Abstract
JAK/STAT signaling pathway is involved in many diseases, including autoimmune diseases, which are characterized by a close interconnection between immune and bone system. JAK/STAT pathway is involved in bone homeostasis and plays an important role in proliferation and differentiation of some cell types, including osteoblasts and osteoclasts. Different molecules, such as cytokines, hormones, and growth factors are responsible for the activation of the JAK/STAT pathway, which leads, at the nuclear level, to start DNA transcription of target genes. Bone cells and remodeling process are often influenced by many cytokines, which act as strong stimulators of bone formation and resorption. Our aim, through careful research in literature, has been to provide an overview of the role of the JAK/STAT pathway in bone remodeling and on bone cells, with a focus on cytokines involved in bone turnover through this signal cascade. The JAK/STAT pathway, through the signal cascade activation mediated by the interaction with many cytokines, acts on bone cells and appears to be involved in bone remodeling process. However, many other studies are needed to completely understand the molecular mechanism underlying these bone process.
Highlights
The Janus kinases (JAKs) are a family of protein tyrosine kinases (PTKs), named JAK1, JAK2, JAK3, and TYK2, that act on signal transducer and activator of transcription (STAT)
A murine study conducted on osteoblasts [55] has demonstrated that phosphorylation of JAKs proteins occurs in the presence of oncostatin-M
Through careful research in the literature, we wanted to focus our attention on the molecular mechanisms that affect the involvement of the JAK/STAT pathway at the cellular level, at the level of bone cells, osteoblasts, and osteoclasts, and how they behave in the remodeling process bone
Summary
The Janus kinases (JAKs) are a family of protein tyrosine kinases (PTKs), named JAK1, JAK2, JAK3, and TYK2, that act on signal transducer and activator of transcription (STAT). A murine study conducted on osteoblasts [55] has demonstrated that phosphorylation of JAKs proteins occurs in the presence of oncostatin-M This indicates the involvement of the three members, JAK1, JAK2, and TYK2, in the bone formation process [1, 56–59]. In a very recent study conducted by Davidson et al, it is highlighted that the participation of STAT3, during the regulation of the osteoclastogenic process, occurs in a different way in female than male osteoclastic cells These data suggest that the STAT3 signal may have a key role in bone turnover [46, 84, 85]. With the activation of STAT3 and the involvement of receptor subunit gp130 to transduce signals, IL-6 can mightily inhibit RANKL-induced osteoclasts differentiation [95]. Both seem to participate in the process of osteoclastogenesis by exhibiting their inhibitory effect and reducing the number of multinucleated osteoclasts [114–116]
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