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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Main Authors: Valentina Dzreyan, Moez Eid, Stanislav Rodkin, Maria Pitinova, Svetlana Demyanenko
Format: Article
Language:English
Published: MDPI AG 2022-04-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/23/8/4451
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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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AT stanislavrodkin e2f1expressionandapoptosisinitiationincrayfishandratperipheralneuronsandglialcellsafteraxonalinjury
AT mariapitinova e2f1expressionandapoptosisinitiationincrayfishandratperipheralneuronsandglialcellsafteraxonalinjury
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