Asset Details
Do you wish to reserve the book?
Inhibition of TGF-β signaling in mesenchymal stem cells of subchondral bone attenuates osteoarthritis
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?
Inhibition of TGF-β signaling in mesenchymal stem cells of subchondral bone attenuates osteoarthritis
Do you wish to request the book?
Inhibition of TGF-β signaling in mesenchymal stem cells of subchondral bone attenuates osteoarthritis
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
Inhibition of TGF-β signaling in mesenchymal stem cells of subchondral bone attenuates osteoarthritis
2013
Overview
Osteoarthritis has been believed to be caused by improper mechanical function of articular joints. Xu Cao and his colleagues now show that this mechanical process leads to upregulation of transforming growth factor β1 activity in mesenchymal stem cells of subchondral bone, resulting in aberrant bone formation, further destabilization of the joint and ultimately the onset of the disease.
Osteoarthritis is a highly prevalent and debilitating joint disorder. There is no effective medical therapy for the condition because of limited understanding of its pathogenesis. We show that transforming growth factor β1 (TGF-β1) is activated in subchondral bone in response to altered mechanical loading in an anterior cruciate ligament transection (ACLT) mouse model of osteoarthritis. TGF-β1 concentrations are also high in subchondral bone from humans with osteoarthritis. High concentrations of TGF-β1 induced formation of nestin-positive mesenchymal stem cell (MSC) clusters, leading to formation of marrow osteoid islets accompanied by high levels of angiogenesis. We found that transgenic expression of active TGF-β1 in osteoblastic cells induced osteoarthritis, whereas inhibition of TGF-β activity in subchondral bone attenuated the degeneration of articular cartilage. In particular, knockout of the TGF-β type II receptor (TβRII) in nestin-positive MSCs led to less development of osteoarthritis relative to wild-type mice after ACLT. Thus, high concentrations of active TGF-β1 in subchondral bone seem to initiate the pathological changes of osteoarthritis, and inhibition of this process could be a potential therapeutic approach to treating this disease.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ Animals
/ Male
/ Mesenchymal Stem Cells - physiology
/ Mice
/ Protein Serine-Threonine Kinases - antagonists & inhibitors
/ Rats
/ Receptor, Transforming Growth Factor-beta Type II
/ Receptors, Transforming Growth Factor beta - antagonists & inhibitors
/ Signal Transduction - physiology
/ Transforming Growth Factor beta - analysis
/ Transforming Growth Factor beta - antagonists & inhibitors
