Knorr_2022_Sci.Rep_12_18565

Reference

Title : Protection of insect neurons by erythropoietin\/CRLF3-mediated regulation of pro-apoptotic acetylcholinesterase - Knorr_2022_Sci.Rep_12_18565
Author(s) : Knorr DY , Schneider K , Buschgens L , Forster J , Georges NS , Geurten BRH , Heinrich R
Ref : Sci Rep , 12 :18565 , 2022
Abstract : Cytokine receptor-like factor 3 (CRLF3) is a conserved but largely uncharacterized orphan cytokine receptor of eumetazoan animals. CRLF3-mediated neuroprotection in insects can be stimulated with human erythropoietin. To identify mechanisms of CRLF3-mediated neuroprotection we studied the expression and proapoptotic function of acetylcholinesterase in insect neurons. We exposed primary brain neurons from Tribolium castaneum to apoptogenic stimuli and dsRNA to interfere with acetylcholinesterase gene expression and compared survival and acetylcholinesterase expression in the presence or absence of the CRLF3 ligand erythropoietin. Hypoxia increased apoptotic cell death and expression of both acetylcholinesterase-coding genes ace-1 and ace-2. Both ace genes give rise to single transcripts in normal and apoptogenic conditions. Pharmacological inhibition of acetylcholinesterases and RNAi-mediated knockdown of either ace-1 or ace-2 expression prevented hypoxia-induced apoptosis. Activation of CRLF3 with protective concentrations of erythropoietin prevented the increased expression of acetylcholinesterase with larger impact on ace-1 than on ace-2. In contrast, high concentrations of erythropoietin that cause neuronal death induced ace-1 expression and hence promoted apoptosis. Our study confirms the general proapoptotic function of AChE, assigns a role of both ace-1 and ace-2 in the regulation of apoptotic death and identifies the erythropoietin/CRLF3-mediated prevention of enhanced acetylcholinesterase expression under apoptogenic conditions as neuroprotective mechanism.
ESTHER : Knorr_2022_Sci.Rep_12_18565
PubMedSearch : Knorr_2022_Sci.Rep_12_18565
PubMedID: 36329181

Related information

Citations formats

Knorr DY, Schneider K, Buschgens L, Forster J, Georges NS, Geurten BRH, Heinrich R (2022)
Protection of insect neurons by erythropoietin\/CRLF3-mediated regulation of pro-apoptotic acetylcholinesterase
Sci Rep 12 :18565

Knorr DY, Schneider K, Buschgens L, Forster J, Georges NS, Geurten BRH, Heinrich R (2022)
Sci Rep 12 :18565

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    [paper] => Knorr_2022_Sci.Rep_12_18565
    [author] => Knorr DY || Schneider K || Buschgens L || Forster J || Georges NS || Geurten BRH || Heinrich R
    [year] => 2022
    [title] => Protection of insect neurons by erythropoietin\/CRLF3-mediated regulation of pro-apoptotic acetylcholinesterase
    [journal] => Sci Rep
    [volume] => 12
    [page] => 18565
    [medline] => 36329181
    [abstract] => Knorr_2022_Sci.Rep_12_18565
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            [content] => Cytokine receptor-like factor 3 (CRLF3) is a conserved but largely uncharacterized orphan cytokine receptor of eumetazoan animals. CRLF3-mediated neuroprotection in insects can be stimulated with human erythropoietin. To identify mechanisms of CRLF3-mediated neuroprotection we studied the expression and proapoptotic function of acetylcholinesterase in insect neurons. We exposed primary brain neurons from Tribolium castaneum to apoptogenic stimuli and dsRNA to interfere with acetylcholinesterase gene expression and compared survival and acetylcholinesterase expression in the presence or absence of the CRLF3 ligand erythropoietin. Hypoxia increased apoptotic cell death and expression of both acetylcholinesterase-coding genes ace-1 and ace-2. Both ace genes give rise to single transcripts in normal and apoptogenic conditions. Pharmacological inhibition of acetylcholinesterases and RNAi-mediated knockdown of either ace-1 or ace-2 expression prevented hypoxia-induced apoptosis. Activation of CRLF3 with protective concentrations of erythropoietin prevented the increased expression of acetylcholinesterase with larger impact on ace-1 than on ace-2. In contrast, high concentrations of erythropoietin that cause neuronal death induced ace-1 expression and hence promoted apoptosis. Our study confirms the general proapoptotic function of AChE, assigns a role of both ace-1 and ace-2 in the regulation of apoptotic death and identifies the erythropoietin/CRLF3-mediated prevention of enhanced acetylcholinesterase expression under apoptogenic conditions as neuroprotective mechanism.
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