Please use this identifier to cite or link to this item: https://hdl.handle.net/11499/9498
Title: Mesenchymal stem cells and c-type natriuretic peptide signaling: A proposal for a new treatment approach for skeletal dysplasias
Authors: Ünal, Murat Serkant
Tufan, Ahmet Çevik
Keywords: Achondroplasia
C-type natriuretic peptide
Dwarfism
Endochondral ossification
Mesenchymal stem cells
Natriuretic peptide receptor-B
Osteochondrodisyplasia
Skeletal dysplasia
atrial natriuretic factor
brain natriuretic peptide
natriuretic factor
natriuretic peptide receptor B
natriuretic peptide type C
achondroplasia
Article
bone dysplasia
enchondral ossification
growth rate
human
in vitro study
mesenchymal stem cell
mesenchymal stem cell transplantation
musculoskeletal development
nonhuman
phenotype
priority journal
protein expression
signal transduction
tissue engineering
trabecular bone
Publisher: Bentham Science Publishers B.V.
Abstract: Endochondral ossification is under the regulation of endocrine, paracrine and otocrine factors including transforming growth factor-ß superfamily members, fibroblast growth factors, retinoids, products of hedgehog gene, parathyroid hormone-related peptide, molecules involved in cell adhesion, and extracellular matrix components. Natriuretic peptide receptor-B, and its ligand C-type natriuretic peptide have also been implicated in the regulation of limb bone development. Results of recent studies are promising in terms of systemic elevation of C-type natriuretic peptide level inducing growth. In addition, same strategy also overcomes the dwarf phenotype of achondroplasia, the most frequently seen skeletal dysplasia in human, in a mouse model. Based on this literature and a series of recent experiments discussed here, this perspective underlines the abundant C-type natriuretic peptide expression in trabecular bone derived mesenchymal stem cells of human, chicken, and rat origin, and proposes the potential use of mesenchymal stem cells as a part of growth inducing treatment strategy in osteochondrodisyplasias in the future. © 2016 Bentham Science Publishers.
URI: https://hdl.handle.net/11499/9498
ISSN: 1574-888X
Appears in Collections:PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Tıp Fakültesi Koleksiyonu
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection

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