Matrix metalloproteinases as modulators of inflammation

Manicone, Anne M.; McGuire, John K.

doi:10.1016/j.semcdb.2007.07.003

Cited by 505 publications

(391 citation statements)

References 82 publications

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“…42 MMP activity is usually linked to inflammation through interactions with and activation of several cytokines, chemokines and other pericellular and cell surface substrates. [43][44][45] Minocycline has broad anti-inflammatory properties, in addition to its action as an MMP inhibitor. 41 In this study, many F4/80 þ macrophages infiltrated around damaged tubules following UUO, which were suppressed in MMP-2 À/À mice or following treatment with minocycline.…”

Section: Mmp-2 In Renal Fibrosismentioning

confidence: 99%

Involvement of matrix metalloproteinase-2 in the development of renal interstitial fibrosis in mouse obstructive nephropathy

Shimizu

Masuda

et al. 2012

Laboratory Investigation

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Section: Mmp-2 In Renal Fibrosismentioning

confidence: 99%

Involvement of matrix metalloproteinase-2 in the development of renal interstitial fibrosis in mouse obstructive nephropathy

Shimizu

Masuda

et al. 2012

Laboratory Investigation

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“…This latter mechanism includes both the immobilization of chemokines to cell surfaces or ECM proteins and the generation of chemotactic concentration gradients that provide directional cues for leukocyte migration. MMPs are proteinases that can indirectly control influx of inflammatory cells by cleaving proteins in the pericellular environment that bind chemokines [74][75][76].…”

Section: Modification Of Chemokine Gradients In Alimentioning

confidence: 99%

Role of the pulmonary epithelium and inflammatory signals in acute lung injury

Manicone¹

2009

Expert Review of Clinical Immunology

118

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Acute lung injury (ALI) is a clinical disease marked by respiratory failure due to disruption of the epithelial and endothelial barrier, flooding of the alveolar compartment with protein-rich fluid and recruitment of neutrophils into the alveolar space. ALI affects approximately 200,000 patients annually in the USA and results in approximately 75,000 deaths. It is associated with prolonged mechanical ventilation, intensive medical care, high morbidity and mortality, and rising healthcare costs. Owing to its impact on public health, great strides have been made towards understanding the pathobiology of ALI to affect outcome. This review will focus on the role of the epithelial cell in the pathogenesis and resolution of ALI and the role of various inflammatory mediators in ALI. Keywordsβ2-agonist; acute lung injury; acute respiratory distress syndrome; chemokine; cytokine; epithelial cell; inflammation; methylprednisolone; neutrophil; salbutamol; steroid; ventilator-induced lung injuryAcute lung injury/acute respiratory distress syndrome (ALI/ARDS) was first described in 1967 by Ashbaugh and colleagues in a group of 12 patients who shared a constellation of clinical symptoms including acute respiratory distress, hypoxemia refractory to supplemental oxygen, decreased lung compliance and diffuse pulmonary infiltrates [1]. Since this first description, the clinical criteria have evolved to include acute onset of respiratory distress, bilateral pulmonary infiltrates seen on chest radiographs, absence of left-sided heart failure and hypoxemia, with the severity of hypoxemia distinguishing ALI and ARDS (Box 1) [2]. Extrapolating from recent epidemiologic studies using these criteria, ALI affects about 200,000 patients annually in the USA and results in approximately 75,000 deaths [3]. This disease, which can be caused by common events such as pneumonia, sepsis and trauma, results in high morbidity, mortality and healthcare expenditures associated with prolonged mechanical ventilation and intensive care. Because of its impact on public health and patient outcomes, great strides have been made towards understanding the pathobiology of ALI.When defined broadly to include all processes related to defense against microbes, other environmental insults and injury, a wide variety of cell types and proteins participate in inflammation and immunity. Leukocytes are the paradigmatic inflammatory cell type, but they are not the only cells that function in defense and immunity. The epithelial lining of all tissues forms a continuous barrier to the environment and is the first line of defense against infectious agents and toxins. Though specialized to serve distinct functions among tissues, epithelial cells respond similarly to injury and infection, and regulate leukocyte influx through the production of proinflammatory cytokines, chemokines and other factors that modulate chemokine gradients and effect leukocyte migration. This review will focus on the role of the pulmonary epithelium and inflammatory mediators in ALI. More s...

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“…However, the overexpression of several MMPs is involved in tumor invasion, metastasis, disregulated angiogenesis, inflammation and even cell destruction [1,[5][6][7][8][9]. …”

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confidence: 99%

The Significance of Matrix Metalloproteinases in Oral Diseases

et al. 2015

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MMPs are significant in the physiological processes of embryo development, wound healing and differentiation related to tissue remodeling. However, the overexpression of several MMPs is involved in tumor invasion, metastasis, disregulated angiogenesis, inflammation and even cell destruction [1,[5][6][7][8][9]. MMP SubfamiliesThe first metalloproteinase was discovered in 1962 during a study of the ECM degradation re- The Role of MMPsMatrix metalloproteinases (MMPs) belong to a family of structurally related zinc-dependent proteolytic enzymes that are known known to play a key role in the catabolic turnover of extracellular matrix (ECM) components. Research studies to date have indicated that MMPs regulate the activity of several non-ECM bioactive substrates, including growth factors, cytokines, chemokines and cell receptors, which determine the tissue microenvironment. These activities are implicated in a number of essential physiopathological processes AbstractMatrix metalloproteinases (MMPs) belong to a family of structurally related zinc-dependent proteolytic enzymes that are known to play a key role in the catabolic turnover of extracellular matrix (ECM) components. Research studies to date have indicated that MMPs regulate the activity of several non-ECM bioactive substrates, including growth factors, cytokines, chemokines and cell receptors, which determine the tissue microenvironment. Disruption of the balance between the concentration of active matalloproteinases and their inhibitors (TIMPs) may lead to pathological changes associated with uncontrolled ECM turnover, tissue remodeling, inflammatory response, cell growth and migration. This brief review presents some information on MMPs' role in inflammatory, metabolic and cancer abnormalities related to the salivary glands, as well as MMP-related aspects that lead to the formation of human dentinal caries lesions. In oral diseases, the most relevant biological fluid commonly used for diagnosing periodontal diseases is saliva. In diseased patients with significantly higher levels of MMPs in their saliva than healthy people, most extracellular matrix components undergo digestion to lower molecular weight forms. Conventional treatment successfully reduces the levels of MMPs inhibits the progressive breakdown of gingival and periodontal ligament collagens. Beside inflammatory abnormalities like Sjögren's syndrome (SS), a large group of disorders is comprised of cancers, most of them involving the parotid gland (Adv Clin Exp Med 2016, 25, 2, 383-390).

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Matrix metalloproteinases as modulators of inflammation

Cited by 505 publications

References 82 publications

Involvement of matrix metalloproteinase-2 in the development of renal interstitial fibrosis in mouse obstructive nephropathy

Involvement of matrix metalloproteinase-2 in the development of renal interstitial fibrosis in mouse obstructive nephropathy

Role of the pulmonary epithelium and inflammatory signals in acute lung injury

The Significance of Matrix Metalloproteinases in Oral Diseases

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