GEO series

Thyroid Stimulating Hormone (TSH) Protects Against Osteoporosis through AMPK Signaling Pathway in Osteoclasts II

GSE216422 Mus musculus (mouse) RNA-seq (gene expression) 3 samples Submitted 2025/10/20 Platform GPL17021

At a glance

RNA-seq (gene expression) · mouse · 3 samples

What it is: RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism: Mus musculus (mouse)
Samples: 3 samples
Data you can get: A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.

Summary (written by the submitters)

It has been believed that osteoporosis associated with hyperthyroidism due to elevated thyroxine level. But patients with subclinical hyperthyroidism, decline in the level of thyroid stimulating hormone (TSH) alone, are at equal risk of osteoporosis. Research has shown that there is thyroid-stimulating hormone receptor (TSHR) on the osteoclast, but whether TSH regulates osteoclast directly and its mechanisms are still not be stated clearly.

Read the full summary ↓

In this study, in combination of in vivo and in vitro, we took the osteoclast precursor cell conditional and systemic knockout TSHR mouse models to study the effects of TSHR knockout on bone metabolism in mice and the changes of osteoclast differentiation and function in vitro. Transcriptomics was used to screen the differential genes and signal pathways, and the in vitro experiments were verified. We found that Tshr flox/ flox Lyz2-Cre (TSHR MKO) mice display decreased femoral biomechanics and bone density, damaged bone microstructure. Serum bone resorption marker CTX-I was significantly increased, accompanied by an increase in the number of osteoclasts in bone sections in TSHR MKO mice. The percentage of CD11b+ in TSHR knockout mice was decreased compared with control littermates. Osteoclasts from Tshr -/- mice had stronger osteoclast differentiation and acid secretion ability. In vitro cell experiments confirmed TSH effecting osteoclast differentiation and function by activation of AMPK signaling pathway. In conclusion, TSH inhibits osteoclast differentiation and bone resorption by activating AMPK signaling pathway, increases bone mass, and has osteoprotective effect. This will provide a reference for the diagnosis and treatment of osteoporosis, especially thyroid function related bone metabolism bnormalities. TSH structural analogues or AMPK activators are expected to provide new ideas for the development of drugs for the prevention and treatment of osteoporosis.

This dataset

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Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE216422_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA893593 and SRA study SRP404213. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Samples in this study

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+ 3 more — browse all 3 samples with per-sample file links →

Datasets on a similar topic

GSE216421 Thyroid Stimulating Hormone (TSH) Protects Against Osteoporosis through AMPK Signaling Pathway in Osteoclasts I 6 samples shares ampk, tsh, osteoporosis, stimulating, osteoclasts, protects, thyroid, hormone
GSE279577 Transcriptomic Landscape of Hyperthyroidism in Mice Overexpressing Thyroid Stimulating Hormone 21 samples shares stimulating, thyroid, hormone
GSE249196 Functional and transcriptomic dose-response analysis of follicle-stimulating hormone in ex vivo mouse folliculogenesis and oogenesis 50 samples shares stimulating, hormone
GSE290347 Effects of Short-Term High Fat/ High Sugar Diet on Follicle - Stimulating Hormone Secretion and Ovarian Gene Expression 24 samples shares stimulating, hormone
GSE275041 Skeletal muscle-derived myostatin is a major endocrine driver of follicle-stimulating hormone synthesis 11 samples shares stimulating, hormone
GSE196742 Mogrol attenuates osteoclast formation and bone resorption by inhibiting the TRAF6/MAPK/NF-κB signaling pathway in vitro and protects against osteoporosis in postmenopausal mice 6 samples shares osteoporosis, protects
GSE310461 Regulation of murine follicle-stimulating hormone β subunit transcription by newly identified enhancers 27 samples shares stimulating, hormone
GSE310459 Regulation of murine follicle-stimulating hormone β subunit transcription by newly identified enhancers [ChIP-seq; LβT2 cells] 13 samples shares stimulating, hormone

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