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KLF2/PPARγ axis contributes to trauma-induced heterotopic ossification by regulating mitochondrial dysfunction

ABSTRACT: KLF2/PPARγ axis contributes to trauma-induced heterotopic ossification by regulating mitochondrial dysfunction

PROVIDER: PRJNA975447 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24705844_1.fastq.gz	Fastqsanger.gz
	SRR24705844_2.fastq.gz	Fastqsanger.gz
	SRR24705845_1.fastq.gz	Fastqsanger.gz
	SRR24705845_2.fastq.gz	Fastqsanger.gz
	SRR24705846_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

KLF2/PPARγ axis contributes to trauma-induced heterotopic ossification by regulating mitochondrial dysfunction

Project description:Trauma-induced heterotopic ossification (HO) is one of the most complex disorders after musculoskeletal injury and is characterized by aberrant extraskeletal bone formation. Recent studies have shed light on the critical role of dysregulated osteogenic differentiation in aberrant bone formation. Krupel-like factor 2 (KLF2) and peroxisome proliferator-activated receptor gamma (PPARγ) are master adapter proteins that link cellular responses to osteogenesis; however, their roles and relationships in HO remain elusive.

2023-05-29 | GSE233201 | GEO

Tenomodulin prevents trauma-induced heterotopic ossification in tendon

Project description:Tenomodulin prevents trauma-induced heterotopic ossification in tendon

| PRJNA743873 | ENA

KLF2/PPARγ axis contributes to trauma-induced heterotopic ossification by regulating mitochondrial dysfunction.

Project description:Trauma-induced heterotopic ossification (HO) is a complex disorder after musculoskeletal injury and characterized by aberrant extraskeletal bone formation. Recent studies shed light on critical role of dysregulated osteogenic differentiation in aberrant bone formation. Krupel-like factor 2 (KLF2) and peroxisome proliferator-activated receptor gamma (PPARγ) are master adapter proteins that link cellular responses to osteogenesis; however, their roles and relationships in HO remain elusive. Using a murine burn/tenotomy model in vivo, we identified elevated KLF2 and reduced PPARγ levels in tendon stem/progenitor cells (TSPCs) during trauma-induced HO formation. Both KLF2 inhibition and PPARγ promotion reduced mature HO, whereas the effects of PPARγ promotion were abolished by KLF2 overexpression. Additionally, mitochondrial dysfunction and reactive oxygen species (ROS) production also increased after burn/tenotomy, and improvements in mitochondrial function (ROS scavenger) could alleviate HO formation, but were abolished by KLF2 activation and PPARγ suppression by affecting redox balance. Furthermore, in vitro, we found increased KLF2 and decreased PPARγ levels in osteogenically induced TSPCs. Both KLF2 inhibition and PPARγ promotion relieved osteogenesis by improving mitochondrial function and maintaining redox balance, and effects of PPARγ promotion were abolished by KLF2 overexpression. Our findings suggest that KLF2/PPARγ axis exerts regulatory effects on trauma-induced HO through modulation of mitochondrial dysfunction and ROS production in TSPCs by affecting redox balance. Targeting KLF2/PPARγ axis and mitochondrial dysfunction can represent attractive approaches to therapeutic intervention in trauma-induced HO.

| S-EPMC10771107 | biostudies-literature

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.

2022-11-02 | GSE161388 | GEO

Wisp inhibits chondrogenic differentiation in heterotopic ossification

Project description:Heterotopic ossification (HO) is the formation of extra-skeletal bone in muscle and soft tissues. Better characterization of the signaling pathways predisposing to HO is critical to identifying therapies directed against this common and potentially debilitating condition. WISP-1 (WNT1-inducible-signaling pathway protein 1) is a CCN family member and is expressed in skeletal cells during bone development or repair. Here, we sought to comprehensively explore the significance of WISP-1 across mouse and human HO. Among CCN family members, local Wisp1 expression was most highly upregulated within experimental trauma-associated HO by RNA sequencing, and increased Wisp1 corresponded to gene markers of osteochondral differentiation. WISP1 immunolocalization demonstrated conserved expression in osteochondral cells across mouse and human HO, including an FOP-like model, post-traumatic model, and human examples of non-genetic HO. Transgenic Wisp1 global knockout demonstrated an increase in cartilage and bone in a trauma-induced HO model. Microarray and in vitro culture of Wisp1 null cells suggested that WISP1 functions as a negative regulator of chondrogenic differentiation, and that Wisp1 deletion results in unrestrained endochondral HO formation. siRNA mediated WISP1 knockdown in human progenitor cells confirmed this finding. Overall, these findings suggest that endogenous WISP1 has pathophysiologic relevance in trauma-induced HO and functions as a negative regulator of ectopic chondrogenesis.

2020-06-08 | GSE127956 | GEO

Wisp inhibits chondrogenic differentiation in heterotopic ossification

Project description:Wisp inhibits chondrogenic differentiation in heterotopic ossification

| PRJNA525862 | ENA

Rat heterotopic ossification model proteome

Project description:The mechanism of heterotopic ossification remains largely unclarified. in this project, we administrated Achilles tenotomy (AT) and partial Achilles tenotomy (PAT) to rat models to simulate the varied size of ectopic bone we observed in the clinical courses. Then we applied Data-independent acquisition (DIA) proteomic strategy to identify the proteins and signaling pathways associated with the progress of heterotopic ossification and propagation of the ectopic bone mass.

2021-04-28 | PXD025678 |

Differential expression profiles of circRNA in mice with traumatic heterotopic ossification

Project description:To investigate whether circRNAs could participate in the pathological osteogenesis of traumatic heterotopic ossification (HO). RNA sequencing was performed to analyze the circRNA expression profile in mice HO tissues and to investigate the relevant mechanisms. We found that 491 circRNAs were significantly differentially expressed in mouse HO tissues by a fold-change ≥2 and p-value ≤0.05. Among these, 168 circRNAs were upregulated, while 323 were downregulated.

2022-11-05 | GSE217301 | GEO

Disturbed glycolipid metabolism activates CXCL13-CXCR5 axis in senescent TSCs to promote heterotopic ossification formation

Project description:Heterotopic ossification (HO) occurs as a common complication after injury, while its risk factor and mechanism remain unclear yet, which restricts the development of pharmacological treatment. Clinical research suggested that diabetes mellitus (DM) patients were prone to develop HO in tendon, but the solid evidence and mechanical research are still needed. Here, we combined the clinical samples and DM mice model to identify that disordered glycolipid metabolism aggravates the senescence of tendon derived stem cells (TSCs) and promotes their osteogenic differentiation. Then, combining the RNA-seq results of aging tendon, we detected the abnormally activated autocrine CXCL13-CXCR5 axis in TSCs cultured in high fat high glucose (HFHG) environment and also in aged tendon. Genetic inhibition of CXCL13 successfully alleviates the HO formation in DM mice, providing a potential therapeutical target for suppressing HO formation in DM patients after trauma or surgery.

2024-08-28 | GSE234916 | GEO

Tenomodulin prevents trauma-induced heterotopic ossification in tendon

Project description:We have reported that loss of Tnmd leads to inferior early tendon repair characterized by fibrovascular scaring and therefore hypothesized that its lack will persistently cause deficient repair during later stages. Tnmd knockout (Tnmd-/-) and wild-type (WT) animals were subjected to complete Achilles tendon surgical transection followed by end-to-end suture. Lineage tracing revealed a reduction in tendon-lineage cells marked by ScleraxisGFP, but an increase in alpha smooth muscle actin myofibroblasts in Tnmd-/- tendon scars. At the proliferative stage, more pro-inflammatory M1 macrophages and larger collagen II cartilaginous template were detected in this group. At the remodeling stage, histological scoring revealed lower repair quality in the injured Tnmd-/- tendons, which was coupled with higher HO quantified by micro-CT. Tendon biomechanical properties were compromised in both groups upon injury, however we identified an abnormal stiffening of non-injured Tnmd-/- tendons, which possessed higher static and dynamic E-moduli. Pathologically thicker and abnormally shaped collagen fibrils were observed by TEM in Tnmd-/- tendons and this together with augmented HO resulted in diminished running capacity of Tnmd-/- mice. These novel findings demonstrate that Tnmd plays a protecting role against trauma-induced endochondral HO and can inspire the generation of novel therapeutics to accelerate repair.

2021-11-08 | GSE179454 | GEO

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