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BMAL1-TTK-H2Bub1 loop deficiency contributes to impaired BM-MSC-mediated bone formation in senile osteoporosis

ABSTRACT: BMAL1-TTK-H2Bub1 loop deficiency contributes to impaired BM-MSC-mediated bone formation in senile osteoporosis

PROVIDER: PRJNA865870 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20791150_1.fastq.gz	Fastqsanger.gz
	SRR20791150_2.fastq.gz	Fastqsanger.gz
	SRR20791151_1.fastq.gz	Fastqsanger.gz
	SRR20791151_2.fastq.gz	Fastqsanger.gz
	SRR20791152_1.fastq.gz	Fastqsanger.gz

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BMAL1-TTK-H2Bub1 loop deficiency contributes to impaired BM-MSC-mediated bone formation in senile osteoporosis

Project description:We performed multiomic high-throughput sequencing to recapitulated the BMAL1-H2Bub1 loop in mesenchymal stem cells osteogenesis. We used lentiviruses to diminish RNF40 and WAC, which are parts of the obligate complex and monoubiquitinated histone H2B, in MSCs, and analysed the H2Bub1 and PolII CUT&Tag-seq.

2022-08-06 | GSE210425 | GEO

BMAL1-TTK-H2Bub1 loop deficiency contributes to impaired BM-MSC-mediated bone formation in senile osteoporosis.

Project description:During the aging process, the reduced osteogenic differentiation of bone marrow mesenchymal stem cells (BM-MSCs) results in decreased bone formation, which contributes to senile osteoporosis. Previous studies have confirmed that interrupted circadian rhythm plays an indispensable role in age-related disease. However, the mechanism underlying the impaired osteogenic differentiation of BM-MSCs during aging and its relationship with interrupted circadian rhythm remains unclear. In this study, we confirmed that the circadian rhythm was interrupted in aging mouse skeletal systems. The level of the core rhythm component BMAL1 but not that of CLOCK in the osteoblast lineage was decreased in senile osteoporotic specimens from both human and mouse. BMAL1 targeted TTK as a circadian-controlled gene to phosphorylate MDM2 and regulate H2Bub1 level, while H2Bub1 in turn regulated the expression of BMAL1. The osteogenic capacity of BM-MSCs was maintained by a positive loop formed by BMAL1-TTK-MDM2-H2Bub1. Furthermore, we demonstrated that using bone-targeting recombinant adeno-associated virus 9 (rAAV9) to enhance Bmal1 or Ttk might have a therapeutic effect on senile osteoporosis and delays bone repair in aging mice. In summary, our study indicated that targeting the BMAL1-TTK-MDM2-H2Bub1 axis via bone-targeting rAAV9 might be a promising strategy for the treatment of senile osteoporosis.

| S-EPMC9996134 | biostudies-literature

Bone formation in senile osteoporosisbone formation in senile osteoporosis

Project description:Bone formation in senile osteoporosisbone formation in senile osteoporosis

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Transcriptome Alteration Between Young and Senile Human Bone MSC

Project description:In order to uncover mechanisms of hBMSC senescence, we performed high-throughput RNA-seq using young and senile human bone MSC (hBMSC).

2023-09-20 | GSE160273 | GEO

Metridium senile

Project description:Metridium senile overview

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Metridium senile

Project description:Metridium senile Genome sequencing

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Novel Role for Alpha-2-Macroglobulin (A2M) as a Disease Modifying Protein in Senile Osteoporosis

Project description:Novel Role for Alpha-2-Macroglobulin (A2M) as a Disease Modifying Protein in Senile Osteoporosis

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Transcriptome Alteration Between Young and Senile Human Bone MSC

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The H2Bub1-deposition complex is required for human and mouse cardiogenesis (RNA-Seq)

Project description:De novo variants affecting monoubiquitination of histone H2B (H2Bub1) are enriched in human congenital heart disease. H2Bub1 is required in stem cell differentiation, cilia function, post-natal cardiomyocyte maturation, and transcriptional elongation. However, how H2Bub1 affects cardiogenesis is unknown. We show that the H2Bub1-deposition complex (RNF20-RNF40-UBE2B) is required for mouse cardiogenesis and for differentiation of human iPSCs into cardiomyocytes. Mice with cardiac-specific Rnf20 deletion are embryonic lethal and have abnormal myocardium. We then analyzed H2Bub1 marks during differentiation of human iPSCs into cardiomyocytes. H2Bub1 is erased from most genes at transition from cardiac mesoderm to cardiac progenitor cells, but is preserved on a subset of long cardiac-specific genes. When H2Bub1 is reduced in iPSC-cardiomyocytes, long cardiac-specific genes have fewer full-length transcripts. This correlates with H2Bub1 accumulation near the center of these genes. H2Bub1 accumulation near the center of tissue-specific genes was also observed in embryonic fibroblasts and fetal osteoblasts. In summary, we show that normal H2Bub1 distribution is required for cardiogenesis and cardiomyocyte differentiation, and point to H2Bub1 regulating tissue-specific gene expression by increasing the amount of full-length transcripts.

2023-10-31 | GSE246411 | GEO

The H2Bub1-deposition complex is required for human and mouse cardiogenesis (ChIP-Seq)

2023-10-31 | GSE246410 | GEO