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How miR-31-5p and miR-33a-5p Regulates SP1/CX43 Expression in Osteoarthritis Disease: Preliminary Insights

Osteoarthritis (OA) is a degenerative bone disease that involved micro and macro-environment of joints. To date, there are no radical curative treatments for OA and novel therapies are mandatory. Recent evidence suggests the role of miRNAs in OA progression. In our previous studies, we demonstrated...

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Autores principales: Costa, Viviana, De Fine, Marcello, Carina, Valeria, Conigliaro, Alice, Raimondi, Lavinia, De Luca, Angela, Bellavia, Daniele, Salamanna, Francesca, Alessandro, Riccardo, Pignatti, Giovanni, Fini, Milena, Giavaresi, Gianluca
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7957523/
https://www.ncbi.nlm.nih.gov/pubmed/33671114
http://dx.doi.org/10.3390/ijms22052471
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author Costa, Viviana
De Fine, Marcello
Carina, Valeria
Conigliaro, Alice
Raimondi, Lavinia
De Luca, Angela
Bellavia, Daniele
Salamanna, Francesca
Alessandro, Riccardo
Pignatti, Giovanni
Fini, Milena
Giavaresi, Gianluca
author_facet Costa, Viviana
De Fine, Marcello
Carina, Valeria
Conigliaro, Alice
Raimondi, Lavinia
De Luca, Angela
Bellavia, Daniele
Salamanna, Francesca
Alessandro, Riccardo
Pignatti, Giovanni
Fini, Milena
Giavaresi, Gianluca
author_sort Costa, Viviana
collection PubMed
description Osteoarthritis (OA) is a degenerative bone disease that involved micro and macro-environment of joints. To date, there are no radical curative treatments for OA and novel therapies are mandatory. Recent evidence suggests the role of miRNAs in OA progression. In our previous studies, we demonstrated the role of miR-31-5p and miR-33a families in different bone regeneration signaling. Here, we investigated the role of miR-31-5p and miR-33a-5p in OA progression. A different expression of miR-31-5p and miR-33a-5p into osteoblasts and chondrocytes isolated from joint tissues of OA patients classified in based on different Kellgren and Lawrence (KL) grading was highlighted; and through a bioinformatic approach the common miRNAs target Specificity proteins (Sp1) were identified. Sp1 regulates the expression of gap junction protein Connexin43 (Cx43), which in OA drives the modification of (i) osteoblasts and chondrocytes genes expression, (ii) joint inflammation cytokines releases and (iii) cell functions. Concerning this, thanks to gain and loss of function studies, the possible role of Sp1 as a modulator of CX43 expression through miR-31-5p and miR-33a-5p action was also evaluated. Finally, we hypothesize that both miRNAs cooperate to modulate the expression of SP1 in osteoblasts and chondrocytes and interfering, consequently, with CX43 expression, and they might be further investigated as new possible biomarkers for OA.
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spelling pubmed-79575232021-03-16 How miR-31-5p and miR-33a-5p Regulates SP1/CX43 Expression in Osteoarthritis Disease: Preliminary Insights Costa, Viviana De Fine, Marcello Carina, Valeria Conigliaro, Alice Raimondi, Lavinia De Luca, Angela Bellavia, Daniele Salamanna, Francesca Alessandro, Riccardo Pignatti, Giovanni Fini, Milena Giavaresi, Gianluca Int J Mol Sci Article Osteoarthritis (OA) is a degenerative bone disease that involved micro and macro-environment of joints. To date, there are no radical curative treatments for OA and novel therapies are mandatory. Recent evidence suggests the role of miRNAs in OA progression. In our previous studies, we demonstrated the role of miR-31-5p and miR-33a families in different bone regeneration signaling. Here, we investigated the role of miR-31-5p and miR-33a-5p in OA progression. A different expression of miR-31-5p and miR-33a-5p into osteoblasts and chondrocytes isolated from joint tissues of OA patients classified in based on different Kellgren and Lawrence (KL) grading was highlighted; and through a bioinformatic approach the common miRNAs target Specificity proteins (Sp1) were identified. Sp1 regulates the expression of gap junction protein Connexin43 (Cx43), which in OA drives the modification of (i) osteoblasts and chondrocytes genes expression, (ii) joint inflammation cytokines releases and (iii) cell functions. Concerning this, thanks to gain and loss of function studies, the possible role of Sp1 as a modulator of CX43 expression through miR-31-5p and miR-33a-5p action was also evaluated. Finally, we hypothesize that both miRNAs cooperate to modulate the expression of SP1 in osteoblasts and chondrocytes and interfering, consequently, with CX43 expression, and they might be further investigated as new possible biomarkers for OA. MDPI 2021-02-28 /pmc/articles/PMC7957523/ /pubmed/33671114 http://dx.doi.org/10.3390/ijms22052471 Text en © 2021 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/).
spellingShingle Article
Costa, Viviana
De Fine, Marcello
Carina, Valeria
Conigliaro, Alice
Raimondi, Lavinia
De Luca, Angela
Bellavia, Daniele
Salamanna, Francesca
Alessandro, Riccardo
Pignatti, Giovanni
Fini, Milena
Giavaresi, Gianluca
How miR-31-5p and miR-33a-5p Regulates SP1/CX43 Expression in Osteoarthritis Disease: Preliminary Insights
title How miR-31-5p and miR-33a-5p Regulates SP1/CX43 Expression in Osteoarthritis Disease: Preliminary Insights
title_full How miR-31-5p and miR-33a-5p Regulates SP1/CX43 Expression in Osteoarthritis Disease: Preliminary Insights
title_fullStr How miR-31-5p and miR-33a-5p Regulates SP1/CX43 Expression in Osteoarthritis Disease: Preliminary Insights
title_full_unstemmed How miR-31-5p and miR-33a-5p Regulates SP1/CX43 Expression in Osteoarthritis Disease: Preliminary Insights
title_short How miR-31-5p and miR-33a-5p Regulates SP1/CX43 Expression in Osteoarthritis Disease: Preliminary Insights
title_sort how mir-31-5p and mir-33a-5p regulates sp1/cx43 expression in osteoarthritis disease: preliminary insights
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7957523/
https://www.ncbi.nlm.nih.gov/pubmed/33671114
http://dx.doi.org/10.3390/ijms22052471
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