Matrix Metalloproteinase-19 in Capillary Endothelial Cells: Expression in Acutely, but Not in Chronically, Inflamed Synovium

Kolb, Cornelia; Mauch, Simon; Krawinkel, Ulrich; Sedláček, Radislav

doi:10.1006/excr.1999.4493

Cited by 48 publications

(36 citation statements)

References 37 publications

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“…Sweat glands were positive for MMP-7 in most cases (data not shown), which is in accordance with our previous data (37). Positive staining for MMP-19 was found in occasional fibroblasts and endothelial cells in 4/9 samples (Table 1), in accordance with previous studies (38). MMP-19 was not detected in areas of keratinocyte apoptosis or vacuolar degeneration (data not shown).…”

Section: Skinsupporting

confidence: 92%

Overexpression of Tissue Inhibitor of Metalloproteinases-3 in Intestinal and Cutaneous Lesions of Graft-versus-Host Disease

Salmela

Karjalainen–Lindsberg

Jeskanen

et al. 2003

Modern Pathology

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Matrix metalloproteinases (MMPs) have been implicated in the pathobiology of various T-cell-mediated inflammatory disorders of the intestine and skin. Their synthetic inhibitor has been shown to prevent lethal acute graft-versus-host disease in animal models. We intended to determine the expression of MMPs 1, 3, 7, 9, 10, 12, and 19 and tissue inhibitors of metalloproteinases (TIMPs) 1 and 3 in intestinal and cutaneous lesions of patients suffering from graft-versus-host disease after bone marrow transplantation. In situ hybridizations for MMPs 1, 3, 7, 10, and 12 as well as TIMPs 1 and 3 were performed using 35 S-labeled cRNA probes on intestinal (n ‫؍‬ 13) and cutaneous specimens (n ‫؍‬ 9) from patients with graft-versus-host disease. Immunohistochemical stainings were carried out to localize MMP-9, MMP-19, TIMP-3, and TGF-␤1 proteins, and TUNEL staining, to detect apoptotic cells. TIMP-3 mRNA and protein were detected in cutaneous lesions in areas with vacuolar degeneration of the basal epidermal layer in all skin samples, and they colocalized with apoptotic keratinocytes and partly with staining for TGF-␤. None of the MMPs examined were overexpressed in skin lesions. Signals for MMP-1 and MMP-3 mRNA was found in 10/13 and 5/13 intestinal biopsies, respectively. In the gut, MMP-19 -positive epithelial cells, particularly in the crypts, were found in 10/13 samples. Expression of MMPs 7, 9, 10, and 12 was absent or very low. TIMPs 1 and 3 were expressed by stromal cells in 12/13 and 10/13 gut samples, respectively. Whereas TIMP-1 was expressed particularly by subepithelial cells where epithelium had shed away, TIMP-3 was detected in deeper areas. We conclude that MMPs are differentially regulated in the skin and gut lesions of graft-versus-host disease. In agreement with previous data on cancer cells, TIMP-3, induced by TGF-␤1, may contribute to the apoptosis of keratinocytes in cutaneous graftversus-host disease lesions, leading to typical histopathological changes. We also conclude that MMPs play a less important role as effector molecules in intestinal graft-versus-host disease than in celiac or inflammatory bowel disease.

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Section: Skinsupporting

confidence: 92%

Overexpression of Tissue Inhibitor of Metalloproteinases-3 in Intestinal and Cutaneous Lesions of Graft-versus-Host Disease

Salmela

Karjalainen–Lindsberg

Jeskanen

et al. 2003

Modern Pathology

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“…MMP-19 is coexpressed with type IV collagen in tunica media and with integrin ␣v␤3 and VEGF-R2 in endothelial cells, 12 and in our study MMP-19 was found in the area where the BM was at least partly destroyed when stained with type IV collagen. The presence of MMP-19 in p63-positive epithelium suggests that it is restricted in vivo to areas of keratinocytes with high proliferative potential and absent from cells undergoing terminal differentiation.…”

Section: Northern and Western Analyses Of Keratinocytessupporting

confidence: 69%

“…DISCUSSION MMP-19 expression has previously been associated with endothelial and smooth muscle cells of several organs in vivo. 12 We show also that cells of epithelial origin are capable of producing MMP-19. 26 Unlike several other MMPs, such as MMP-1, MMP-9 and MMP-10, 5,14 MMP-19 is not expressed by migrating keratin- 50 m (a,d,e,h,i) and 25 m (b,c,f,g,j,k-n).…”

Section: Northern and Western Analyses Of Keratinocytesmentioning

confidence: 52%

“…11 MMP-19 has been described in smooth muscle cells of the tunica media of large blood vessels, normal skin and uterine ligaments as well as in endothelial cells of acutely inflamed synovial capillaries. 12 It is also detected on the surface of activated peripheral blood mononuclear cells, TH1 lymphocytes and Jurkat T-lymphoma cells. 11 has been suggested to play a role in matrix remodeling and in the pathogenesis of rheumatoid arthritis.…”

mentioning

confidence: 99%

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Matrix metalloproteinase‐19 is expressed by proliferating epithelium but disappears with neoplastic dedifferentiation

Impola

Toriseva

Suomela

et al. 2002

Intl Journal of Cancer

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“…As examples, these observations include increases in microvascular EC expression of MMP-1 during embryonic angiogenesis and vasculogenesis 47 and MMP-9 and -19 expression in ECs of the endothelium of rheumatoid arthritis synovium. 48,49 In some cases, EC expression of MMPs is differentially regulated spatially and/or temporally during the progression of a physiologic or pathologic condition, suggesting the involvement of the MMP at particular stages of the process. For instance, the cycle-specific pattern of expression of MMP-1, -2, -3, -9, TIMP-1 and TIMP-2 that was observed in blood vessels of the endometrium implies their involvement at different stages of the angiogenic process during the menstrual cycle.…”

Section: Endogenous Inhibitors Of Metalloproteinasesmentioning

confidence: 99%

Metalloproteinases and their inhibitors in tumor angiogenesis

Handsley

Edwards

2005

Intl Journal of Cancer

260

211

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Angiogenesis is the process by which new blood vessels are formed from preexisting vasculature. It is an essential feature of the female reproductive cycle, embryonic development and wound repair. Angiogenesis has also been identified as a causal or contributing factor in several pathologies, including cancer, where it is a rate-limiting step during tumor progression. Matrix metalloproteinases (MMPs) are a family of soluble and membrane-anchored proteolytic enzymes that can degrade components of the extracellular matrix (ECM) as well as a growing number of modulators of cell function. Several of the MMPs, in particular the gelatinases and membrane-type 1 MMP (MT1-MMP), have been linked to angiogenesis. Potential roles for these proteases during the angiogenic process include degradation of the basement membrane and perivascular ECM components, unmasking of cryptic biologically relevant sites in ECM components, modulation of angiogenic factors and production of endogenous angiogenic inhibitors. This review brings together what is currently known about the functions of the MMPs and the closely related ADAM (a disintegrin and metalloproteinase domain) and ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) families in angiogenesis and considers how this information might be useful in manipulation of the angiogenic process, with a view to constraining tumor progression. ' 2005 Wiley-Liss, Inc.Key words: metalloproteinase; tumor; angiogenesis; tissue inhibitor of metalloproteinases; protease; extracellular matrix Angiogenesis is an essential feature of several physiologic processes such as the developmental growth of organs, wound healing and the female reproductive cycle. 1 It is also particularly significant in cancer progression, being a crucial step in the transition of a tumor from a hyperplastic but contained in situ state to a malignant phenotype. 2,3 To allow its growth beyond a certain critical size, a solid avascular tumor must develop its own blood supply in order to meet its growing metabolic requirements. 1 Vascularization of a tumor also provides a route for dissemination of the tumor cells to different sites around the body.Although angiogenesis appears to be the primary form of tumor vascularization, the malignant cells of a tumor can gain access to a blood supply through other means, such as via tumor-induced vasculogenesis, in which bone marrow-derived precursor endothelial cells contribute to the formation of tumor vessels. 4,5 Vasculogenic mimicry is another form of vessel formation that has been reported in certain tumor types, such as aggressive human uveal melanomas, prostate and breast tumors. [6][7][8] In these cases, networks of tumor cell-lined vascular channels were identified within the tumors. Finally, vessel co-option, implemented by tumor cells as a temporary means of gaining access to a blood supply, involves the tumor cells growing around and thus co-opting existing host vessels to form an initially well-vascularized tumor. 9 This review will highlight new insigh...

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Matrix Metalloproteinase-19 in Capillary Endothelial Cells: Expression in Acutely, but Not in Chronically, Inflamed Synovium

Cited by 48 publications

References 37 publications

Overexpression of Tissue Inhibitor of Metalloproteinases-3 in Intestinal and Cutaneous Lesions of Graft-versus-Host Disease

Overexpression of Tissue Inhibitor of Metalloproteinases-3 in Intestinal and Cutaneous Lesions of Graft-versus-Host Disease

Matrix metalloproteinase‐19 is expressed by proliferating epithelium but disappears with neoplastic dedifferentiation

Metalloproteinases and their inhibitors in tumor angiogenesis

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