AI Article Synopsis
- - Short-term treatment with low doses of glucocorticoid analogues, like dexamethasone, can improve neurological symptoms in Ataxia-Telangiectasia (A-T), a rare disease affecting the brain and immune system.
- - The study examined whether dexamethasone could induce an alternative ATM transcript (ATMdexa1) but found no evidence of this effect in A-T cell types or ATM-knockout cells.
- - Researchers highlighted that some results linked to ATMdexa1 may be due to cellular artifacts, suggesting that caution is needed when interpreting the effects of dexamethasone in lab settings before applying it to A-T patient treatment.
Article Abstract
Short term treatment with low doses of glucocorticoid analogues has been shown to ameliorate neurological symptoms in Ataxia-Telangiectasia (A-T), a rare autosomal recessive multisystem disease that mainly affects the cerebellum, immune system, and lungs. Molecular mechanisms underlying this clinical observation are unclear. We aimed at evaluating the effect of dexamethasone on the induction of alternative ATM transcripts (ATMdexa1). We showed that dexamethasone cannot induce an alternative ATM transcript in control and A-T lymphoblasts and primary fibroblasts, or in an ATM-knockout HeLa cell line. We also demonstrated that some of the reported readouts associated with ATMdexa1 are due to cellular artifacts and the direct induction of γH2AX by dexamethasone via DNA-PK. Finally, we suggest caution in interpreting dexamethasone effects in vitro for the results to be translated into a rational use of the drug in A-T patients.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7677391 | PMC |
| http://dx.doi.org/10.1038/s41598-020-77352-z | DOI Listing |
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