Airway Remodeling in Chronic Obstructive Pulmonary Disease and Asthma: the Role of Matrix Metalloproteinase-9

Grzela, Katarzyna; Litwiniuk, Małgorzata; Zagórska, Wioletta; Grzela, Tomasz

doi:10.1007/s00005-015-0345-y

Cited by 98 publications

(107 citation statements)

References 91 publications

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“…They can contribute to cancer metastasis, aneurysm and varicose vein formation, and airway remodeling in asthma. [8][9][10][11][12] Moreover, the excessive production and hyperactivity of MMPs is observed in patients with nonhealing chronic wounds.…”

Section: Introductionmentioning

confidence: 99%

Matrix metalloproteinases in the wound microenvironment: therapeutic perspectives

Krejner¹,

Litwiniuk²,

Grzela³

2016

CWCMR

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Matrix metalloproteinases (MMPs) are key effector molecules responsible for extracellular matrix (ECM) turnover. They are involved in tissue remodeling and regeneration. Although the main targets for MMPs are ECM components, they are also able to digest a variety of non-ECM molecules including cytokines, their receptors, or carriers. Therefore, the activity of the MMPs remains under tight control. However, when controlling mechanisms are ineffective, MMPs may become highly dangerous molecules, which have a strong destructive effect on affected tissues. Apart from cancer metastasis, aneurysm formation, or airway remodeling in asthma, MMPs have also been identified as main detrimental factors in delayed healing of chronic wounds. In this short review, we describe main representatives of MMPs family, their role in pathophysiology of chronic wounds, as well as current and possible therapeutic strategies for modulation of MMPs' activity, which may be useful in management of chronic wounds.

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Section: Introductionmentioning

confidence: 99%

Matrix metalloproteinases in the wound microenvironment: therapeutic perspectives

Krejner¹,

Litwiniuk²,

Grzela³

2016

CWCMR

Self Cite

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“…Metalloproteinases (MMPs) mediate degradation of extracellular matrix, cell invasion, remodeling and tissue damage (Atkinson and Senior, 2003; Elkington and Friedland, 2006; Grzela et al, 2016). To evaluate the hypothesis that the HIV reprogramming of normal BC to take on a destructive phenotype is mediated by HIV inducing the BC to express matrix metalloproteases, the cell lysates of BC + HIV were assessed using a human protease array.…”

Section: Resultsmentioning

confidence: 99%

“…Matrix metalloproteinases (MMPs) are proteolytic enzymes capable of degrading the extracellular matrix, facilitating cell migration and tissue remodeling (Atkinson and Senior, 2003; Elkington and Friedland, 2006; Grzela et al, 2016; Legrand et al, 1999). MMPs also regulate cytokines and chemokines activity, influencing the recruitment and functions of inflammatory cells (Parks et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

HIV Reprograms Human Airway Basal Stem/Progenitor Cells to Acquire a Tissue-Destructive Phenotype

Chung

Khan

et al. 2017

Cell Reports

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Summary While highly active anti-retroviral therapy has dramatically improved the survival of HIV-infected individuals, there is an increased risk for other co-morbidities, such as COPD, manifesting as emphysema. Given that emphysema orginates around the airways, and that human airway basal cells (BC) are adult airway stem/progenitor cells, we hypothesized that HIV reprograms BCs to a distinct phenotype that contribute to the development of emphysema. Our data indicate that HIV binds to, but does not replicate, in BC. HIV binding to BCs induces them to acquire an invasive phenotype, mediated by up-regulation of MMP-9 expression through activation of MAPK signaling pathways. This HIV-induced “destructive” phenotype may contribute to degradation of extracellular matrix and tissue damage relevant to the development of emphysema commonly seen in HIV+ individuals.

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“…Previous studies have shown an increase in ERK with MMP-9 in CS and LPS induced mice models and CS condensate-stimulated cells [19]. CS stimulated the phosphorylation of Erk in airway epithelial cells, macrophages, and neutrophils, which eventually elevates the MMP-9 and iNOS expression [1927]. …”

Section: Discussionmentioning

confidence: 99%

HemoHIM, a herbal preparation, alleviates airway inflammation caused by cigarette smoke and lipopolysaccharide

Shin

Kim

et al. 2017

Lab Anim Res

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HemoHIM, herbal preparation has designed for immune system recovery. We investigated the anti-inflammatory effect of HemoHIM on cigarette smoke (CS) and lipopolysaccharide (LPS) induced chronic obstructive pulmonary disease (COPD) mouse model. To induce COPD, C57BL/6 mice were exposed to CS for 1 h per day (eight cigarettes per day) for 4 weeks and intranasally received LPS on day 26. HemoHIM was administrated to mice at a dose of 50 or 100 mg/kg 1h before CS exposure. HemoHIM reduced the inflammatory cell count and levels of tumor necrosis factor receptor (TNF)-α, interleukin (IL)-6 and IL-1β in the broncho-alveolar lavage fluid (BALF) induced by CS+LPS exposure. HemoHIM decreased the inflammatory cell infiltration in the airway and inhibited the expression of iNOS and MMP-9 and phosphorylation of Erk in lung tissue exposed to CS+LPS. In summary, our results indicate that HemoHIM inhibited a reduction in the lung inflammatory response on CS and LPS induced lung inflammation via the Erk pathway. Therefore, we suggest that HemoHIM has the potential to treat pulmonary inflammatory disease such as COPD.

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Airway Remodeling in Chronic Obstructive Pulmonary Disease and Asthma: the Role of Matrix Metalloproteinase-9

Cited by 98 publications

References 91 publications

Matrix metalloproteinases in the wound microenvironment: therapeutic perspectives

Matrix metalloproteinases in the wound microenvironment: therapeutic perspectives

HIV Reprograms Human Airway Basal Stem/Progenitor Cells to Acquire a Tissue-Destructive Phenotype

HemoHIM, a herbal preparation, alleviates airway inflammation caused by cigarette smoke and lipopolysaccharide

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