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Fetuin A is an immunomodulator and therapeutic target for Heterotopic ossification and associated bone loss

ABSTRACT: Fetuin A is an immunomodulator and therapeutic target for Heterotopic ossification and associated bone loss

PROVIDER: PRJNA677998 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13050800_1.fastq.gz	Fastqsanger.gz
	SRR13050800_2.fastq.gz	Fastqsanger.gz
	SRR13050801_1.fastq.gz	Fastqsanger.gz
	SRR13050801_2.fastq.gz	Fastqsanger.gz
	SRR13050802_1.fastq.gz	Fastqsanger.gz

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Fetuin A is an immunomodulator and therapeutic target for Heterotopic ossification and associated bone loss

Project description:Heterotopic ossification (HO), the pathologic growth of extra-skeletal bone, occurs as a common complication of trauma or in genetic disorders and can be disabling and lethal.We report that mice harboring injury-induced HO exhibit bone loss similar to the presentation of HO patients. Esepecially, Fetuin A dysregulation promotes immunosupression in HO lesion to link HO and bone loss.

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Interorgan communication in the neurogenic heterotopic ossification: focusing on the role of brain-derived extracellular vesicles

Project description:Brain-derived extracellular vesicles participate in inter-organ communication after traumatic brain injury by transporting pathogens to initiate secondary injury. Inflammasome related proteins encapsulated in brain-derived extracellular vesicles are capable of crossing the blood-brain barrier to reach distal tissues. These proteins initiate inflammatory dysfunction such as neurogenic heterotopic ossification. This recurrent condition is highly debilitating to patients because of its relatively unknown pathogenesis and the lack of effective prophylactic intervention strategies. Accordingly, a rat model of neurogenic heterotopic ossification that combined traumatic brain injury and achillotenotomy was developed to address these two issues. Histological examination of the injured tendon identified the coexistence of ectopic calcification and fibroblast pyroptosis. The relationships among brain-derived extracellular vesicles, fibroblast pyroptosis and ectopic calcification were further investigated in vitro and in vivo. Intravenous injection of the pyroptosis inhibitor Ac-YVAD-cmk reversed the development of neurogenic heterotopic ossification in vivo. The present work highlighted the role of brain-derived extracellular vesicles in the pathogenesis of neurogenic heterotopic ossification and offered a potential strategy for the prevention of neurogenic heterotopic ossification after traumatic brain injury.

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Transcriptome analysis of heterotopic ossification mesenchymal stromal cells

Project description:Heterotopic Ossification (HO) is the abnormal formation of ectopic bone in soft tissues generally in muscles surrounding joints such hip, knee, elbow or shoulder. The etiology of this pathology is not known but it is well established that the risk of HO is increased after traumatic brain or spinal cord injuries and also after fractures or burns. Patients with HOs suffer from pain and the range of motion from limbs with ectopic bone is highly reduced. Currently, the only effective treatment for HOs is surgical resection but they can reoccur after resection underpinning that a better understanding of its pathophysiology is required to cure patients. To date, the nature of osteogenic precursor cells (of mesenchymal origin) forming HOs is not fully elucidated and remains to be defined. A transcriptional analysis of mesenchymal stromal cells (MSCs) from HOs would help identifying molecules that could be therapeutically targeted.

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