Open AccessTransdifferentiation of myoblasts into osteoblasts – possible use for bone therapy
Author(s) -
Lin Daphne P. L.,
Carnagarin Revathy,
Dharmarajan Arun,
Dass Crispin R.
Publication year - 2017
Publication title -
journal of pharmacy and pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 118
eISSN - 2042-7158
pISSN - 0022-3573
DOI - 10.1111/jphp.12790
Subject(s) - transdifferentiation , osteoblast , junb , bone morphogenetic protein , transcription factor , bone morphogenetic protein 7 , microbiology and biotechnology , bone healing , osteoporosis , bone morphogenetic protein 2 , biology , cancer research , endocrinology , stem cell , anatomy , genetics , gene , in vitro
Objectives Transdifferentiation is defined as the conversion of one cell type to another and is an ever‐expanding field with a growing number of cells found to be capable of such a process. To date, the fact remains that there are limited treatment options for fracture healing, osteoporosis and bone repair post‐destruction by bone tumours. Hence, this review focuses on the transdifferentiation of myoblast to osteoblast as a means to further understand the transdifferentiation process and to investigate a potential therapeutic option if successful. Key findings The potent osteoinductive effects of the bone morphogenetic protein‐2 are largely implicated in the transdifferentiation of myoblast to osteoblast. Bone morphogenetic protein‐2‐induced activation of the Smad1 protein ultimately results in JunB synthesis, the first transcriptional step in myoblast dedifferentiation. The upregulation of the activating protein‐1 binding activity triggers the transcription of the runt‐related transcription factor 2 gene, a transcription factor that plays a major role in osteoblast differentiation. Summary This potential transdifferentiation treatment may be utilised for dental implants, fracture healing, osteoporosis and bone repair post‐destruction by bone tumours.