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Paw Skin as a Translational Model for Investigating Fibrotic and Inflammatory Wound Healing Defects in Recessive Dystrophic Epidermolysis Bullosa
(MDPI AG, 2025-04-30)
DE GREGORIO CONCHA, CRISTIAN ALEJANDRO
;
Giselle Ramos-Gonzalez
;
Bernardo Morales-Catalán
;
EZQUER, EDUARDO FERNANDO
;
EZQUER, EDUARDO MARCELO
Recessive dystrophic epidermolysis bullosa (RDEB) is a severe genetic disease caused by COL7A1 mutations. It leads to skin fragility, chronic inflammation, and impaired wound healing. The condition often results in fibrotic scarring, pseudosyndactyly, and cutaneous squamous cell carcinoma (SCC). However, current animal models fail to fully replicate chronic RDEB wounds. In this study, we used Collagen VII-hypomorphic mice (Col7a1flNeo/flNeo) and created full-thickness wounds on their paw skin, an area prone to fibrosis due to mechanical stress. We analyzed the healing process using histology, immunofluorescence, and electron microscopy. The RDEB mice showed delayed wound closure, increased inflammation, and poor granulation tissue formation. At 30 days post-injury, we observed persistent fibrosis, with elevated levels of Collagen I, α-SMA+ myofibroblasts, and tenascin-C. These mice also had fewer intraepidermal nerve fibers, which may help explain the neuropathic pain associated with RDEB. Our model reproduces the main features of chronic RDEB wounds. It offers a useful tool for evaluating therapies aimed at reducing inflammation, fibrosis, and tumor risk in these patients.
Scopus© Citations 3 4
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Is Frontal Fibrosing Alopecia Connected to Sunscreen Usage?
(2024)
Rohan Shah
;
LARRONDO GALVEZ, JORGE FELIPE
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Fibrotic response induced by angiotensin-II requires NAD(P)H oxidase-induced reactive oxygen species (ROS) in skeletal muscle cells
(2011)
Claudio Cabello-Verrugio
;
María José Acuña
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María Gabriela Morales
;
Alvaro Becerra
;
Felipe Simon
Scopus© Citations 65 1
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Angiotensin II-induced pro-fibrotic effects require p38MAPK activity and transforming growth factor beta 1 expression in skeletal muscle cells
(2012)
María Gabriela Morales
;
Yaneisi Vazquez
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María José Acuña
;
Juan Carlos Rivera
;
Felipe Simon
9Scopus© Citations 77
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CTGF/CCN‐2 over‐expression can directly induce features of skeletal muscle dystrophy
(2011)
María Gabriela Morales
;
Claudio Cabello‐Verrugio
;
Cristian Santander
;
Daniel Cabrera
;
Roel Goldschmeding
<jats:title>Abstract</jats:title><jats:p>Muscular dystrophies are diseases characterized by muscle weakness together with cycles of degeneration and regeneration of muscle fibres, resulting in a progressive decrease of muscle mass, diminished muscle force generation and an increase in fibrosis. Fibrotic disorders are the endpoint of many chronic diseases in different tissues, where accumulation of the extracellular matrix (ECM) occurs. Connective tissue growth factor CTGF/CCN2, which is over‐expressed in muscular dystrophies, plays a major role in many progressive scarring conditions. To test the hypothesis that CTGF might not only contribute conversion of already damaged muscle into scar tissue, but that it could by itself also directly contribute to skeletal muscle deterioration, we evaluated the effect of CTGF over‐expression in tibialis anterior muscle of wild‐type mice, using an adenovirus containing the <jats:italic>CTGF</jats:italic> mouse sequence (Ad–mCTGF). CTGF over‐expression induced extensive skeletal muscle damage, which was followed by a massive regeneration of the damaged muscle, as evidenced by increased embryonic myosin and fibres with centrally located nuclei. It also induced strong fibrosis with increased levels of fibronectin, collagen, decorin and α‐smooth muscle actin (α‐SMA). Moreover, CTGF over‐expression caused a decrease of the specific isometric contractile force. Strikingly, when CTGF over‐expression stopped, the entire phenotype proved to be reversible, in parallel with normalization of CTGF levels. Thus, CTGF not merely acts downstream of muscle injury but also contributes directly to the deterioration of skeletal muscle phenotype and function. Moreover, normalization of expression levels led to spontaneous reversal of the CTGF‐induced phenotype and to full recovery of muscle structure. These observations underscore the importance of CTGF in the pathophysiology of muscular dystrophies and suggest that targeting CTGF might have significant potential in the development of novel therapies for Duchenne muscular dystrophy and related diseases. Copyright © 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</jats:p>
1Scopus© Citations 101
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Maintenance of chronicity signatures in fibroblasts isolated from recessive dystrophic epidermolysis bullosa chronic wound dressings under culture conditions
(2023)
DE GREGORIO CONCHA, CRISTIAN ALEJANDRO
;
Evelyng Catalán
;
Gabriel Garrido
;
Pilar Morandé
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CASTILLO BENNETT, JIMENA VICTORIA
<jats:title>Abstract</jats:title><jats:sec> <jats:title>Background</jats:title> <jats:p>Recessive Dystrophic Epidermolysis Bullosa (RDEB) is a rare inherited skin disease caused by variants in the <jats:italic>COL7A1</jats:italic> gene, coding for type VII collagen (C7), an important component of anchoring fibrils in the basement membrane of the epidermis. RDEB patients suffer from skin fragility starting with blister formation and evolving into chronic wounds, inflammation and skin fibrosis, with a high risk of developing aggressive skin carcinomas. Restricted therapeutic options are limited by the lack of in vitro models of defective wound healing in RDEB patients.</jats:p> </jats:sec><jats:sec> <jats:title>Results</jats:title> <jats:p>In order to explore a more efficient, non-invasive in vitro model for RDEB studies, we obtained patient fibroblasts derived from discarded dressings) and examined their phenotypic features compared with fibroblasts derived from non-injured skin of RDEB and healthy-donor skin biopsies. Our results demonstrate that fibroblasts derived from RDEB chronic wounds (RDEB-CW) displayed characteristics of senescent cells, increased myofibroblast differentiation, and augmented levels of TGF-β1 signaling components compared to fibroblasts derived from RDEB acute wounds and unaffected RDEB skin as well as skin from healthy-donors. Furthermore, RDEB-CW fibroblasts exhibited an increased pattern of inflammatory cytokine secretion (IL-1β and IL-6) when compared with RDEB and control fibroblasts. Interestingly, these aberrant patterns were found specifically in RDEB-CW fibroblasts independent of the culturing method, since fibroblasts obtained from dressing of acute wounds displayed a phenotype more similar to fibroblasts obtained from RDEB normal skin biopsies.</jats:p> </jats:sec><jats:sec> <jats:title>Conclusions</jats:title> <jats:p>Our results show that in vitro cultured RDEB-CW fibroblasts maintain distinctive cellular and molecular characteristics resembling the inflammatory and fibrotic microenvironment observed in RDEB patients’ chronic wounds. This work describes a novel, non-invasive and painless strategy to obtain human fibroblasts chronically subjected to an inflammatory and fibrotic environment, supporting their use as an accessible model for in vitro studies of RDEB wound healing pathogenesis. As such, this approach is well suited to testing new therapeutic strategies under controlled laboratory conditions.</jats:p> </jats:sec>
Scopus© Citations 1 1
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Clinical features and sex hormone profile in male patients with frontal fibrosing alopecia: A multicenter retrospective study with 33 patients
(2022)
Isabella Doche
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Marcello M.S. Nico
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Paula Gerlero
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Marina Rebeis
;
Daniel F. Melo
13 1Scopus© Citations 9
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Cardiac remodeling and arrhythmogenesis are ameliorated by administration of Cx43 mimetic peptide Gap27 in heart failure rats
(2020)
Claudia M. Lucero
;
David C. Andrade
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Camilo Toledo
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Hugo S. Díaz
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Katherin V. Pereyra
<jats:title>Abstract</jats:title><jats:p>Alterations in connexins and specifically in 43 isoform (Cx43) in the heart have been associated with a high incidence of arrhythmogenesis and sudden death in several cardiac diseases. We propose to determine salutary effect of Cx43 mimetic peptide Gap27 in the progression of heart failure. High-output heart failure was induced by volume overload using the arterio-venous fistula model (AV-Shunt) in adult male rats. Four weeks after AV-Shunt surgery, the Cx43 mimetic peptide Gap27 or scrambled peptide, were administered via osmotic minipumps (AV-Shunt<jats:sub>Gap27</jats:sub> or AV-Shunt<jats:sub>Scr</jats:sub>) for 4 weeks. Cardiac volumes, arrhythmias, function and remodeling were determined at 8 weeks after AV-Shunt surgeries. At 8<jats:sup>th</jats:sup> week, AV-Shunt<jats:sub>Gap27</jats:sub> showed a marked decrease in the progression of cardiac deterioration and showed a significant improvement in cardiac functions measured by intraventricular pressure-volume loops. Furthermore, AV-Shunt<jats:sub>Gap27</jats:sub> showed less cardiac arrhythmogenesis and cardiac hypertrophy index compared to AV-Shunt<jats:sub>Scr</jats:sub>. Gap27 treatment results in no change Cx43 expression in the heart of AV-Shunt rats. Our results strongly suggest that Cx43 play a pivotal role in the progression of cardiac dysfunction and arrhythmogenesis in high-output heart failure; furthermore, support the use of Cx43 mimetic peptide Gap27 as an effective therapeutic tool to reduce the progression of cardiac dysfunction in high-output heart failure.</jats:p>
Scopus© Citations 30 1
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Managing All the Genotypic Knowledge: Approach to a Septic Patient Colonized by Different Enterobacteriales with Unique Carbapenemases
(2019)
Stacy C. Park
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Alexander M. Wailan
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Katie E. Barry
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Kasi Vegesana
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Joanne Carroll
<jats:p> The recent development of new antimicrobials active against carbapenemase-producing <jats:italic>Enterobacteriales</jats:italic> (CPE) has brought new hope for the treatment of infections due to these organisms. However, the evolving epidemiology of bacteria with carbapenemases may complicate management, as providers are faced with treating patients colonized by bacteria producing multiple carbapenemases. </jats:p>
Scopus© Citations 7 1

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