Inflammation in stasis dermatitis upregulates MMP-1, MMP-2 and MMP-13 expression

Herouy, Yared; Mellios, P; Bandemir, E; Dichmann, Stefan; Nockowski, Piotr; Schöpf, Erwin; Norgauer, Johannes

doi:10.1016/s0923-1811(00)00128-6

Cited by 63 publications

(64 citation statements)

References 30 publications

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“…These morphological changes are linked to alterations in the activities of both MMP and their counterregulatory inhibitors, TIMP. The MMP are a group of zinc-dependent endopeptidases, which are capable of digesting the ECM and basement membrane [12][13][14].…”

Section: Discussionmentioning

confidence: 99%

“…The recruitment of circulating polymorphonuclear leukocytes (e.g. neutrophils and macrophages) into inflammatory sites involves traversing both the capillary walls and the interstitium [12,13]. To traverse these barriers, inflammatory cells adhere to endothelial cells and degrade extracellular matrix (ECM) proteins [12,13].…”

mentioning

confidence: 99%

“…neutrophils and macrophages) into inflammatory sites involves traversing both the capillary walls and the interstitium [12,13]. To traverse these barriers, inflammatory cells adhere to endothelial cells and degrade extracellular matrix (ECM) proteins [12,13]. The degradation of ECM proteins, including basement membrane proteins, is regulated by matrix metalloproteinases (MMP) and their inhibitors (tissue inhibitors of metalloproteinases (TIMP)), which are secreted by a wide variety of cells, including inflammatory cells, epithelial cells and fibroblasts, in response to inflammatory stimuli [13,14].…”

mentioning

confidence: 99%

“…To traverse these barriers, inflammatory cells adhere to endothelial cells and degrade extracellular matrix (ECM) proteins [12,13]. The degradation of ECM proteins, including basement membrane proteins, is regulated by matrix metalloproteinases (MMP) and their inhibitors (tissue inhibitors of metalloproteinases (TIMP)), which are secreted by a wide variety of cells, including inflammatory cells, epithelial cells and fibroblasts, in response to inflammatory stimuli [13,14]. However, currently, the influence of macrolide antibiotics on MMP and TIMP production is not fully understood [15].…”

mentioning

confidence: 99%

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Suppression of matrix metalloproteinase production from nasal fibroblasts by macrolide antibioticsin vitro

Kanai¹,

Asano²,

Hisamitsu³

et al. 2004

Eur Respir J

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It is well known that low-dose and long-term administration of macrolide antibiotics favourably modify the clinical status of chronic airway inflammatory diseases. However, the therapeutic mode of action of macrolide antibiotics is not well understood. The present study aimed to examine the influence of macrolide antibiotics, roxithromycin (RXM) and josamycin (JM) on matrix metalloproteinase (MMP) production from nasal polyp fibroblasts (NPF) in vitro.NPF, at a concentration of 2.5610 5 cells?mL -1 , were stimulated with tumour necrosis factor (TNF)-a in the presence of various concentrations of RXM or JM for 24 h. MMP-2 and -9 levels in culture supernatants were analysed by ELISA, and MMP mRNA expression was examined by RT-PCR. The influence of RXM on nuclear factor (NF)-kB and activator protein (AP)-1 activation was also examined.Addition of RXM (but not JM) at 5.0 and 7.5 mg?mL -1 significantly suppressed the production of MMP-2 and -9 from NPF induced by TNF-a stimulation. RXM also suppressed MMP mRNA expression through the inhibition of NF-kB and AP-1 activation.The present results suggest that the suppressive activity of roxithromycin on MMP-2 and -9 production is, in part, responsible for the therapeutic action of macrolides on chronic airway inflammatory diseases. Eur Respir J 2004; 23: 671-678.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Suppression of matrix metalloproteinase production from nasal fibroblasts by macrolide antibioticsin vitro

Kanai¹,

Asano²,

Hisamitsu³

et al. 2004

Eur Respir J

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“…34 An early study by Saito et al 23 suggested that increased MMP-2 levels affect tissue remodeling and contribute to a proulcer environment. Subsequently, Herouy et al 41 examined stasis dermatitis, a common consequence of impaired venous drainage characterized by dermal neovascularization, and noted elevated MMP-1, 22, and 213 and diminished TIMP-1 and 22 in the skin lesions. More recently, Xu et al 40 showed that specific polymorphisms in the MMP-9 and TIMP-2 genes potentially put patients at a higher risk for developing varicose veins.…”

Section: Mmpsmentioning

confidence: 99%

Genetic polymorphisms of vein wall remodeling in chronic venous disease: a narrative and systematic review

Bharath

Kahn

Lazo‐Langner

2014

Blood

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Chronic venous disease encompasses a spectrum of disorders caused by an abnormal venous system. They include chronic venous insufficiency, varicose veins, lipodermatosclerosis, postthrombotic syndrome, and venous ulceration. Some evidence suggests a genetic predisposition to chronic venous disease from gene polymorphisms associated mainly with vein wall remodeling. The literature exploring these polymorphisms has not been reviewed and compiled thus far. In this narrative and systematic review, we present the current evidence available on the role of polymorphisms in genes involved in vein wall remodeling and other pathways as contributors to chronic venous disease. We searched the EMBASE, Medline, and PubMed databases from inception to 2013 for basic science or clinical studies relating to genetic associations in chronic venous disease and obtained 38 relevant studies for this review. Important candidate genes/proteins include the matrix metalloproteinases (extracellular matrix degradation), vascular endothelial growth factors (angiogenesis and vessel wall integrity), FOXC2 (vascular development), hemochromatosis (involved in venous ulceration and iron absorption), and various types of collagen (contributors to vein wall strength). The data on associations between these genes/proteins and the postthrombotic syndrome are limited and additional studies are required. These associations might have future prognostic and therapeutic implications.

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Inflammation

Steinhoff¹,

Griffiths²,

Church³

et al. 2004

Rook's Textbook of Dermatology

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Inflammation in stasis dermatitis upregulates MMP-1, MMP-2 and MMP-13 expression

Cited by 63 publications

References 30 publications

Suppression of matrix metalloproteinase production from nasal fibroblasts by macrolide antibioticsin vitro

Suppression of matrix metalloproteinase production from nasal fibroblasts by macrolide antibioticsin vitro

Genetic polymorphisms of vein wall remodeling in chronic venous disease: a narrative and systematic review

Inflammation

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