UVA-mediated down-regulation of MMP-2 and MT1-MMP coincides with impaired angiogenic phenotype of human dermal endothelial cells

Cauchard, Jean-Hubert; Robinet, Arnaud; Poitevin, Stephane; Bobichon, Helene; Maziere, Jean-Claude; Bellon, Georges; Hornebeck, William

doi:10.1016/j.bbrc.2006.04.115

Title: UVA-mediated down-regulation of MMP-2 and MT1-MMP coincides with impaired angiogenic phenotype of human dermal endothelial cells

Full Record
Other Related Research

Abstract

UVA irradiation, dose-dependently (5-20 J/cm{sup 2}), was shown to impair the morphogenic differentiation of human microvascular endothelial cells (HMECs) on Matrigel. Parallely, UVA down-regulated the expression of MMP-2 and MT1-MMP, both at the protein and the mRNA levels. On the contrary, the production of MMP-1 and TIMP-1 by HMECs increased following UVA treatment. The inhibitory effect of UVA on MMP expression and pseudotubes formation was mediated by UVA-generated singlet oxygen ({sup 1}O{sub 2}). The contribution of MT1-MMP, but not TIMP-1, to the regulation of HMECs' angiogenic phenotype following UVA irradiation was suggested using elastin-derived peptides and TIMP-1 blocking antibody, respectively.

Authors:

Cauchard, Jean-Hubert ^[1]; Robinet, Arnaud ^[1]; Poitevin, Stephane ^[2]; Bobichon, Helene ^[3]; Maziere, Jean-Claude ^[4]; Bellon, Georges ^[1]; Hornebeck, William ^[1]

CNRS UMR 6198, IFR 53 Biomolecules, Faculty of Medicine, 51, rue Cognacq Jay, Reims 51100 (France)
EA 3796, IFR53 'Biomolecules', Faculty of Medicine, Reims (France)
CNRS UMR 6142, IFR53 'Biomolecules', Faculty of Medicine, Reims (France)
EA2087, North Hospital, Amiens (France)

Publication Date:: Fri Jun 30 00:00:00 EDT 2006

OSTI Identifier:: 20854327

Resource Type:: Journal Article

Journal Name:: Biochemical and Biophysical Research Communications

Additional Journal Information:: Journal Volume: 345; Journal Issue: 2; Other Information: DOI: 10.1016/j.bbrc.2006.04.115; PII: S0006-291X(06)00856-4; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X

Country of Publication:: United States

Language:: English

Subject:: 60 APPLIED LIFE SCIENCES; ANTIBODIES; GENE REGULATION; IRRADIATION; PEPTIDES; PHENOTYPE; RADIATION DOSES; ULTRAVIOLET RADIATION

Citation Formats


                    Cauchard, Jean-Hubert, Robinet, Arnaud, Poitevin, Stephane, Bobichon, Helene, Maziere, Jean-Claude, Bellon, Georges, and Hornebeck, William. UVA-mediated down-regulation of MMP-2 and MT1-MMP coincides with impaired angiogenic phenotype of human dermal endothelial cells.  United States: N. p., 2006. 
        Web.  doi:10.1016/j.bbrc.2006.04.115.

Copy to clipboard


                    Cauchard, Jean-Hubert, Robinet, Arnaud, Poitevin, Stephane, Bobichon, Helene, Maziere, Jean-Claude, Bellon, Georges, & Hornebeck, William. UVA-mediated down-regulation of MMP-2 and MT1-MMP coincides with impaired angiogenic phenotype of human dermal endothelial cells.  United States.  https://doi.org/10.1016/j.bbrc.2006.04.115

Copy to clipboard


                    Cauchard, Jean-Hubert, Robinet, Arnaud, Poitevin, Stephane, Bobichon, Helene, Maziere, Jean-Claude, Bellon, Georges, and Hornebeck, William. 2006.  
        "UVA-mediated down-regulation of MMP-2 and MT1-MMP coincides with impaired angiogenic phenotype of human dermal endothelial cells".  United States.  https://doi.org/10.1016/j.bbrc.2006.04.115.

Copy to clipboard


                    
@article{osti_20854327,

  title        = {UVA-mediated down-regulation of MMP-2 and MT1-MMP coincides with impaired angiogenic phenotype of human dermal endothelial cells},

  author       = {Cauchard, Jean-Hubert and Robinet, Arnaud and Poitevin, Stephane and Bobichon, Helene and Maziere, Jean-Claude and Bellon, Georges and Hornebeck, William},

  abstractNote = {UVA irradiation, dose-dependently (5-20 J/cm{sup 2}), was shown to impair the morphogenic differentiation of human microvascular endothelial cells (HMECs) on Matrigel. Parallely, UVA down-regulated the expression of MMP-2 and MT1-MMP, both at the protein and the mRNA levels. On the contrary, the production of MMP-1 and TIMP-1 by HMECs increased following UVA treatment. The inhibitory effect of UVA on MMP expression and pseudotubes formation was mediated by UVA-generated singlet oxygen ({sup 1}O{sub 2}). The contribution of MT1-MMP, but not TIMP-1, to the regulation of HMECs' angiogenic phenotype following UVA irradiation was suggested using elastin-derived peptides and TIMP-1 blocking antibody, respectively.},

  doi          = {10.1016/j.bbrc.2006.04.115},

  url          = {https://www.osti.gov/biblio/20854327},
  journal      = {Biochemical and Biophysical Research Communications},

  issn         = {0006-291X},

  number       = 2,

  volume       = 345,

  place        = {United States},

  year         = {Fri Jun 30 00:00:00 EDT 2006},

  month        = {Fri Jun 30 00:00:00 EDT 2006}

}

Copy to clipboard

Journal Article:

https://doi.org/10.1016/j.bbrc.2006.04.115

Other availability

Find in Google Scholar

Search WorldCat to find libraries that may hold this journal

Save / Share:

Export Metadata

Save to My Library

Similar records in OSTI.GOV collections:

Dextran-shelled oxygen-loaded nanodroplets reestablish a normoxia-like pro-angiogenic phenotype and behavior in hypoxic human dermal microvascular endothelium

Journal Article Basilico, Nicoletta; Magnetto, Chiara; D'Alessandro, Sarah; ... - Toxicology and Applied Pharmacology

In chronic wounds, hypoxia seriously undermines tissue repair processes by altering the balances between pro-angiogenic proteolytic enzymes (matrix metalloproteinases, MMPs) and their inhibitors (tissue inhibitors of metalloproteinases, TIMPs) released from surrounding cells. Recently, we have shown that in human monocytes hypoxia reduces MMP-9 and increases TIMP-1 without affecting TIMP-2 secretion, whereas in human keratinocytes it reduces MMP-2, MMP-9, and TIMP-2, without affecting TIMP-1 release. Provided that the phenotype of the cellular environment is better understood, chronic wounds might be targeted by new oxygenating compounds such as chitosan- or dextran-shelled and 2H,3H-decafluoropentane-cored oxygen-loaded nanodroplets (OLNs). Here, we investigated the effects ofmore »« less
https://doi.org/10.1016/J.TAAP.2015.08.005
Human papillomavirus causes an angiogenic switch in keratinocytes which is sufficient to alter endothelial cell behavior

Journal Article Chen, W; Li, F; Mead, L; ... - Virology

One of the requirements for tumor growth is the ability to recruit a blood supply, a process known as angiogenesis. Angiogenesis begins early in the progression of cervical disease from mild to severe dysplasia and on to invasive cancer. We have previously reported that expression of human papillomavirus type 16 E6 and E7 (HPV16 E6E7) proteins in primary foreskin keratinocytes (HFKs) decreases expression of two inhibitors and increases expression of two angiogenic inducers [Toussaint-Smith, E., Donner, D.B., Roman, A., 2004. Expression of human papillomavirus type 16 E6 and E7 oncoproteins in primary foreskin keratinocytes is sufficient to alter the expressionmore »« less
https://doi.org/10.1016/j.virol.2007.05.030
Suppression of alpha-tocopherol ether-linked acetic acid in VEGF-induced angiogenesis and the possible mechanisms in human umbilical vein endothelial cells

Journal Article Chuang, Cheng-Hung; Liu, Chia-Hua; Lu, Ta-Jung; ... - Toxicology and Applied Pharmacology

Alpha-tocopherol ether-linked acetic acid (α-TEA) has been reported to exhibit both anti-tumor and anti-metastatic activities in cell culture and animal studies. However, it is unclear whether α-TEA possesses anti-angiogenic effects. In this study, we investigated the effect of α-TEA on vascular endothelial growth factor (VEGF)-induced angiogenesis and matrix metalloproteinase (MMP) expression both in vitro and ex vivo. We found that the α-TEA inhibited tube formation, invasion, and migration in human umbilical vein endothelial cells (HUVECs) and that such actions were accompanied by reduced expression of MMP-2. α-TEA also inhibited ex vivo angiogenesis, as indicated by chicken egg chorioallantoic membrane assay.more »« less
https://doi.org/10.1016/J.TAAP.2014.10.018
MT1-MMP promotes cell growth and ERK activation through c-Src and paxillin in three-dimensional collagen matrix

Journal Article Takino, Takahisa; Tsuge, Hisashi; Ozawa, Terumasa; ... - Biochemical and Biophysical Research Communications

Membrane-type 1 matrix metalloproteinase (MT1-MMP) is essential for tumor invasion and growth. We show here that MT1-MMP induces extracellular signal-regulated kinase (ERK) activation in cancer cells cultured in collagen gel, which is indispensable for their proliferation. Inhibition of MT1-MMP by MMP inhibitor or small interfering RNA suppressed activation of focal adhesion kinase (FAK) and ERK in MT1-MMP-expressing cancer cells, which resulted in up-regulation of p21{sup WAF1} and suppression of cell growth in collagen gel. Cell proliferation was also abrogated by the inhibitor against ERK pathway without affecting FAK phosphorylation. MT1-MMP and integrin {alpha}{sub v}{beta}{sub 3} were shown to be involvedmore »« less
https://doi.org/10.1016/J.BBRC.2010.05.059
RNA interference screening identifies clathrin-B and cofilin-1 as mediators of MT1-MMP in endometrial cancer

Journal Article Baker, Tabari; Waheed, Sana; Syed, Viqar - Experimental Cell Research

The matrix metalloproteinases (MMPs) are implicated in tumor invasion and metastasis. Given their multiple tumor promoting roles, MMPs are promising targets for the treatment of metastatic cancer. Using a siRNA library screen of 140 membrane trafficking genes, we identified 41 genes in HEC-1B and 36 in Ishikawa cancer cells that decreased metalloproteinases activity. The 16 genes common in both cancer cell lines that decreased MMPs activity are involved in cargo sorting, vesicle formation and vesicle recycling. The top two genes clathrin-B and cofilin-1 were chosen for post hoc functional studies. Higher expression of both genes was confirmed in cancer cellsmore »« less
https://doi.org/10.1016/J.YEXCR.2018.07.031

Similar Records