Middermal Elastolysis: Dermal Fibroblasts Cooperate with Inflammatory Cells to the Elastolytic Disorder

Little is known about the cause and pathophysiology of middermal elastolysis (MDE). In this condition, variable inflammatory infiltrate may be present or not together with loss of elastic fibres in the middermis that spares both papillary and lower reticular dermis. MDE may be a consequence of abnor...

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Main Authors: Giovanna De Cunto, Arianna Lamberti, Maria Margherita de Santi, Clelia Miracco, Michele Fimiani, Giuseppe Lungarella, Eleonora Cavarra
Format: Article
Language:English
Published: Wiley 2017-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2017/9524594
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author Giovanna De Cunto
Arianna Lamberti
Maria Margherita de Santi
Clelia Miracco
Michele Fimiani
Giuseppe Lungarella
Eleonora Cavarra
author_facet Giovanna De Cunto
Arianna Lamberti
Maria Margherita de Santi
Clelia Miracco
Michele Fimiani
Giuseppe Lungarella
Eleonora Cavarra
author_sort Giovanna De Cunto
collection DOAJ
description Little is known about the cause and pathophysiology of middermal elastolysis (MDE). In this condition, variable inflammatory infiltrate may be present or not together with loss of elastic fibres in the middermis that spares both papillary and lower reticular dermis. MDE may be a consequence of abnormal extracellular matrix degradation related to an imbalance between elastolytic enzymes released from inflammatory and resident cells and their naturally occurring inhibitors. However, the cause of this imbalance is still an object of investigation. In order to shed light on the role of fibroblasts in MDE, we used fibroblast cultures from MDE and control subjects to evaluate matrix metalloproteinases (MMPs) and their major inhibitor TIMP-1, which in combination with neutrophil or macrophage proteases released in inflamed areas may influence the elastolytic burden. We demonstrate that fibroblasts derived from MDE produce in vitro low levels of TIMP-1, the major inhibitor of MMPs. Elevated levels of MMP-2, MMP-14, and TIMP-2 capable to activate in a cooperative manner pro-MMP-2 are present in MDE tissue samples. Additionally, significant reaction for MMP-1 is present in the same MDE areas. These data all together suggest that ECM changes in MDE are due to cooperation of different cell populations (i.e., inflammatory cells and fibroblasts).
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spelling doaj-art-038b3b89ad8d4a5cb87b32bf7b377e4c2025-08-20T02:03:19ZengWileyMediators of Inflammation0962-93511466-18612017-01-01201710.1155/2017/95245949524594Middermal Elastolysis: Dermal Fibroblasts Cooperate with Inflammatory Cells to the Elastolytic DisorderGiovanna De Cunto0Arianna Lamberti1Maria Margherita de Santi2Clelia Miracco3Michele Fimiani4Giuseppe Lungarella5Eleonora Cavarra6Department of Molecular and Developmental Medicine, Section of General Pathology, University of Siena, Via Aldo Moro 6, 53100 Siena, ItalyDepartment of Medicine, Surgery, and Neurosciences, Unit of Dermatology, University of Siena, Viale Bracci, 53100 Siena, ItalyUnit of Pathological Anatomy, AOU Siena, Viale Bracci, 53100 Siena, ItalyDepartment of Medicine, Surgery, and Neurosciences, Unit of Pathological Anatomy, University of Siena, Viale Bracci, 53100 Siena, ItalyDepartment of Medicine, Surgery, and Neurosciences, Unit of Dermatology, University of Siena, Viale Bracci, 53100 Siena, ItalyDepartment of Molecular and Developmental Medicine, Section of General Pathology, University of Siena, Via Aldo Moro 6, 53100 Siena, ItalyDepartment of Molecular and Developmental Medicine, Section of General Pathology, University of Siena, Via Aldo Moro 6, 53100 Siena, ItalyLittle is known about the cause and pathophysiology of middermal elastolysis (MDE). In this condition, variable inflammatory infiltrate may be present or not together with loss of elastic fibres in the middermis that spares both papillary and lower reticular dermis. MDE may be a consequence of abnormal extracellular matrix degradation related to an imbalance between elastolytic enzymes released from inflammatory and resident cells and their naturally occurring inhibitors. However, the cause of this imbalance is still an object of investigation. In order to shed light on the role of fibroblasts in MDE, we used fibroblast cultures from MDE and control subjects to evaluate matrix metalloproteinases (MMPs) and their major inhibitor TIMP-1, which in combination with neutrophil or macrophage proteases released in inflamed areas may influence the elastolytic burden. We demonstrate that fibroblasts derived from MDE produce in vitro low levels of TIMP-1, the major inhibitor of MMPs. Elevated levels of MMP-2, MMP-14, and TIMP-2 capable to activate in a cooperative manner pro-MMP-2 are present in MDE tissue samples. Additionally, significant reaction for MMP-1 is present in the same MDE areas. These data all together suggest that ECM changes in MDE are due to cooperation of different cell populations (i.e., inflammatory cells and fibroblasts).http://dx.doi.org/10.1155/2017/9524594
spellingShingle Giovanna De Cunto
Arianna Lamberti
Maria Margherita de Santi
Clelia Miracco
Michele Fimiani
Giuseppe Lungarella
Eleonora Cavarra
Middermal Elastolysis: Dermal Fibroblasts Cooperate with Inflammatory Cells to the Elastolytic Disorder
Mediators of Inflammation
title Middermal Elastolysis: Dermal Fibroblasts Cooperate with Inflammatory Cells to the Elastolytic Disorder
title_full Middermal Elastolysis: Dermal Fibroblasts Cooperate with Inflammatory Cells to the Elastolytic Disorder
title_fullStr Middermal Elastolysis: Dermal Fibroblasts Cooperate with Inflammatory Cells to the Elastolytic Disorder
title_full_unstemmed Middermal Elastolysis: Dermal Fibroblasts Cooperate with Inflammatory Cells to the Elastolytic Disorder
title_short Middermal Elastolysis: Dermal Fibroblasts Cooperate with Inflammatory Cells to the Elastolytic Disorder
title_sort middermal elastolysis dermal fibroblasts cooperate with inflammatory cells to the elastolytic disorder
url http://dx.doi.org/10.1155/2017/9524594
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