GPER1 contributes to T3-induced osteogenesis by mediating glycolysis in osteoblast precursors

Author:

Xue Ying1,Liu Guo-ming12,Ke Dian-shan13ORCID,Yu Yun-long13ORCID,Hou Jian-Ming1

Affiliation:

1. Shengli Clinical Medical College of Fujian Medical University, Fuzhou 350001, China

2. Department of Orthopedics, South Hospital of Fujian Provincial Hospital, Fuzhou 350001, China

3. Department of Orthopedics, Fujian Provincial Hospital, Fuzhou 350001, China

Abstract

Triiodothyronine (T3) is critical to osteogenesis, which is the key factor in bone growth. Our transcriptomic and metabolomic analysis results indicated that T3 leads to enhanced expression of G protein-coupled estrogen receptor 1 (GPER1) as well as increases in glycolysis metabolite levels. Accordingly, our study aimed to explore the role of GPER1-mediated glycolysis in T3-regulated osteogenesis. The MC3T3-E1 cell line was used as an osteoblast precursor model. After treatment with T3, a GPER1-specific antagonist (G15) and inhibitor of glycolysis (3PO) were used to explore the roles of GPER1 and glycolysis in T3-regulated osteogenesis, as measured by ALP activity, Alizarin red staining intensity and osteogenic molecule expression. Our results showed that T3 promoted osteogenesis-related activity, which was reversed by treatment with G15. In addition, T3 enhanced the glycolytic potential and production of lactic acid (LD) in MC3T3-E1 cells, and treatment with G15 restored the aforementioned effects of T3. Ultimately, the pharmacological inhibition of glycolysis with 3PO blocked the ability of T3 to enhance osteogenic activities. In conclusion, GPER1 mediates glycolysis in osteoblast precursors, which is critical for T3-promoted osteogenesis.

Funder

Natural Science Foundation of Fujian Province

National Natural Science Foundation of China

Publisher

Frontiers Media SA

Subject

General Biochemistry, Genetics and Molecular Biology

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