Novel functions for NFκB

Inhibition of bone formation

Susan Miranda, Jia Chang, Gustavo Miranda-Carboni, Cun Yu Wang

Research output: Contribution to journalReview article

85 Citations (Scopus)

Abstract

NFκB is a family of transcription factors involved in immunity and the normal functioning of many tissues. It has been well studied in osteoclasts, and new data indicate an important role for NFκB in the negative regulation of bone formation. In this article, we discuss how NFκB activation affects osteoblast function and bone formation. In particular, we describe how reduced NFκB activity in osteoblasts results in an increase in bone formation via enhanced c-Jun N-terminal kinase (JNK) activity, which regulates FOSL1 (also known as Fra1) expression. Furthermore, we discuss how estrogen and NFκB crosstalk in osteoblasts acts to oppositely regulate bone formation. Future NFκB-targeting treatments for osteoporosis, rheumatoid arthritis and other inflammatory bone diseases could lead to increased bone formation concurrent with decreased bone resorption.

Original languageEnglish (US)
Pages (from-to)607-611
Number of pages5
JournalNature Reviews Rheumatology
Volume6
Issue number10
DOIs
StatePublished - Oct 1 2010

Fingerprint

Osteogenesis
Osteoblasts
JNK Mitogen-Activated Protein Kinases
Bone Diseases
Osteoclasts
Bone Resorption
Osteoporosis
Immunity
Rheumatoid Arthritis
Estrogens
Transcription Factors

All Science Journal Classification (ASJC) codes

  • Rheumatology

Cite this

Novel functions for NFκB : Inhibition of bone formation. / Miranda, Susan; Chang, Jia; Miranda-Carboni, Gustavo; Wang, Cun Yu.

In: Nature Reviews Rheumatology, Vol. 6, No. 10, 01.10.2010, p. 607-611.

Research output: Contribution to journalReview article

@article{cb9ae3fd833b46eda35f39337b48eb86,
title = "Novel functions for NFκB: Inhibition of bone formation",
abstract = "NFκB is a family of transcription factors involved in immunity and the normal functioning of many tissues. It has been well studied in osteoclasts, and new data indicate an important role for NFκB in the negative regulation of bone formation. In this article, we discuss how NFκB activation affects osteoblast function and bone formation. In particular, we describe how reduced NFκB activity in osteoblasts results in an increase in bone formation via enhanced c-Jun N-terminal kinase (JNK) activity, which regulates FOSL1 (also known as Fra1) expression. Furthermore, we discuss how estrogen and NFκB crosstalk in osteoblasts acts to oppositely regulate bone formation. Future NFκB-targeting treatments for osteoporosis, rheumatoid arthritis and other inflammatory bone diseases could lead to increased bone formation concurrent with decreased bone resorption.",
author = "Susan Miranda and Jia Chang and Gustavo Miranda-Carboni and Wang, {Cun Yu}",
year = "2010",
month = "10",
day = "1",
doi = "10.1038/nrrheum.2010.133",
language = "English (US)",
volume = "6",
pages = "607--611",
journal = "Nature reviews. Rheumatology",
issn = "1759-4790",
publisher = "Nature Publishing Group",
number = "10",

}

TY - JOUR

T1 - Novel functions for NFκB

T2 - Inhibition of bone formation

AU - Miranda, Susan

AU - Chang, Jia

AU - Miranda-Carboni, Gustavo

AU - Wang, Cun Yu

PY - 2010/10/1

Y1 - 2010/10/1

N2 - NFκB is a family of transcription factors involved in immunity and the normal functioning of many tissues. It has been well studied in osteoclasts, and new data indicate an important role for NFκB in the negative regulation of bone formation. In this article, we discuss how NFκB activation affects osteoblast function and bone formation. In particular, we describe how reduced NFκB activity in osteoblasts results in an increase in bone formation via enhanced c-Jun N-terminal kinase (JNK) activity, which regulates FOSL1 (also known as Fra1) expression. Furthermore, we discuss how estrogen and NFκB crosstalk in osteoblasts acts to oppositely regulate bone formation. Future NFκB-targeting treatments for osteoporosis, rheumatoid arthritis and other inflammatory bone diseases could lead to increased bone formation concurrent with decreased bone resorption.

AB - NFκB is a family of transcription factors involved in immunity and the normal functioning of many tissues. It has been well studied in osteoclasts, and new data indicate an important role for NFκB in the negative regulation of bone formation. In this article, we discuss how NFκB activation affects osteoblast function and bone formation. In particular, we describe how reduced NFκB activity in osteoblasts results in an increase in bone formation via enhanced c-Jun N-terminal kinase (JNK) activity, which regulates FOSL1 (also known as Fra1) expression. Furthermore, we discuss how estrogen and NFκB crosstalk in osteoblasts acts to oppositely regulate bone formation. Future NFκB-targeting treatments for osteoporosis, rheumatoid arthritis and other inflammatory bone diseases could lead to increased bone formation concurrent with decreased bone resorption.

UR - http://www.scopus.com/inward/record.url?scp=77957587105&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77957587105&partnerID=8YFLogxK

U2 - 10.1038/nrrheum.2010.133

DO - 10.1038/nrrheum.2010.133

M3 - Review article

VL - 6

SP - 607

EP - 611

JO - Nature reviews. Rheumatology

JF - Nature reviews. Rheumatology

SN - 1759-4790

IS - 10

ER -