Relationships of MMP-9 and TIMP-1 proteins with chronic obstructive pulmonary disease risk: A systematic review and meta-analysis

Yang, Lu; Zhao, Zhuo; Wang, Junnan; Li, Jianxin; Wang, Weiming; Li, Shumei; Song, Lei

doi:10.4103/1735-1995.178737

Cited by 33 publications

(29 citation statements)

References 58 publications

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“…[ 2 ] It has been shown that various immune cells and a variety of cellular and molecular pathways are involved in inflammation and play critical roles in COPD pathogenesis. [ 3 4 ] Among many cellular and molecular targets, microRNAs (miRNAs) have emerged to be involved in COPD pathogenesis. [ 5 6 ] Deregulation of miRNAs is associated with the initiation and progression of several diseases such as stroke, cardiovascular diseases, diabetes, cancer, and inflammatory diseases.…”

Section: Introductionmentioning

confidence: 99%

Chronic obstructive pulmonary disease: MicroRNAs and exosomes as new diagnostic and therapeutic biomarkers

et al. 2018

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Chronic obstructive pulmonary disease (COPD) is known as a progressive lung disease and the fourth leading cause of death worldwide. Despite valuable efforts, there is still no accurate diagnostic and prognostic tool for COPD. Hence, it seems that finding new biomarkers could contribute to provide better therapeutic platforms for COPD patients. Among various biomarkers, microRNAs (miRNAs) have emerged as new biomarkers for the prognosis and diagnosis of patients with COPD. It has been shown that deregulation of miRNAs targeting a variety of cellular and molecular pathways such as Notch, Wnt, hypoxia-inducible factor-1α, transforming growth factor, Kras, and Smad could be involved in COPD pathogenesis. Multiple lines of evidence have indicated that extracellular vesicles such as exosomes could carry a variety of cargos (i.e., mRNAs, miRNAs, and proteins) which transfer various cellular and molecular signals to recipient cells. Here, we summarized various miRNAs which could be applied as diagnostic and prognostic biomarkers in the treatment of patients with COPD. Moreover, we highlighted the role of extracellular vesicles containing miRNAs as diagnostic and prognostic biomarkers in COPD patients.

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Section: Introductionmentioning

confidence: 99%

Chronic obstructive pulmonary disease: MicroRNAs and exosomes as new diagnostic and therapeutic biomarkers

et al. 2018

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“…MMP-9 is inhibited by the tissue inhibitors of metalloproteinase (TIMP1) and so the imbalance between MMP-9 and TIMP1 ratio could be involved in COPD pathogenesis [28]. Herein, in complement of the MMP-9 and TIMP1 ratio analysis [28, 29], we demonstrate that the concentration of the MMP-9/TIMP1 complex in the serum of COPD patients is higher than that in healthy controls, which corroborates the findings of other authors [30]. More complexes of MMP-9/TIMP1 could be delivered by increased secretion of MMP-9, but it was also found that COPD patients exhibited a significantly higher level of unbound TIMP1 ([29, 30] and our unpublished data).…”

Section: Discussionmentioning

confidence: 99%

Impact of Matrix Metalloproteinase 9 on COPD Development in Polish Patients: Genetic Polymorphism, Protein Level, and Their Relationship with Lung Function

Gilowska

Kasper

Bogacz

et al. 2018

BioMed Research International

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Chronic obstructive pulmonary disease (COPD) is characterized by a decline of lung function and symptoms such as chronic bronchitis and emphysema leading from lung tissue destruction. Increased activity of matrix metalloproteinases (MMPs) and an imbalance between MMPs and their tissue inhibitors (TIMPs) are considered as factors influencing the pathogenesis of COPD. We investigated the role of genetic polymorphism and expression level of MMP-9 and concentration of its complexes with TIMPs in the development of COPD among Polish patients. We analyzed SNP in the promoter region of MMP-9 gene (rs3918242) using PCR-RFLP method among 335 COPD patients and 309 healthy individuals. Additionally, 60 COPD patients and 61 controls were tested for copy number variants (CNV) of MMP-9 (by quantitative real-time PCR) and serum levels of MMP-9 and its complexes with TIMP1 and TIMP2 (using ELISA). All subjects were analyzed for lung function using spirometry (FEV1% and FEV1/FVC parameters). We observed that allele and genotype frequencies of the SNP rs3918242, as well as the number of gene copies, were similar in COPD patient and controls groups. Serum levels of MMP-9 and MMP-9/TIMP1 complex were significantly higher in COPD patients in comparison to controls groups, although independently of analyzed gene polymorphisms. Additionally, the significant inverse relationships between parameters of lung function (FEV1% and FEV1/FVC) and proteins level were found in ridge regression models, especially we found that FEV1% decreased when MMP-9 level increased in controls and patients with COPD group. In conclusion, we found that COPD patients were predisposed to produce more MMP-9 and MMP-9/TIMP1 complex than healthy individuals. This phenomenon is probably associated with the disease-related lung environment but not with genetic features of the MMP-9.

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“…Recent reports indicated that EGF and its receptor EGFR were increased in some tumors, such as gastric cancer, and GBM, which further induced tumorigenesis, and stimulated cell proliferation and migration [ 19 – 21 ]. In addition, matrix metalloproteinases are involved into cell invasion, metastases, and angiogenesi, and can cause dynamic changes of biological behaviors [ 22 – 25 ]. In the present work, our study showed that U87 and U251 cells transfected with miR-137 mimics indeed decreased the expression of EGFR, MMP2 and MMP9 proteins than control, suggesting that miR-137 reduced GBM cell proliferation and invasion.…”

Section: Discussionmentioning

confidence: 99%

miR-137 acts as a tumor suppressor via inhibiting CXCL12 in human glioblastoma

Shan

Fang

et al. 2017

Oncotarget

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Up to date, miR-137 has been demonstrated as a tumor suppressor in many kinds of human malignancies. In the present study, we conducted transfection, western blot and RT-PCR to explore the role of miR-137 in the development of human glioblastoma (GBM). Here, we found that miR-137 expression was obviously down-regulated in GBM tissues and cells rather than matched non-tumor tissues and NHA cells. However, the expression of C-X-C motif ligand 12 (CXCL12) mRNA and protein were up-regulated in GBM tissues and cells. In vitro, miR-137 mimics inhibited GBM cell proliferation, migration and invasion, and the 3′-untranslated regions (3′-UTR) of CXCL12 were a direct target of miR-137. In addition, miR-137 mimics also inhibited the expression of EGFR, Bcl-2 and MMP2/9 proteins, but increased the expression of Bax protein. Notably, CXCL12 over-expression attenuated miR-137-inhibited cell proliferation and invasion, while CXCL12 siRNAs promoted miR-137 inhibition effects. In vivo, miR-137 mimics also suppressed tumor growth in nude mice xenograft model. In conclusion, miR-137 serves as a tumor suppressor by inhibition of CXCL12 in human GBM. Thus, miR-137-CXCL12 can be recommended as a useful and effective target for treatment of GBM.

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Relationships of MMP-9 and TIMP-1 proteins with chronic obstructive pulmonary disease risk: A systematic review and meta-analysis

Cited by 33 publications

References 58 publications

Chronic obstructive pulmonary disease: MicroRNAs and exosomes as new diagnostic and therapeutic biomarkers

Chronic obstructive pulmonary disease: MicroRNAs and exosomes as new diagnostic and therapeutic biomarkers

Impact of Matrix Metalloproteinase 9 on COPD Development in Polish Patients: Genetic Polymorphism, Protein Level, and Their Relationship with Lung Function

miR-137 acts as a tumor suppressor via inhibiting CXCL12 in human glioblastoma

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