Asset Details
Do you wish to reserve the book?
STAT3 is critical for skeletal development and bone homeostasis by regulating osteogenesis
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?
STAT3 is critical for skeletal development and bone homeostasis by regulating osteogenesis
Do you wish to request the book?
STAT3 is critical for skeletal development and bone homeostasis by regulating osteogenesis
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
STAT3 is critical for skeletal development and bone homeostasis by regulating osteogenesis
2021
Overview
Skeletal deformities are typical AD-HIES manifestations, which are mainly caused by heterozygous and loss-of-function mutations in Signal transducer and activator of transcription 3 (STAT3). However, the mechanism is still unclear and the treatment strategy is limited. Herein, we reported that the mice with
Stat3
deletion in osteoblasts, but not in osteoclasts, induced AD-HIES-like skeletal defects, including craniofacial malformation, osteoporosis, and spontaneous bone fracture. Mechanistic analyses revealed that STAT3 in cooperation with Msh homeobox 1(MSX1) drove osteoblast differentiation by promoting Distal-less homeobox 5(
Dlx5)
transcription. Furthermore, pharmacological activation of STAT3 partially rescued skeletal deformities in heterozygous knockout mice, while inhibition of STAT3 aggravated bone loss. Taken together, these data show that STAT3 is critical for modulating skeletal development and maintaining bone homeostasis through STAT3-indcued osteogenesis and suggest it may be a potential target for treatments.
Autosomal dominant hyper-immunoglobulin E syndrome (AD-HIES) is associated with mutations in STAT3, and clinical manifestations include skeletal deformities. Here, the authors show that inactivation of STAT3 in osteoblast induces AD-HIES-like skeletal defects by impairing osteogenesis, and show that pharmacological STAT3 activation rescues the phenotype.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 38/91
/ Animals
/ Cell Differentiation - drug effects
/ Defects
/ Homeobox
/ Homeodomain Proteins - genetics
/ Humanities and Social Sciences
/ Mesenchymal Stem Cells - cytology
/ Mesenchymal Stem Cells - metabolism
/ Mice
/ MSX1 Transcription Factor - genetics
/ MSX1 Transcription Factor - metabolism
/ Musculoskeletal Abnormalities - drug therapy
/ Musculoskeletal Abnormalities - genetics
/ Musculoskeletal Abnormalities - metabolism
/ Mutation
/ Science
/ STAT3 Transcription Factor - antagonists & inhibitors
/ STAT3 Transcription Factor - genetics
