Protein kinase A is a dependent factor and therapeutic target in mouse models of fibrous dysplasia

Abstract Fibrous dysplasia is a skeletal disorder caused by activating mutations in Gαs, leading to bone fractures, deformities, and pain. Protein kinase A (PKA), the principal effector of Gαs, plays critical roles in various biological processes. However, its role in fibrous dysplasia is unknown. H...

Full description

Saved in:
Bibliographic Details
Main Authors: Zhongyu Liu, Lu Xing, Wenlong Huang, Ning Ji, Hang Zhao, Qianming Chen, Xianglong Han, Ding Bai, Xuefeng Zhao
Format: Article
Language:English
Published: Nature Portfolio 2025-07-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-025-61402-z
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849334431189303296
author Zhongyu Liu
Lu Xing
Wenlong Huang
Ning Ji
Hang Zhao
Qianming Chen
Xianglong Han
Ding Bai
Xuefeng Zhao
author_facet Zhongyu Liu
Lu Xing
Wenlong Huang
Ning Ji
Hang Zhao
Qianming Chen
Xianglong Han
Ding Bai
Xuefeng Zhao
author_sort Zhongyu Liu
collection DOAJ
description Abstract Fibrous dysplasia is a skeletal disorder caused by activating mutations in Gαs, leading to bone fractures, deformities, and pain. Protein kinase A (PKA), the principal effector of Gαs, plays critical roles in various biological processes. However, its role in fibrous dysplasia is unknown. Here we demonstrate that PKA activation replicates fibrous dysplasia-like lesions in a transgenic mouse model expressing an activating mutation of PKA in the skeletal stem cell lineage. Mechanistically, PKA promotes osteoclastogenesis and aberrant osteogenic differentiation and proliferation of skeletal stem cells, while impairing mineralization. Downregulating PKA activity, using either a genetically engineered PKA inhibitor peptide or small-molecule inhibitors, effectively alleviates fibrous dysplasia lesions in a fibrous dysplasia mouse model and safeguards bone structure by increasing trabecular bone volume in a PKA-inhibition mouse model. Although long-term pharmacological PKA inhibition remains untested, these findings demonstrate that PKA is a dependent factor in fibrous dysplasia initiation and progression, underscoring its potential as a therapeutic target.
format Article
id doaj-art-e1af8882deee43189f4bb9c8ab140c69
institution Kabale University
issn 2041-1723
language English
publishDate 2025-07-01
publisher Nature Portfolio
record_format Article
series Nature Communications
spelling doaj-art-e1af8882deee43189f4bb9c8ab140c692025-08-20T03:45:34ZengNature PortfolioNature Communications2041-17232025-07-0116111810.1038/s41467-025-61402-zProtein kinase A is a dependent factor and therapeutic target in mouse models of fibrous dysplasiaZhongyu Liu0Lu Xing1Wenlong Huang2Ning Ji3Hang Zhao4Qianming Chen5Xianglong Han6Ding Bai7Xuefeng Zhao8State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan UniversityState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan UniversityState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan UniversityState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan UniversityState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan UniversityState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan UniversityState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan UniversityState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan UniversityState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan UniversityAbstract Fibrous dysplasia is a skeletal disorder caused by activating mutations in Gαs, leading to bone fractures, deformities, and pain. Protein kinase A (PKA), the principal effector of Gαs, plays critical roles in various biological processes. However, its role in fibrous dysplasia is unknown. Here we demonstrate that PKA activation replicates fibrous dysplasia-like lesions in a transgenic mouse model expressing an activating mutation of PKA in the skeletal stem cell lineage. Mechanistically, PKA promotes osteoclastogenesis and aberrant osteogenic differentiation and proliferation of skeletal stem cells, while impairing mineralization. Downregulating PKA activity, using either a genetically engineered PKA inhibitor peptide or small-molecule inhibitors, effectively alleviates fibrous dysplasia lesions in a fibrous dysplasia mouse model and safeguards bone structure by increasing trabecular bone volume in a PKA-inhibition mouse model. Although long-term pharmacological PKA inhibition remains untested, these findings demonstrate that PKA is a dependent factor in fibrous dysplasia initiation and progression, underscoring its potential as a therapeutic target.https://doi.org/10.1038/s41467-025-61402-z
spellingShingle Zhongyu Liu
Lu Xing
Wenlong Huang
Ning Ji
Hang Zhao
Qianming Chen
Xianglong Han
Ding Bai
Xuefeng Zhao
Protein kinase A is a dependent factor and therapeutic target in mouse models of fibrous dysplasia
Nature Communications
title Protein kinase A is a dependent factor and therapeutic target in mouse models of fibrous dysplasia
title_full Protein kinase A is a dependent factor and therapeutic target in mouse models of fibrous dysplasia
title_fullStr Protein kinase A is a dependent factor and therapeutic target in mouse models of fibrous dysplasia
title_full_unstemmed Protein kinase A is a dependent factor and therapeutic target in mouse models of fibrous dysplasia
title_short Protein kinase A is a dependent factor and therapeutic target in mouse models of fibrous dysplasia
title_sort protein kinase a is a dependent factor and therapeutic target in mouse models of fibrous dysplasia
url https://doi.org/10.1038/s41467-025-61402-z
work_keys_str_mv AT zhongyuliu proteinkinaseaisadependentfactorandtherapeutictargetinmousemodelsoffibrousdysplasia
AT luxing proteinkinaseaisadependentfactorandtherapeutictargetinmousemodelsoffibrousdysplasia
AT wenlonghuang proteinkinaseaisadependentfactorandtherapeutictargetinmousemodelsoffibrousdysplasia
AT ningji proteinkinaseaisadependentfactorandtherapeutictargetinmousemodelsoffibrousdysplasia
AT hangzhao proteinkinaseaisadependentfactorandtherapeutictargetinmousemodelsoffibrousdysplasia
AT qianmingchen proteinkinaseaisadependentfactorandtherapeutictargetinmousemodelsoffibrousdysplasia
AT xianglonghan proteinkinaseaisadependentfactorandtherapeutictargetinmousemodelsoffibrousdysplasia
AT dingbai proteinkinaseaisadependentfactorandtherapeutictargetinmousemodelsoffibrousdysplasia
AT xuefengzhao proteinkinaseaisadependentfactorandtherapeutictargetinmousemodelsoffibrousdysplasia