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Comprehensive transcriptome analysis of osteoclasts with the SIK3 deletion and pterosin B treatment.

ABSTRACT: Comprehensive transcriptome analysis of osteoclasts with the SIK3 deletion and pterosin B treatment.

PROVIDER: PRJNA980570 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24834800_1.fastq.gz	Fastqsanger.gz
	SRR24834800_2.fastq.gz	Fastqsanger.gz
	SRR24834801_1.fastq.gz	Fastqsanger.gz
	SRR24834801_2.fastq.gz	Fastqsanger.gz
	SRR24834802_1.fastq.gz	Fastqsanger.gz

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Comprehensive transcriptome analysis of osteoclasts with the SIK3 deletion and pterosin B treatment.

Project description:Maintenance of bone homeostasis and the balance between bone resorption and formation are crucial for maintaining skeletal integrity. Osteoclasts are responsible for bone resorption and play a vital role in this process. The role of salt-inducible kinase 3 (SIK3) in osteoclast differentiation and maturation and its potential as a therapeutic target for osteoporosis remain poorly understood. Here, we generated osteoclast-specific Sik3 conditional knockout (cKO) mice and investigated the effects of SIK3 deletion on bone homeostasis. Our findings revealed increased bone mineral density and an osteopetrosis phenotype in Sik3 cKO mice, indicating the involvement of SIK3 in bone resorption. Furthermore, we examined the effect of pterosin B, an SIK3 inhibitor, on osteoclast differentiation. Pterosin B treatment inhibits osteoclast differentiation in vitro, reduces the number of multinucleated osteoclasts, and suppresses bone resorption. Therefore, in this study, to better understand the molecular mechanism of SIK3 in osteoclast differentiation and maturation, we performed gene expression profiling of bone marrow monocytes from SIK3 deletion and pterosin B treated mice using RNA sequencing (RNA-seq).

2024-07-21 | GSE234221 | GEO

Identification of Sik3-targeting compound, pterosin B, for treatment of osteoarthritis

Project description:Osteoarthritis is a common joint disorder that causes debilitating conditions among the elderly. Risk factors of osteoarthritis include age, which is often associated with the thinning of articular cartilage. We generated conditional knockout mice that lack salt-inducible kinase 3 (Sik3) specifically in chondrocytes after birth by tamoxifen administration. Deletion of Sik3 at 2 or 8 weeks after birth increased the thickness of articular cartilage by increasing the chondrocyte population. Additionally, Sik3 deletion protected cartilage against osteoarthritis development. We identified the edible Pteridium aquilinum ingredient, pterosin B, as a compound that inhibits the Sik3 pathway. Intraarticular injection of pterosin B protected cartilage against osteoarthritis development. Sik3 deletion or pterosin B treatment inhibited activation of the hypertrophic program through the histone deacetylase 4 (Hdac4) pathway, increased Prg4 expression in chondrocytes, and protected cartilage against osteoarthritic attack. Collectively, our results suggest Sik3 is a regulator that regulates homeostasis of articular cartilage thickness and a target for treatment of osteoarthritis, and that pterosin B can be the lead compound for relevant drugs.

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Whole transcriptome analysis of osteoclasts after treatment with or without etelcalcetide

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Effects of SIK3 KO on the transcriptome in CA1 region

Project description:SIK3 is reported to regulate sleep in mice, but it's unclear how SIK3 works at the synapse in the brain. Here, to explore the potential effects of endogenous SIK3 on the global transcriptome, in-vivo deletion of SIK3 was achieved by CRISPR KO in the CA1 region of Cas9 mice. The CA1 tissues were dissected and analyzed by bulk RNAseq. The result shows that in-vivo deletion of SIK3 induces a minor change in the transcriptome, suggesting a transcription-independent mechanism for SIK3.

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Comparison expression data from wild-type and NFATc1-deficient osteoclasts

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Project description:Bisphosphonates are the mainstay of therapy worldwide for osteoporosis. They inhibit the activities of the osteoclasts, the bone resorption cells. While bisphosphonates are known to block farnesyl pyrophsophate synthase to exert their anti-resorptive action, the detailed mechanism is not well understood. Examining the change in expression profile before and after bisphosphonate treatment in the osteoclasts might shed some light on the biological pathways that are perturbed. Osteoclastic precursor cells were treated with (or without) bisphosphonates (alendronate or risedronate) during their differentiation into mature osteoclasts.

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Project description:Phosphate binders, vitamin D analogs, and calcimimetics have recently been used to control the disturbed mineral metabolism in chronic kidney disease-mineral and bone disorder (CKD-MBD). Etelcalcetide , a new calcimimetic agent approved by is considered by patients due to its convenience as an intravenous form which easily affordable during dialysis sessions. In this study, we evaluated the effects of etelcalcetide on osteoclasts.

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USP8-mediated mitochondrial regulation in osteoclasts is essential for skeletal development

Project description:Aberrant protein regulatory pathways disrupt bone homeostasis and contribute to skeletal diseases. Many of cysteine protease family of deubiquitinating enzymes (DUBs) are critical for regulation of bone-resorbing osteoclasts and bone-forming osteoblasts. Here, we demonstrate that the DUB ubiquitin-specific protease 8 (USP8) is highly expressed in osteoclasts and its deletion impairs osteoclast development and bone resorption activity. Deletion of USP8 in osteoclasts (Usp8Ctsk) results in low bone mass due to defective endochondral ossification and short stature resulting from abnormal growth plate structure. Mechanistically, USP8 deficiency in osteoclasts dampens mitochondrial number, activity, oxidative phosphorylation, and mitophagy, while reactive oxygen species (ROS) inflammatory responses are increased in these cells. Moreover, USP8-deficient osteoclasts in metaphysis produce secretory factors that hinder both cartilage formation in the growth plate and trabecular bone formation. Collectively, these findings identify USP8 as a key regulator of osteoclast development and secretory factor production, shaping the microenvironment essential for skeletal development.

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