HDAC1 mediates p53 cytoplasmic translocation in dorsal root ganglia after sciatic nerve transection
Valentina A. Dzreyan Laboratory of Molecular Neurobiology, Academy of Biology and Biotechnology, Southern Federal University, prospect Stachki 194/1, Rostov‐on‐Don, Russia
Abstract
In our previous works, immunofluorescence microscopy and immunoblotting showed the overexpression of HDAC1 and HDAC2 in the dorsal root ganglia (DRG) at 1-4 hours after sciatic nerve transection as the earliest proapoptotic event. This was followed by the upregulation of proapoptotic protein p53 at 24 hours post-axotomy. In DRG neurons, HDAC1 was initially upregulated at one hour post-axotomy but then redistributed together with p53 from the nuclei to the cytoplasm at 24 h post-axotomy. Administration of sodium valproate, a non-selective inhibitor of I class HDACs, prevented axotomy-induced p53 cytoplasma translocation and reduced overexpression of p53 in the axotomized DRG.
To examine the possible interaction between HDAC1 or HDAC2 and p53, we performed co-immunoprecipitation and Duolink® proximity ligation assay (PLA®) for endogenous HDAC1 or HDAC2 and p53. Co-IP and PLA data indicated that HDAC1, but not HDAC2 and p53, do interact.
Thus, HDAC1 mediates p53 cytoplasmic translocation in DRG after axotomy and so is involved in the axotomy-induced injury of DRG neurons and glial cells. HDAC1 and downstream target factors, for example p53, may be considered promising molecular targets for the development of potential neuroprotective agents.
Supported by the Ministry of Education and Science of the Russian Federation (project no. 0852-2020-0028), and a scholarship of the President of the Russian Federation for young scientists.
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Dzreyan Valentina Aleksandrovna
Laboratory of Molecular Neurobiology, Southern Federal University, prospect Stachki 194/1, Rostov‐on‐Don, Russia
Russia
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