Abstract
The Interleukin-6/STAT3 (IL-6/STAT3) signaling pathway is essential for proper immune response to invading pathogens and viral infections. Moreover, STAT3 has high implications as a therapeutic target for rheumatoid and osteoarthritis. Recent literature has found that the IL-6/STAT3 signaling pathway plays an imperative role in the development of cartilage and bone. However, the direct role and the downstream effectors of STAT3 signaling during cartilage formation remains elusive. Through the use of cleared skeletal preparations, and histology, conditional loss of STAT3 in mouse cartilage, via the Col2-Cre driver, show that STAT3 is essential for proper limb growth plate formation. Furthermore, loss of STAT3 results in spontaneous bone fractures of the humerus. Interestingly, these severe fractures are rapidly repaired, underscoring an untapped mechanism for regeneration in musculoskeletal tissue. Moreover, conditional loss of STAT3 in limb mesenchyme, via the Prx1-Cre driver was generated. Loss of STAT3 in mesoderm show contortion phenotypes in the humerus. The stronger limb phenotype of Prx1Cre;Stat3fxfx compared to Col2Cre;Stat3fxfx mice indicates that Stat3 may exert effects at multiple stages of endochondral bone formation. Future experiments elucidating the downstream effectors of STAT3 mediated pathways will reveal the mechanisms by which STAT3 modulates different processes in limb development.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
