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Cytoplasmic hnRNPK interacts with GSK3β and is essential for the osteoclast differentiation

Xiaoqin Fan1, Haiting Xiong1, Jinmei Wei1

  • 1Key laboratory of functional protein research of Guangdong higher education institutes, Institute of life and health engineering, Jinan University, Guangzhou, 510632, China.

Scientific Reports
|December 8, 2015
PubMed

Insights

Heterogeneous nuclear ribonucleoprotein K (hnRNPK) is crucial for osteoclast differentiation by interacting with Glycogen synthase kinase-3β (GSK3β). This interaction regulates key pathways essential for bone cell formation and function.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Osteoclast differentiation is a critical process for bone remodeling.
  • Glycogen synthase kinase-3β (GSK3β) phosphorylation at Ser9 is implicated in osteoclastogenesis.
  • The precise molecular mechanisms linking GSK3β to osteoclast differentiation are not fully understood.

Purpose of the Study:

  • To elucidate the role of heterogeneous nuclear ribonucleoprotein K (hnRNPK) in osteoclast differentiation.
  • To investigate the interaction between hnRNPK and GSK3β during this process.

Main Methods:

  • Investigated hnRNPK's interaction with GSK3β during RANKL-induced osteoclast differentiation.
  • Utilized techniques to track nuclear-cytoplasmic translocation of hnRNPK.
  • Examined the impact of hnRNPK on GSK3β functions, NF-κB activation, NFATc1 expression, and tubulin acetylation.

Main Results:

  • PI3K/Akt-mediated GSK3β phosphorylation induces ERK-dependent nuclear-cytoplasmic translocation of hnRNPK.
  • hnRNPK co-localizes and interacts with GSK3β in the cytoplasm.
  • hnRNPK is essential for osteoclast differentiation, NF-κB activation, NFATc1 expression, and tubulin acetylation.
  • hnRNPK localizes to the actin belt and is vital for mature osteoclast formation.

Conclusions:

  • hnRNPK plays a critical role in osteoclast differentiation.
  • A model is proposed where cytoplasmic hnRNPK interacts with GSK3β to regulate its function in osteoclastogenesis.

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