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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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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

Adenosine impairs the proliferative capacity of terminally mature NK cells

Project description:Adenosine impairs the proliferative capacity of terminally mature NK cells

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Liver-Specific Overexpression of HKDC1 Increases Hepatocyte Size and Proliferative Capacity

Project description:Liver-Specific Overexpression of HKDC1 Increases Hepatocyte Size and Proliferative Capacity

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Dietary cystine restriction increases the proliferative capacity of the small intestine of mice

Project description:Dietary cystine restriction increases the proliferative capacity of the small intestine of mice

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Dietary cystine restriction increases the proliferative capacity of the small intestine of mice

Project description:Dietary cystine restriction increases the proliferative capacity of the small intestine of mice

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Validation of small molecule activators and identification of altered signaling pathways underlying the age-related decline in proliferative capacity in human dermal progenitors

Project description:Validation of small molecule activators and identification of altered signaling pathways underlying the age-related decline in proliferative capacity in human dermal progenitors

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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.

2018-05-08 | GSE99476 | GEO

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

2018-05-08 | GSE99336 | GEO

Elucidating the corneal endothelial cell proliferation capacity through an interspecies transcriptome comparison

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).

2023-01-20 | GSE222458 | GEO

Dietary cystine restriction increases the proliferative capacity of the small intestine of mice

Project description:Cysteine is a semi-essential amino acid provided by dietary intake of mainly meat, eggs and whole grains or via the amino acid methionine. The majority of dietary cystine is absorbed in the small intestine and can be used for protein synthesis or converted to taurine and glutathione. Since there is a trend towards adopting a vegetarian/vegan diet, which is low in cysteine, in this study, we investigate the effect of dietary cystine restriction on intestinal epithelial layer function. Mice (8/group) received a normal diet or a diet low in cystine for 2 weeks. We observed no changes in plasma methionine, cysteine, taurine or glutathione levels after 2 weeks. Stem cell markers as well as the proliferation marker Ki67 were or tended to be increased upon cystine restriction. Gene set enrichment analysis reveals enrichment of Wnt signaling in the small intestine of mice on the low cystine diet. These proliferative effects were not observed in the colon, and are thus specific for the small intestine. In the colon, we observed that dietary cystine restriction results in an increase in the number of goblet cells but no significant changes in the thickness of the mucus barrier or in its protective capacity. There was no difference in the microbiome between the normal and low cystine diet. Overall, we cannot conclude if dietary cystine restriction is beneficial, since increased proliferation and goblet cells can indicate a potential for damage repair, nevertheless hyperproliferation has the potential to induce cancer as well.

2023-09-01 | GSE234566 | GEO

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