59
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Role of Matrix Metalloproteinases in Photoaging and Photocarcinogenesis

      review-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Matrix metalloproteinases (MMPs) are zinc-containing endopeptidases with an extensive range of substrate specificities. Collectively, these enzymes are able to degrade various components of extracellular matrix (ECM) proteins. Based on their structure and substrate specificity, they can be categorized into five main subgroups, namely (1) collagenases (MMP-1, MMP-8 and MMP-13); (2) gelatinases (MMP-2 and MMP-9); (3) stromelysins (MMP-3, MMP-10 and MMP-11); (4) matrilysins (MMP-7 and MMP-26); and (5) membrane-type (MT) MMPs (MMP-14, MMP-15, and MMP-16). The alterations made to the ECM by MMPs might contribute in skin wrinkling, a characteristic of premature skin aging. In photocarcinogenesis, degradation of ECM is the initial step towards tumor cell invasion, to invade both the basement membrane and the surrounding stroma that mainly comprises fibrillar collagens. Additionally, MMPs are involved in angiogenesis, which promotes cancer cell growth and migration. In this review, we focus on the present knowledge about premature skin aging and skin cancers such as basal cell carcinoma (BCC), squamous cell carcinoma (SCC), and melanoma, with our main focus on members of the MMP family and their functions.

          Related collections

          Most cited references92

          • Record: found
          • Abstract: found
          • Article: not found

          Tumor-associated macrophage-induced invasion and angiogenesis of human basal cell carcinoma cells by cyclooxygenase-2 induction.

          Tumor-associated macrophages (TAMs) and cyclooxygenase-2 (COX-2) are associated with invasion, angiogenesis, and poor prognosis in many human cancers. However, the role of TAMs in human basal cell carcinoma (BCC) remains elusive. We found that the number of TAMs infiltrating the tumor is correlated with the depth of invasion, microvessel density, and COX-2 expression in human BCC cells. TAMs also aggregate near COX-2 expressing BCC tumor nests. We hypothesize that TAMs might activate COX-2 in BCC cells and subsequently increase their invasion and angiogenesis. TAMs are a kind of M2 macrophage derived from macrophages exposed to Th2 cytokines. M2-polarized macrophages derived from peripheral blood monocytes were cocultured with BCC cells without direct contact. Coculture with the M2 macrophages induced COX-2-dependent invasion and angiogenesis of BCC cells. Human THP-1 cell line cells, after treated with phorbol myristate acetate (PMA), differentiated to macrophages with M2 functional profiles. Coculture with PMA-treated THP-1 macrophages induced COX-2-dependent release of matrix metalloproteinase-9 and subsequent increased invasion of BCC cells. Macrophages also induced COX-2-dependent secretion of basic fibroblast growth factor and vascular endothelial growth factor-A, and increased angiogenesis in BCC cells.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Matrix metalloproteinase-1 is the major collagenolytic enzyme responsible for collagen damage in UV-irradiated human skin.

            Punch biopsies of human skin were obtained 1 day after irradiation with two minimal-erythema doses (MED) from either a UVB light source or a Solar Simulator and incubated in organ culture for 72 h. Organ culture fluids obtained at 24, 48 and 72 h were analyzed for collagenolytic activity and for reactivity with antibodies to matrix metalloproteinase-1 (MMP-1; interstitial collagenase) and MMP-13 (collagenase-3). High levels of collagenolytic activity were seen in organ culture fluid from skin exposed to either light source. MMP-1 was strongly induced in parallel, increasing from less than 100 ng/ml in organ culture fluid from control skin to approximately 1.1 microg/ml in culture fluid from UV-treated skin. Whereas most of the detectable MMP-1 in control culture fluid was represented by the latent form of the enzyme, approximately 50% of the enzyme was present as the active form in organ culture fluid of UV-exposed skin. In contrast, there was no detectable MMP-13 in control organ culture fluid and very little change after UV exposure (less than 100 ng/ml in both cases). Finally, neutralization studies with a blocking antibody to MMP-1 removed 95 +/- 4% of the collagenolytic activity in the organ culture fluid from UV-treated skin. These findings strongly implicate MMP-1 rather than MMP-13 as the major collagenolytic enzyme responsible for collagen damage in photoaging.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Hypoxia influences vasculogenic mimicry channel formation and tumor invasion-related protein expression in melanoma.

              Hypoxia can enhance tumor cell invasion and metastasis. The cause and the molecular mechanism are still not clear. In our study, mouse melanoma B16 cells were inoculated into mouse ischemic limbs and non-ischemic controls and the engrafted melanomas were subsequently observed. Vasculogenic mimicry channels in melanoma tumors of the two groups were counted and the expression of HIF-1alpha, MMP-2, MMP-9 and VEGF was assessed by immunohistochemical staining. Formalin-fixed, paraffin-embedded tissues were used for immunohistochemical staining. In the early stage of engrafted melanoma growth, the size of melanomas in ischemic limbs increased slower than in the controls. However, later there was no obvious difference in their size. Melanoma tumors in the ischemic group had more vasculogenic mimicry channels than those in the controls (P=0.039). Similarly, the expression of HIF-1alpha, MMP-2, MMP-9 and VEGF was higher in the ischemic group than in the non-ischemic controls (P=0.024, 0.047, 0.007 and 0.025, respectively). There was a positive association in melanoma cells of the ischemic group between expression of HIF-1alpha and VEGF, and also between MMP-9 and MMP-2. In the ischemic group, there was statistical significance for the correlation between HIF-1alpha and VEGF expression (r=0.456, P=0.038). Furthermore, MMP-2 expression was positively correlated with MMP-9 and VEGF expression (r=0.589 and 0.502, P=0.008 and 0.024, respectively). Melanoma cells in a hypoxic microenvironment increased HIF-1alpha expression and induced the formation of vasculogenic mimicry channels to acquire an adequate blood supply. On the other hand, the expression of MMP-2 and MMP-9 in tumor tissue increased to enhance the invasiveness. HIF-1alpha, MMP-2 and MMP-9 may be associated with the failure of stop-flow perfusion in some patients with melanoma.
                Bookmark

                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                Int J Mol Sci
                Int J Mol Sci
                ijms
                International Journal of Molecular Sciences
                MDPI
                1422-0067
                02 June 2016
                June 2016
                : 17
                : 6
                : 868
                Affiliations
                [1 ]Division of Dermatology, Chulabhorn International College of Medicine, Thammasat University, Pathum Thani 12000, Thailand; p_ha_r@ 123456hotmail.com (P.P.); kae_mdcu@ 123456yahoo.com (J.M.); chad_naja@ 123456hotmail.com (O.P.)
                [2 ]Department of Dermatology, Jichi Medical University, Tochigi 329-0498, Japan; mamitaro@ 123456jichi.ac.jp
                Author notes
                [* ]Correspondence: mkomine12@ 123456jichi.ac.jp ; Tel.: +81-285-58-7360
                [†]

                These authors contributed equally to this work.

                Article
                ijms-17-00868
                10.3390/ijms17060868
                4926402
                27271600
                c993b0f5-d89d-4f35-ac4a-8512b073eac3
                © 2016 by the authors; licensee MDPI, Basel, Switzerland.

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC-BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 14 April 2016
                : 30 May 2016
                Categories
                Review

                Molecular biology
                matrix metalloproteinase (mmp),photoaging,photocarcinogenesis,basal cell carcinoma,squamous cell carcinoma,malignant melanoma

                Comments

                Comment on this article