase-9, Tissue Inhibitor of Metalloproteinase-1, and Changes in Alveolar Septa in Patients with Chronic Obstructive Pulmonary Disease

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