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Small molecule oxybutynin rescues proliferative capacity of complex III-defective MPCs

ABSTRACT: Small molecule oxybutynin rescues proliferative capacity of complex III-defective MPCs

PROVIDER: PRJNA1188628 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31417565_1.fastq.gz	Fastqsanger.gz
	SRR31417565_2.fastq.gz	Fastqsanger.gz
	SRR31417566_1.fastq.gz	Fastqsanger.gz
	SRR31417566_2.fastq.gz	Fastqsanger.gz
	SRR31417567_1.fastq.gz	Fastqsanger.gz

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Small molecule oxybutynin rescues proliferative capacity of complex III-defective MPCs

Project description:Mitochondrial disease encompasses a group of genetically inherited disorders hallmarked by an inability of the respiratory chain to produce sufficient ATP. These disorders present with multisystemic pathologies that predominantly impact highly energetic tissues such as skeletal muscle. There is no cure or effective treatment for mitochondrial disease. We have discovered a small molecule known as oxybutynin that can bypass Complex III mitochondrial dysfunction in primary murine and human skeletal muscle progenitor cells (MPCs). Oxybutynin administration improves MPC proliferative capacity, enhances cellular glycolytic function, and improves myotube formation. Mechanistically, results from our isothermal shift assay indicates that oxybutynin interacts with a suite of proteins involved in mRNA processing which then trigger the upregulation biological pathways to circumvent CIII mitochondrial dysfunction. Taken together, we provide evidence for the small molecule oxybutynin as a potential therapeutic candidate for the future treatment of CIII mitochondrial dysfunction.

2024-11-25 | GSE282462 | GEO

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ERF deletion rescues RAS deficiency in mouse embryonic stem cells [ChIP-seq]

Project description:RAS proteins are key regulators of growth factor signaling. Here we show that deletion of all RAS genes in mouse embryonic stem cells (mES) leads to an overall reduction in protein translation, limits their long-term proliferative capacity and incapacitates them to differentiate. Deletion of ERF, a transcriptional repressor of the ETS family, rescues proliferation and differentiation of RAS-deficient mES cells and allows the development of teratomas lacking RAS genes. Upon RAS deletion, ERF translocates to the nucleus where it binds to multiple enhancers of key RAS targets suppressing their expression. We also reveal recurrent losses of ERF in cancer and show that ERF deficiency increases the resistance of cancer cells to pharmacological inhibition of the RAS pathway. In summary, we here reveal a central role for ERF in coordinating RAS signaling in pluripotent cells, and identify a synthetic viable interaction that bypasses the requirement for RAS proteins in mammalian cells.

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ERF deletion rescues RAS deficiency in mouse embryonic stem cells [expression profiling]

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Project description:The regenerative capacity of corneal endothelial cells (CECs) differs between species; in bigger mammals such as humans and sheep, CECs are arrested in a non-proliferative state. Damage to these cells can compromise its function leading to corneal opacity and impaired vision. Corneal transplantation is the current treatment for the recovery of a clear eyesight, but the donor tissue demand is higher than the offer and there is the need to develop novel treatment modalities. In contrast, rabbit CECs retain a high proliferative profile and have the capacity to repopulate the endothelium upon injury. There is currently a lack of fundamental knowledge to explain the difference in the proliferation capacity of these cells across species. Gaining information on the transcriptomic differences across species could allow the identification of crucial proliferation drivers of CEC proliferation to develop novel regenerative medicine therapies. In this study we have analyzed at the transcriptomic level corneal endothelial samples originating from human, sheep, and rabbit. To understand the differences across the CECs proliferation capacity in each species, we have generated an automated pipeline for the analysis of pathways with different activity. Our results revealed that 52 pathways had commonly different activity when comparing species with non-proliferative endothelium (human and sheep) to species with proliferative endothelium (rabbit).

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