Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Cot/Tpl2 is essential for RANKL induction by lipid A in osteoblasts.

T Kikuchi1, Y Yoshikai, J Miyoshi

  • 1Laboratory of Host Defense and Germfree Life, Research Institute for Disease Mechanism and Control, Nagoya University School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan.

Journal of Dental Research
|June 25, 2003
PubMed
Summary

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Data on changes to mucosal inflammation and the intestinal microbiota following dietary micronutrients in genetically susceptible hosts.

Data in brief·2018
Same author

Role of Mfa5 in Expression of Mfa1 Fimbriae in Porphyromonas gingivalis.

Journal of dental research·2016
Same author

Five-year clinical results for treatment of intrabony defects with EMD, guided tissue regeneration and open-flap debridement: a case series.

Journal of periodontal research·2014
Same author

Inflammatory bone loss in experimental periodontitis induced by Aggregatibacter actinomycetemcomitans in interleukin-1 receptor antagonist knockout mice.

Infection and immunity·2014
Same author

Ethanol and amylase production by a newly isolated Clostridium sp.

World journal of microbiology & biotechnology·2014
Same author

Follicular dendritic cell-secreted protein is decreased in experimental periodontitis concurrently with the increase of interleukin-17 expression and the Rankl/Opg mRNA ratio.

Journal of periodontal research·2013

Lipopolysaccharide (LPS) triggers bone loss in periodontal disease by increasing osteoblast RANKL. The kinase Cot/Tpl2 is essential for LPS-induced ERK activation and RANKL production in osteoblasts.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Immunology

Background:

  • Lipopolysaccharide (LPS) exacerbates bone resorption in periodontal diseases.
  • LPS induces osteoblast receptor activator of NF-kappa B ligand (RANKL) via extracellular signal-regulated kinase (ERK) activation.
  • The precise regulatory mechanisms of LPS-induced RANKL expression remain unclear.

Purpose of the Study:

  • To investigate the role of Cot/Tpl2 in LPS-induced ERK activation and RANKL expression in osteoblasts.
  • To elucidate the signaling pathways involved in LPS-mediated osteoblast responses.

Main Methods:

  • Utilized mouse osteoblasts lacking the Cot/Tpl2 kinase.
  • Administered synthetic lipid A (active LPS component) to osteoblasts.
  • Assessed RANKL mRNA levels and ERK activation.

Related Experiment Videos

  • Evaluated the activation of other signaling pathways including JNK, p38, Raf-1, and NF-kappa B.

    • Main Results:

    • Osteoblasts deficient in Cot/Tpl2 exhibited significantly reduced RANKL mRNA induction and ERK activation upon LPS stimulation.
    • Cot/Tpl2 deficiency did not affect the activation of JNK, p38, Raf-1, or NF-kappa B pathways.
    • These findings highlight a specific role for Cot/Tpl2 in the LPS signaling cascade.

    Conclusions:

    • Cot/Tpl2 is a critical kinase required for LPS-induced ERK activation in osteoblasts.
    • Cot/Tpl2 plays an essential role in the induction of RANKL by LPS in osteoblasts.
    • This study identifies Cot/Tpl2 as a key mediator in the pathogenesis of periodontal disease.