Human endothelial gelatinases and angiogenesis

Nguyen, Minh Vu Chuong

doi:10.1016/s1357-2725(01)00007-3

Cited by 269 publications

(219 citation statements)

References 62 publications

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“…In response to angiogenic stimuli, endothelial cells degrade the basement membrane by secreting proteolytic enzymes that include metalloproteinases (MMPs) and serine proteases [1,2,37]. The cells then migrate through the degraded basement membrane and continue to break down the interstitial stroma as they move.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to proteolytic enzyme secretion and migration, tube morphogenesis depends on endothelial cell proliferation [1,2,37,38]. Analysis of cell growth and cell cycle profile upon TO-IFI16 infection suggests that sustained expression of IFI16 affects HUVEC proliferation.…”

Section: Discussionmentioning

confidence: 99%

“…HUVEC cultured on a Matrigel rapidly align, extend processes into the matrix, and, finally, form capillary-like structures [37,38]. These structures are composed of polarized cells connected via complex junctions surrounding a central lumen.…”

Section: Inhibition Of Huvec Chemotaxis Invasion and Tube Morphogenmentioning

confidence: 99%

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The interferon-inducible IFI16 gene inhibits tube morphogenesis and proliferation of primary, but not HPV16 E6/E7-immortalized human endothelial cells

Ravera

Gioia

Andrea

et al. 2004

Experimental Cell Research

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Immunohistochemical analysis has demonstrated that the human IFI16 gene, in addition to the hematopoietic tissues, is highly expressed in endothelial cells and squamous stratified epithelia. In this study, we have developed a reliable HSV-derived replication-defective vector (TO-IFI16) to efficiently transduce IFI16 into primary human umbilical vein endothelial cells (HUVEC), which are usually poorly transfectable. HUVEC infection with TO-IFI16 virus suppressed endothelial migration, invasion and formation of capillary-like structures in vitro. In parallel, sustained IFI16 expression inhibited HUVEC cell cycle progression, accompanied by significant induction of p53, p21, and hypophosphorylated pRb. Further support for the involvement of these pathways in IFI16 activity came from the finding that infection with TO-IFI16 virus does not impair the in vitro angiogenic activity and cell cycle progression of HUVEC immortalized by HPV16 E6/E7 oncogenes, which are known to inactivate both p53 and pRb systems. This use of a reliable viral system for gene delivery into primary human endothelial cells assigns a potent angiostatic activity to an IFN-inducible gene, namely IFI16, and thus throws further light on antiangiogenic therapy employing IFNs. D

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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The interferon-inducible IFI16 gene inhibits tube morphogenesis and proliferation of primary, but not HPV16 E6/E7-immortalized human endothelial cells

Ravera

Gioia

Andrea

et al. 2004

Experimental Cell Research

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“…26,27 MMPs-2 and Ϫ9, also known as gelatinases, are important proteases that degrade the components present both in basement membranes, such as type IV collagen and laminin, 15,36 and in the interstitial extracellular matrix, particularly the fragments derived from the proteolysis of type I fibrillar collagen, denominated gelatins. 18,36 MMP-2 has been observed by immunohistochemistry in OKC epithelial basement membranes, 33 by in situ hybridization in OKC connective tissue fibroblasts, 33 by western immunoblotting and gelatin zymography in cultured fibroblasts, 32 and in co-cultured OKC epithelial cells and fibroblasts. 34 In light of these findings, MMP-2 has been implied in the degradation of the extracellular matrix surrounding OKCs.…”

Section: Table II Immunoreactivity To Matrix Metalloproteinases In Omentioning

confidence: 99%

Immunohistochemical expression of MMPs 1, 7, and 26 in syndrome and nonsyndrome odontogenic keratocysts

Cavalcante

Pereira

Nonaka

et al. 2008

Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, an

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Objective. The objective of this study was to analyze the expression of matrix metalloproteinases (MMPs) 1, 7, and 26 in odontogenic keratocysts (OKCs) associated with Gorlin syndrome (SOKCs) and nonsyndrome OKCs (NSOKCs). Study design. Twenty-one SOKCs and 20 NSOKCs were evaluated for epithelial expression of MMP-1, MMP-7, and MMP-26 and for mesenchymal expression of MMP-1 by immunohistochemistry. Results. Strong epithelial positivity to MMP-1 was observed in 76% of SOKCs and in 15% of NSOKCs (P Ͻ .05). Strong mesenchymal immunoreactivity to MMP-1 was observed in 38% of SOKCs and in 20% of NSOKCs (P Ͼ .05). Epithelial immunoreactivity to MMP-7 was strongly positive in 67% of SOKCs and in 40% of NSOKCs (P Ͼ .05). For MMP-26, strong positivity was found in 62% of SOKCs, in contrast to 35% of NSOKCs (P Ͼ .05). Conclusion. MMPs-1, Ϫ7 and Ϫ26 may play important roles in the biology of OKCs. Furthermore, the presence of these proteases at higher levels in SOKCs may help to explain increased OKC aggressiveness associated with nevoid basal cell carcinoma syndrome.

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“…Angiogenesis plays a role in non-pathological conditions, like the reproductive cycle in women, wound healing as well as placental development. In these conditions, angiogenesis is strictly regulated [2]. Dysregulation of angiogenesis may lead to pathological conditions like: rheumatoid arthritis, diabetic retinopathy and psoriasis [3,4].…”

Section: Introductionmentioning

confidence: 99%

The possible role of matrix metalloproteinase (MMP)-2 and MMP-9 in cancer, e.g. acute leukemia

Klein

Vellenga

Fraaije

et al. 2004

Critical Reviews in Oncology/Hematology

311

170

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Human endothelial gelatinases and angiogenesis

Cited by 269 publications

References 62 publications

The interferon-inducible IFI16 gene inhibits tube morphogenesis and proliferation of primary, but not HPV16 E6/E7-immortalized human endothelial cells

The interferon-inducible IFI16 gene inhibits tube morphogenesis and proliferation of primary, but not HPV16 E6/E7-immortalized human endothelial cells

Immunohistochemical expression of MMPs 1, 7, and 26 in syndrome and nonsyndrome odontogenic keratocysts

The possible role of matrix metalloproteinase (MMP)-2 and MMP-9 in cancer, e.g. acute leukemia

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