E2F1 Expression and Apoptosis Initiation in Crayfish and Rat Peripheral Neurons and Glial Cells after Axonal Injury
Neurotrauma is among the main causes of human disability and mortality. The transcription factor E2F1 is one of the key proteins that determine the fate of cells. The involvement of E2F1 in the regulation of survival and death of peripheral nerve cells after axotomy has not been previously studied....
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MDPI AG
2022-04-01
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author | Valentina Dzreyan Moez Eid Stanislav Rodkin Maria Pitinova Svetlana Demyanenko |
author_facet | Valentina Dzreyan Moez Eid Stanislav Rodkin Maria Pitinova Svetlana Demyanenko |
author_sort | Valentina Dzreyan |
collection | DOAJ |
description | Neurotrauma is among the main causes of human disability and mortality. The transcription factor E2F1 is one of the key proteins that determine the fate of cells. The involvement of E2F1 in the regulation of survival and death of peripheral nerve cells after axotomy has not been previously studied. We, for the first time, studied axotomy-induced changes in the expression and localization of E2F1 following axonal injury in rats and crayfish. Immunoblotting and immunofluorescence microscopy were used for the analysis of the expression and intracellular localization of E2F1 and its changes after axotomy. To evaluate whether this transcription factor promotes cell apoptosis, we examined the effect of pharmacological inhibition of E2F activity in axotomized rat models. In this work, axotomy caused increased expression of E2F1 as early as 4 h and even 1 h after axotomy of mechanoreceptor neurons and ganglia of crayfish ventral nerve cord (VNC), as well as rat dorsal root ganglia (DRG). The level of E2F1 expression increased both in the cytoplasm and the nuclei of neurons. Pharmacological inhibition of E2F demonstrated a pronounced neuroprotective activity against axotomized DRGs. E2F1 and downstream targets could be considered promising molecular targets for the development of potential neuroprotective agents. |
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spelling | doaj.art-5712a23a83b4430fadd54dab9b332ae22023-12-03T13:31:08ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-04-01238445110.3390/ijms23084451E2F1 Expression and Apoptosis Initiation in Crayfish and Rat Peripheral Neurons and Glial Cells after Axonal InjuryValentina Dzreyan0Moez Eid1Stanislav Rodkin2Maria Pitinova3Svetlana Demyanenko4Laboratory of Molecular Neurobiology, Academy of Biology and Biotechnology, Southern Federal University, Stachki Ave., 194/1, 344090 Rostov-on-Don, RussiaLaboratory of Molecular Neurobiology, Academy of Biology and Biotechnology, Southern Federal University, Stachki Ave., 194/1, 344090 Rostov-on-Don, RussiaLaboratory of Molecular Neurobiology, Academy of Biology and Biotechnology, Southern Federal University, Stachki Ave., 194/1, 344090 Rostov-on-Don, RussiaLaboratory of Molecular Neurobiology, Academy of Biology and Biotechnology, Southern Federal University, Stachki Ave., 194/1, 344090 Rostov-on-Don, RussiaLaboratory of Molecular Neurobiology, Academy of Biology and Biotechnology, Southern Federal University, Stachki Ave., 194/1, 344090 Rostov-on-Don, RussiaNeurotrauma is among the main causes of human disability and mortality. The transcription factor E2F1 is one of the key proteins that determine the fate of cells. The involvement of E2F1 in the regulation of survival and death of peripheral nerve cells after axotomy has not been previously studied. We, for the first time, studied axotomy-induced changes in the expression and localization of E2F1 following axonal injury in rats and crayfish. Immunoblotting and immunofluorescence microscopy were used for the analysis of the expression and intracellular localization of E2F1 and its changes after axotomy. To evaluate whether this transcription factor promotes cell apoptosis, we examined the effect of pharmacological inhibition of E2F activity in axotomized rat models. In this work, axotomy caused increased expression of E2F1 as early as 4 h and even 1 h after axotomy of mechanoreceptor neurons and ganglia of crayfish ventral nerve cord (VNC), as well as rat dorsal root ganglia (DRG). The level of E2F1 expression increased both in the cytoplasm and the nuclei of neurons. Pharmacological inhibition of E2F demonstrated a pronounced neuroprotective activity against axotomized DRGs. E2F1 and downstream targets could be considered promising molecular targets for the development of potential neuroprotective agents.https://www.mdpi.com/1422-0067/23/8/4451apoptosisE2F1 inhibitioncrayfish neurondorsal root ganglionE2F1nerve injury |
spellingShingle | Valentina Dzreyan Moez Eid Stanislav Rodkin Maria Pitinova Svetlana Demyanenko E2F1 Expression and Apoptosis Initiation in Crayfish and Rat Peripheral Neurons and Glial Cells after Axonal Injury International Journal of Molecular Sciences apoptosis E2F1 inhibition crayfish neuron dorsal root ganglion E2F1 nerve injury |
title | E2F1 Expression and Apoptosis Initiation in Crayfish and Rat Peripheral Neurons and Glial Cells after Axonal Injury |
title_full | E2F1 Expression and Apoptosis Initiation in Crayfish and Rat Peripheral Neurons and Glial Cells after Axonal Injury |
title_fullStr | E2F1 Expression and Apoptosis Initiation in Crayfish and Rat Peripheral Neurons and Glial Cells after Axonal Injury |
title_full_unstemmed | E2F1 Expression and Apoptosis Initiation in Crayfish and Rat Peripheral Neurons and Glial Cells after Axonal Injury |
title_short | E2F1 Expression and Apoptosis Initiation in Crayfish and Rat Peripheral Neurons and Glial Cells after Axonal Injury |
title_sort | e2f1 expression and apoptosis initiation in crayfish and rat peripheral neurons and glial cells after axonal injury |
topic | apoptosis E2F1 inhibition crayfish neuron dorsal root ganglion E2F1 nerve injury |
url | https://www.mdpi.com/1422-0067/23/8/4451 |
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