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ScRNA sequencing of cells harvested from the tendon injury site after a severe burn/tenotomy injury with and without sciatic neurectomy

ABSTRACT: scRNA sequencing of cells harvested from the tendon injury site after a severe burn/tenotomy injury with and without sciatic neurectomy

PROVIDER: PRJNA686113 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13268672_1.fastq.gz	Fastqsanger.gz
	SRR13268672_2.fastq.gz	Fastqsanger.gz
	SRR13268673_1.fastq.gz	Fastqsanger.gz
	SRR13268673_2.fastq.gz	Fastqsanger.gz
	SRR13268674_1.fastq.gz	Fastqsanger.gz

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scRNA sequencing of cells harvested from the tendon injury site after a severe burn/tenotomy injury with and without sciatic neurectomy

Project description:scRNA sequencing was performed on cells harvested from the injury site of mice that underwent a burn/tenotomy injury with sciatic neurectomy or sham neurectomy (skin incision) to study the role of nerves in the formation of heterotopic ossification and aberrant stem cell differentiation following traumatic injury.

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scRNA and snATAC sequencing of cells harvested from the tendon injury site after a severe burn/tenotomy injury

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Identification of plasma extracellular vesicle biomarkers after burn injury

Project description:Severe burn injury is a one of the most devastating forms of trauma with over 1.1 million burns each year requiring medical attention in the United States. Deaths from burn injury are commonly caused by immune-related sequelae such as pneumonia, organ failure and other opportunistic bacterial infections. Though there have been numerous studies to assess the immunological dysfunction associated with burn injury, there have yet to be a predictive biomarker, that can be used to assess high risk patients and their outcomes. We hypothesized that circulating extracellular vesicles (EVs) released early after burn injury would promote activate peripheral macrophages and specific cargo could be used as a biomarker to identify at-risk patients. To test this hypothesis, we assessed the immune consequences of adoptive transfer of EVs isolated after burn injury in vitro and used unbiased proteomic on EVs from mouse models and human burn patients from the UNC Jaycee Burn Center. Findings here suggest EVs serve as mediators of immune dysfunction and potential biomarkers.

2022-02-16 | PXD028515 | Pride

Burn Injury (1-7d)

Project description:Animal experiments were performed with male Sprague-Dawley rats (Charles River Laboratories, Boston, MA) weighing 150 ? 200 grams. All experimental protocols used in this study were approved by the Subcommittee on Research Animal Care, Massachusetts General Hospital. Rats were individually housed in a temperature-controlled (25oC) and light-controlled room (12h light-dark cycle) and allowed to adjust to their new surroundings for at least 5 days prior to the experiment. Water and rat chow were provided ad libitum to the animals. On the day of the treatment, the animals were randomly divided into two groups, burned and sham-burned. The burn injury consisted of a full-skin-thickness scald burn of the dorsum, calculated to be ~ 20% of the rat?s total body surface area (TBSA), induced by immersing the designated area in boiling water for 10 s (45). Rats were resuscitated with an intra-peritoneal injection of sterile saline solution (1.5 mL/Kg body weight/% TBSA) immediately after burn. The mortality rate of this treatment was negligible. At each time point (1, 2, 4, and 7d), three animals belonging to each group were sacrificed, the liver and serum collected, and stored at ?80oC after being inflicted with 20% TBSA burn injury. Sham-burn rats (n=3) considered as the control were treated identically except that they were immersed into a 37oC water bath and immediately sacrificed to collect the livers. Keywords = Burn Liver microarray genechip time course Keywords: time-course

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Partial Tendon Injury at the Tendon-to-Bone Enthesis Activates Skeletal Stem Cells

Project description:Partial tendon-to-bone interface (TBI) injuries heal in a mechanically inferior manner and redevelop healthy uninjured tissue morphology. The origin of the cells involved in tendon-to-bone healing remains unknown. We employed a rigorous approach to evaluate if mouse skeletal stem cells (mSSC) play a role in tendon-to-bone healing after partial-injury. Using fluorescence-activated cell sorting we identified that found that they are present within the TBI. Using a TBI-injury rainbow lineage tracing mouse model, we demonstrated that injury-responsive cells within the TBI and calcaneus proliferate polyclonally following partial-tendon injury at the TBI. These injury-responsive clonal cells express skeletal marker SP7. We quantified the differences in mSCC frequency after TBI-injury and found that mSSC respond to injury with a higher frequency and have associated changes in gene expression, with the specific down-regulation of the TGFβ signaling pathway. Exogenous delivery of TGFβ after injury was found to reduce the mSSC response after injury. These findings suggest that mSSC may facilitate tendon-to-bone healing by downregulating TGFβ signaling within the mSSC niche.

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