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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.

In vitro dexamethasone treatment does not induce alternative ATM transcripts in cells from Ataxia–Telangiectasia patients