Asset Details
Do you wish to reserve the book?
Myostatin is a direct regulator of osteoclast differentiation and its inhibition reduces inflammatory joint destruction in mice
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Myostatin is a direct regulator of osteoclast differentiation and its inhibition reduces inflammatory joint destruction in mice
Do you wish to request the book?
Myostatin is a direct regulator of osteoclast differentiation and its inhibition reduces inflammatory joint destruction in mice
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Myostatin is a direct regulator of osteoclast differentiation and its inhibition reduces inflammatory joint destruction in mice
2015
Overview
Myostatin is shown to directly promote osteoclast differentiation, and its inhibition improves arthritic bone loss in two mouse models.
Myostatin (also known as growth and differentiation factor 8) is a secreted member of the transforming growth factor-β (TGF-β) family that is mainly expressed in skeletal muscle, which is also its primary target tissue. Deletion of the myostatin gene (
Mstn
) in mice leads to muscle hypertrophy, and animal studies support the concept that myostatin is a negative regulator of muscle growth and regeneration
1
,
2
,
3
,
4
,
5
. However, myostatin deficiency also increases bone formation, mainly through loading-associated effects on bone
6
,
7
,
8
,
9
,
10
,
11
. Here we report a previously unknown direct role for myostatin in osteoclastogenesis and in the progressive loss of articular bone in rheumatoid arthritis (RA). We demonstrate that myostatin is highly expressed in the synovial tissues of RA subjects and of human tumor necrosis factor (TNF)-α transgenic (hTNFtg) mice, a model for human RA
12
. Myostatin strongly accelerates receptor activator of nuclear factor κB ligand (RANKL)-mediated osteoclast formation
in vitro
through transcription factor SMAD2-dependent regulation of nuclear factor of activated T-cells (NFATC1). Myostatin deficiency or antibody-mediated inhibition leads to an amelioration of arthritis severity in hTNFtg mice, chiefly reflected by less bone destruction. Consistent with these effects in hTNFtg mice, the lack of myostatin leads to increased grip strength and less bone erosion in the K/BxN serum-induced arthritis model in mice. The results strongly suggest that myostatin is a potent therapeutic target for interfering with osteoclast formation and joint destruction in RA.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ 13/95
/ 59
/ 64
/ 64/110
/ 82/80
/ 96
/ 96/1
/ 96/109
/ Analysis
/ Animals
/ Arthritis, Rheumatoid - therapy
/ Extracellular Signal-Regulated MAP Kinases - physiology
/ Humans
/ letter
/ Macrophage Colony-Stimulating Factor - pharmacology
/ Mice
/ Myostatin - antagonists & inhibitors
/ NFATC Transcription Factors - metabolism
/ Rodents
/ Studies
