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The Thyroid Hormone Receptors Modulate the Skin Response to Retinoids

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García Serrano, Laura & Gomez Ferrería, María Ana & Contreras Jurado, Silvia Constanza & Segrelles, Carmen & Paramio, Jesus M. & Aranda, Ana .The Thyroid Hormone Receptors Modulate the Skin Response to Retinoids.

ISO 690

García Serrano, Laura & Gomez Ferrería, María Ana & Contreras Jurado, Silvia Constanza & Segrelles, Carmen & Paramio, Jesus M. & Aranda, Ana. The Thyroid Hormone Receptors Modulate the Skin Response to Retinoids.

https://hdl.handle.net/20.500.12080/26193
dc.contributor.author García Serrano, Laura
dc.contributor.author Gomez Ferrería, María Ana
dc.contributor.author Contreras Jurado, Silvia Constanza
dc.contributor.author Segrelles, Carmen
dc.contributor.author Paramio, Jesus M.
dc.contributor.author Aranda, Ana
dc.date.accessioned 2021-11-10T17:32:07Z
dc.date.available 2021-11-10T17:32:07Z
dc.date.created 2011-08-17
dc.identifier.uri https://hdl.handle.net/20.500.12080/26193
dc.description.abstract Background: Retinoids play an important role in skin homeostasis and when administered topically cause skin hyperplasia, abnormal epidermal differentiation and inflammation. Thyroidal status in humans also influences skin morphology and function and we have recently shown that the thyroid hormone receptors (TRs) are required for a normal proliferative response to 12-O-tetradecanolyphorbol-13-acetate (TPA) in mice. Methodology/Principal findings: We have compared the epidermal response of mice lacking the thyroid hormone receptor binding isoforms TRa1 and TRb to retinoids and TPA. Reduced hyperplasia and a decreased number of proliferating cells in the basal layer in response to 9-cis-RA and TPA were found in the epidermis of TR-deficient mice. Nuclear levels of proteins important for cell proliferation were altered, and expression of keratins 5 and 6 was also reduced, concomitantly with the decreased number of epidermal cell layers. In control mice the retinoid (but not TPA) induced parakeratosis and diminished expression of keratin 10 and loricrin, markers of early and terminal epidermal differentiation, respectively. This reduction was more accentuated in the TR deficient animals, whereas they did not present parakeratosis. Therefore, TRs modulate both the proliferative response to retinoids and their inhibitory effects on skin differentiation. Reduced proliferation, which was reversed upon thyroxine treatment, was also found in hypothyroid mice, demonstrating that thyroid hormone binding to TRs is required for the normal response to retinoids. In addition, the mRNA levels of the pro-inflammatory cytokines TNFa and IL-6 and the chemotactic proteins S1008A and S1008B were significantly elevated in the skin of TR knock-out mice after TPA or 9-cis-RA treatment and immune cell infiltration was also enhanced. Conclusions/significance: Since retinoids are commonly used for the treatment of skin disorders, these results demonstrating that TRs regulate skin proliferation, differentiation and inflammation in response to these compounds could have not only physiological but also therapeutic implications es_ES
dc.format application/pdf es_ES
dc.language eng es_ES
dc.rights CC-BY es_ES
dc.rights.uri http://creativecommons.org/licenses/by/4.0/deed.es es_ES
dc.title The Thyroid Hormone Receptors Modulate the Skin Response to Retinoids es_ES
dc.type info:eu-repo/semantics/article es_ES
dc.rights.accessrights info:eu-repo/semantics/openAccess es_ES
dc.identifier.location N/A es_ES


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