Hepcidin deficiency causes bone loss through interfering with the canonical Wnt/β-catenin pathway via Forkhead box O3a

Journal of Orthopaedic Translation
Guangfei LiYou-jia Xu

Abstract

Hepcidin deficiency is known to cause body iron accumulation and bone microarchitecture defects, but the exact underlying mechanisms of hepcidin deficiency-induced bone loss remain unclear. Our objective was to understand the molecular mechanism of hepcidin deficiency-induced bone loss. The bone phenotypes of wild type (WT) and hepcidin knockout (Hepcidin-KO) mice were measured by microcomputed tomography. The osteoclastic marker of the bone was measured by tartrate-resistant acid phosphatase staining. The osteoblastic marker of the bone was measured by immunostaining of osteocalcin. Primary osteoblastic and osteoclastic differentiation was performed using bone marrow cells. The mature osteoclast was determined by tartrate-resistant acid phosphatase staining, pit formation assay and relative gene expression. The mature osteoblast was determined by alkaline phosphatase activity, alkaline phosphatase staining, Alizarin Red staining and relative gene expression. The protein expression of β-catenin, TCF4/TCF7L2 and Forkhead box O3a (FOXO3a) was measured by Western blot and their combination by co-immunoprecipitation. In vivo study was performed by tail vein administration of FOXO3a-RNAi using an adeno-associated virus in Hepcidin-K...Continue Reading

Citations

Apr 2, 2021·Molecular and Cellular Biochemistry·Xian-Min LiTian-Lan Zhao
Dec 24, 2021·International Journal of Sport Nutrition and Exercise Metabolism·Nikita C FenshamLouise M Burke

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Methods Mentioned

BETA
Assay
reverse transcription-PCR
Protein Assay
electrophoresis
co-immunoprecipitation
Co-IP

Software Mentioned

ImageJ
GraphPad Prism

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