Nf2 orchestrates β-arrestin2-biased PTH1R signaling to couple bone mass with skeletal integrity

J Junguang Liao (Department of Biopharmaceutics, Zhejiang Provincial Engineering Research Center of New Technologies and Applications for Targeted Therapy of Major Diseases, College of Life Science and Medicine, Zhejiang Sci-Tech University) Y Yiliang He (Department of Biopharmaceutics, Zhejiang Provincial Engineering Research Center of New Technologies and Applications for Targeted Therapy of Major Diseases, College of Life Science and Medicine, Zhejiang Sci-Tech University) C Chenyang Zhang (Department of Biopharmaceutics, Zhejiang Provincial Engineering Research Center of New Technologies and Applications for Targeted Therapy of Major Diseases, College of Life Science and Medicine, Zhejiang Sci-Tech University) Q Qitao Qian (Department of Biopharmaceutics, Zhejiang Provincial Engineering Research Center of New Technologies and Applications for Targeted Therapy of Major Diseases, College of Life Science and Medicine, Zhejiang Sci-Tech University) Y Yuping Huang (Department of Biopharmaceutics, Zhejiang Provincial Engineering Research Center of New Technologies and Applications for Targeted Therapy of Major Diseases, College of Life Science and Medicine, Zhejiang Sci-Tech University) Q Qi Zhang P Panpan Shen C Chenhe Zhou (Department of Orthopedics, Second Affiliated Hospital, Zhejiang University School of Medicine) M Mengrui Wu (Department of Cell and Developmental Biology, College of Life Sciences, Zhejiang University) G Guiqian Chen (Department of Biopharmaceutics, Zhejiang Provincial Engineering Research Center of New Technologies and Applications for Targeted Therapy of Major Diseases, College of Life Science and Medicine, Zhejiang Sci-Tech University)

Abstract

Precise spatiotemporal regulation of parathyroid hormone (PTH) and PTH-related peptide signaling through the parathyroid hormone receptor 1 (PTH1R) is fundamental to skeletal development and metabolic bone remodeling, yet the intracellular mechanisms that fine-tune this signaling remain a central unanswered question. Here, we identify neurofibromin 2 (Nf2) as an essential regulator of PTH1R trafficking and signaling. Conditional knockout of Nf2 in chondrocytes results in short-limbed dwarfism, disrupted growth plate organization, and suppressed chondrocyte proliferation and hypertrophy, and a paradoxical bone phenotype marked by trabecular hyperproliferation and cortical thinning. Mechanistically, Nf2 binds to the PTH1R C-terminal domain (464–591 aa) to promote selective receptor internalization via β-arrestin2 without altering G protein–coupled receptor kinase-mediated PTH1R phosphorylation. Loss of Nf2 decouples PTH1R from β-arrestin2‐mediated endocytosis, leading to sustained and amplified signaling through the cAMP‐CREB‐pSOX9 (S181) and VEGF axis. Consequently, Nf2 -deficient mice exhibited bone changes similar to those induced by the PTH1R agonist abaloparatide. These findings establish Nf2 as a chondrocyte‐intrinsic gatekeeper of PTH1R signaling and uncover a cellular mechanism for bone homeostasis by targeting Nf2‐mediated β-arrestin2 recruitment.

Article Details

Volume / Issue Vol. 123, Issue 24
Published June 16, 2026
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (10)

J

Junguang Liao

Department of Biopharmaceutics, Zhejiang Provincial Engineering Research Center of New Technologies and Applications for Targeted Therapy of Major Diseases, College of Life Science and Medicine, Zhejiang Sci-Tech University

Y

Yiliang He

Department of Biopharmaceutics, Zhejiang Provincial Engineering Research Center of New Technologies and Applications for Targeted Therapy of Major Diseases, College of Life Science and Medicine, Zhejiang Sci-Tech University

C

Chenyang Zhang

Department of Biopharmaceutics, Zhejiang Provincial Engineering Research Center of New Technologies and Applications for Targeted Therapy of Major Diseases, College of Life Science and Medicine, Zhejiang Sci-Tech University

Q

Qitao Qian

Department of Biopharmaceutics, Zhejiang Provincial Engineering Research Center of New Technologies and Applications for Targeted Therapy of Major Diseases, College of Life Science and Medicine, Zhejiang Sci-Tech University

Y

Yuping Huang

Department of Biopharmaceutics, Zhejiang Provincial Engineering Research Center of New Technologies and Applications for Targeted Therapy of Major Diseases, College of Life Science and Medicine, Zhejiang Sci-Tech University

Q

Qi Zhang

P

Panpan Shen

C

Chenhe Zhou

Department of Orthopedics, Second Affiliated Hospital, Zhejiang University School of Medicine

M

Mengrui Wu

Department of Cell and Developmental Biology, College of Life Sciences, Zhejiang University

G

Guiqian Chen

Department of Biopharmaceutics, Zhejiang Provincial Engineering Research Center of New Technologies and Applications for Targeted Therapy of Major Diseases, College of Life Science and Medicine, Zhejiang Sci-Tech University