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The role of miRNA and lncRNA in heterotopic ossification pathogenesis

Heterotopic ossification (HO) is the formation of bone in non-osseous tissues, such as skeletal muscles. The HO could have a genetic or a non-genetic (acquired) background, that is, it could be caused by musculoskeletal trauma, such as burns, fractures, joint arthroplasty (traumatic HO), or cerebral...

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Autores principales: Pulik, Łukasz, Mierzejewski, Bartosz, Sibilska, Aleksandra, Grabowska, Iwona, Ciemerych, Maria Anna, Łęgosz, Paweł, Brzóska, Edyta
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9753082/
https://www.ncbi.nlm.nih.gov/pubmed/36522666
http://dx.doi.org/10.1186/s13287-022-03213-3
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author Pulik, Łukasz
Mierzejewski, Bartosz
Sibilska, Aleksandra
Grabowska, Iwona
Ciemerych, Maria Anna
Łęgosz, Paweł
Brzóska, Edyta
author_facet Pulik, Łukasz
Mierzejewski, Bartosz
Sibilska, Aleksandra
Grabowska, Iwona
Ciemerych, Maria Anna
Łęgosz, Paweł
Brzóska, Edyta
author_sort Pulik, Łukasz
collection PubMed
description Heterotopic ossification (HO) is the formation of bone in non-osseous tissues, such as skeletal muscles. The HO could have a genetic or a non-genetic (acquired) background, that is, it could be caused by musculoskeletal trauma, such as burns, fractures, joint arthroplasty (traumatic HO), or cerebral or spinal insult (neurogenetic HO). HO formation is caused by the differentiation of stem or progenitor cells induced by local or systemic imbalances. The main factors described so far in HO induction are TGFβ1, BMPs, activin A, oncostatin M, substance P, neurotrophin-3, and WNT. In addition, dysregulation of noncoding RNAs, such as microRNA or long noncoding RNA, homeostasis may play an important role in the development of HO. For example, decreased expression of miRNA-630, which is responsible for the endothelial–mesenchymal transition, was observed in HO patients. The reduced level of miRNA-421 in patients with humeral fracture was shown to be associated with overexpression of BMP2 and a higher rate of HO occurrence. Down-regulation of miRNA-203 increased the expression of runt-related transcription factor 2 (RUNX2), a crucial regulator of osteoblast differentiation. Thus, understanding the various functions of noncoding RNAs can reveal potential targets for the prevention or treatment of HO.
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spelling pubmed-97530822022-12-15 The role of miRNA and lncRNA in heterotopic ossification pathogenesis Pulik, Łukasz Mierzejewski, Bartosz Sibilska, Aleksandra Grabowska, Iwona Ciemerych, Maria Anna Łęgosz, Paweł Brzóska, Edyta Stem Cell Res Ther Review Heterotopic ossification (HO) is the formation of bone in non-osseous tissues, such as skeletal muscles. The HO could have a genetic or a non-genetic (acquired) background, that is, it could be caused by musculoskeletal trauma, such as burns, fractures, joint arthroplasty (traumatic HO), or cerebral or spinal insult (neurogenetic HO). HO formation is caused by the differentiation of stem or progenitor cells induced by local or systemic imbalances. The main factors described so far in HO induction are TGFβ1, BMPs, activin A, oncostatin M, substance P, neurotrophin-3, and WNT. In addition, dysregulation of noncoding RNAs, such as microRNA or long noncoding RNA, homeostasis may play an important role in the development of HO. For example, decreased expression of miRNA-630, which is responsible for the endothelial–mesenchymal transition, was observed in HO patients. The reduced level of miRNA-421 in patients with humeral fracture was shown to be associated with overexpression of BMP2 and a higher rate of HO occurrence. Down-regulation of miRNA-203 increased the expression of runt-related transcription factor 2 (RUNX2), a crucial regulator of osteoblast differentiation. Thus, understanding the various functions of noncoding RNAs can reveal potential targets for the prevention or treatment of HO. BioMed Central 2022-12-15 /pmc/articles/PMC9753082/ /pubmed/36522666 http://dx.doi.org/10.1186/s13287-022-03213-3 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Review
Pulik, Łukasz
Mierzejewski, Bartosz
Sibilska, Aleksandra
Grabowska, Iwona
Ciemerych, Maria Anna
Łęgosz, Paweł
Brzóska, Edyta
The role of miRNA and lncRNA in heterotopic ossification pathogenesis
title The role of miRNA and lncRNA in heterotopic ossification pathogenesis
title_full The role of miRNA and lncRNA in heterotopic ossification pathogenesis
title_fullStr The role of miRNA and lncRNA in heterotopic ossification pathogenesis
title_full_unstemmed The role of miRNA and lncRNA in heterotopic ossification pathogenesis
title_short The role of miRNA and lncRNA in heterotopic ossification pathogenesis
title_sort role of mirna and lncrna in heterotopic ossification pathogenesis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9753082/
https://www.ncbi.nlm.nih.gov/pubmed/36522666
http://dx.doi.org/10.1186/s13287-022-03213-3
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