Transcriptional Modulation of the Hippo Signaling Pathway by Drugs Used to Treat Bipolar Disorder and Schizophrenia

Recent reports suggest a link between positive regulation of the Hippo pathway with bipolar disorder (BD), and the Hippo pathway is known to interact with multiple other signaling pathways previously associated with BD and other psychiatric disorders. In this study, neuronal-like NT2 cells were trea...

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Published inInternational journal of molecular sciences Vol. 22; no. 13; p. 7164
Main Authors Panizzutti, Bruna, Bortolasci, Chiara C., Spolding, Briana, Kidnapillai, Srisaiyini, Connor, Timothy, Richardson, Mark F., Truong, Trang T. T., Liu, Zoe S. J., Morris, Gerwyn, Gray, Laura, Hyun Kim, Jee, Dean, Olivia M., Berk, Michael, Walder, Ken
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 02.07.2021
MDPI
Subjects
Alzheimer's disease
Apoptosis
Bipolar disorder
Bipolar Disorder - drug therapy
Cell Line, Tumor
Drugs
Gene Expression Regulation - drug effects
Hippo Signaling Pathway
Humans
Insects
Nervous system
Pathophysiology
Protein Serine-Threonine Kinases - genetics
Protein Serine-Threonine Kinases - metabolism
Psychotropic drugs
Psychotropic Drugs - pharmacology
Psychotropic Drugs - therapeutic use
Schizophrenia
Schizophrenia - drug therapy
Signal Transduction - drug effects
Transcription factors
Transcription Factors - metabolism
bipolar disorder
Hippo pathway
drug repurposing
inflammation
neuroscience
connectivity map
psychiatry
schizophrenia
psychotropic drugs
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Abstract Recent reports suggest a link between positive regulation of the Hippo pathway with bipolar disorder (BD), and the Hippo pathway is known to interact with multiple other signaling pathways previously associated with BD and other psychiatric disorders. In this study, neuronal-like NT2 cells were treated with amisulpride (10 µM), aripiprazole (0.1 µM), clozapine (10 µM), lamotrigine (50 µM), lithium (2.5 mM), quetiapine (50 µM), risperidone (0.1 µM), valproate (0.5 mM), or vehicle control for 24 h. Genome-wide mRNA expression was quantified and analyzed using gene set enrichment analysis (GSEA), with genes belonging to Hippo, Wnt, Notch, TGF- β, and Hedgehog retrieved from the KEGG database. Five of the eight drugs downregulated the genes of the Hippo pathway and modulated several genes involved in the interacting pathways. We speculate that the regulation of these genes, especially by aripiprazole, clozapine, and quetiapine, results in a reduction of MAPK and NFκB pro-inflammatory signaling through modulation of Hippo, Wnt, and TGF-β pathways. We also employed connectivity map analysis to identify compounds that act on these pathways in a similar manner to the known psychiatric drugs. Thirty-six compounds were identified. The presence of antidepressants and antipsychotics validates our approach and reveals possible new targets for drug repurposing.
AbstractList Recent reports suggest a link between positive regulation of the Hippo pathway with bipolar disorder (BD), and the Hippo pathway is known to interact with multiple other signaling pathways previously associated with BD and other psychiatric disorders. In this study, neuronal-like NT2 cells were treated with amisulpride (10 µM), aripiprazole (0.1 µM), clozapine (10 µM), lamotrigine (50 µM), lithium (2.5 mM), quetiapine (50 µM), risperidone (0.1 µM), valproate (0.5 mM), or vehicle control for 24 h. Genome-wide mRNA expression was quantified and analyzed using gene set enrichment analysis (GSEA), with genes belonging to Hippo, Wnt, Notch, TGF- β, and Hedgehog retrieved from the KEGG database. Five of the eight drugs downregulated the genes of the Hippo pathway and modulated several genes involved in the interacting pathways. We speculate that the regulation of these genes, especially by aripiprazole, clozapine, and quetiapine, results in a reduction of MAPK and NFκB pro-inflammatory signaling through modulation of Hippo, Wnt, and TGF-β pathways. We also employed connectivity map analysis to identify compounds that act on these pathways in a similar manner to the known psychiatric drugs. Thirty-six compounds were identified. The presence of antidepressants and antipsychotics validates our approach and reveals possible new targets for drug repurposing.Recent reports suggest a link between positive regulation of the Hippo pathway with bipolar disorder (BD), and the Hippo pathway is known to interact with multiple other signaling pathways previously associated with BD and other psychiatric disorders. In this study, neuronal-like NT2 cells were treated with amisulpride (10 µM), aripiprazole (0.1 µM), clozapine (10 µM), lamotrigine (50 µM), lithium (2.5 mM), quetiapine (50 µM), risperidone (0.1 µM), valproate (0.5 mM), or vehicle control for 24 h. Genome-wide mRNA expression was quantified and analyzed using gene set enrichment analysis (GSEA), with genes belonging to Hippo, Wnt, Notch, TGF- β, and Hedgehog retrieved from the KEGG database. Five of the eight drugs downregulated the genes of the Hippo pathway and modulated several genes involved in the interacting pathways. We speculate that the regulation of these genes, especially by aripiprazole, clozapine, and quetiapine, results in a reduction of MAPK and NFκB pro-inflammatory signaling through modulation of Hippo, Wnt, and TGF-β pathways. We also employed connectivity map analysis to identify compounds that act on these pathways in a similar manner to the known psychiatric drugs. Thirty-six compounds were identified. The presence of antidepressants and antipsychotics validates our approach and reveals possible new targets for drug repurposing.
Recent reports suggest a link between positive regulation of the Hippo pathway with bipolar disorder (BD), and the Hippo pathway is known to interact with multiple other signaling pathways previously associated with BD and other psychiatric disorders. In this study, neuronal-like NT2 cells were treated with amisulpride (10 µM), aripiprazole (0.1 µM), clozapine (10 µM), lamotrigine (50 µM), lithium (2.5 mM), quetiapine (50 µM), risperidone (0.1 µM), valproate (0.5 mM), or vehicle control for 24 h. Genome-wide mRNA expression was quantified and analyzed using gene set enrichment analysis (GSEA), with genes belonging to Hippo, Wnt, Notch, TGF- β, and Hedgehog retrieved from the KEGG database. Five of the eight drugs downregulated the genes of the Hippo pathway and modulated several genes involved in the interacting pathways. We speculate that the regulation of these genes, especially by aripiprazole, clozapine, and quetiapine, results in a reduction of MAPK and NFκB pro-inflammatory signaling through modulation of Hippo, Wnt, and TGF-β pathways. We also employed connectivity map analysis to identify compounds that act on these pathways in a similar manner to the known psychiatric drugs. Thirty-six compounds were identified. The presence of antidepressants and antipsychotics validates our approach and reveals possible new targets for drug repurposing.
Author Liu, Zoe S. J.
Morris, Gerwyn
Dean, Olivia M.
Panizzutti, Bruna
Connor, Timothy
Hyun Kim, Jee
Truong, Trang T. T.
Walder, Ken
Gray, Laura
Spolding, Briana
Richardson, Mark F.
Berk, Michael
Kidnapillai, Srisaiyini
Bortolasci, Chiara C.
AuthorAffiliation 1 Institute for Innovation in Physical and Mental Health and Clinical Translation, School of Medicine, Deakin University, IMPACT, Geelong 3220, Australia; b.panizzuttiparry@deakin.edu.au (B.P.); chiara.b@deakin.edu.au (C.C.B.); briana.spolding@deakin.edu.au (B.S.); srisaiyini.kidnapillai@med.lu.se (S.K.); timothy.connor@deakin.edu.au (T.C.); truongtra@deakin.edu.au (T.T.T.T.); zoe.liu@deakin.edu.au (Z.S.J.L.); activatedmicroglia@gmail.com (G.M.); l.gray@deakin.edu.au (L.G.); jee.kim@deakin.edu.au (J.H.K.); o.dean@deakin.edu.au (O.M.D.); michael.berk@deakin.edu.au (M.B.)
6 Orygen Youth Health Research Centre, Parkville 3052, Australia
3 Florey Institute for Neuroscience and Mental Health, University of Melbourne, Parkville 3052, Australia
5 Centre of Youth Mental Health, University of Melbourne, Parkville 3052, Australia
4 Department of Psychiatry, Royal Melbourne Hospital, University of Melbourne, Parkville 3052, Australia
2 Genomics Centre, School of Life and Environmental Sciences, Deakin
AuthorAffiliation_xml – name: 5 Centre of Youth Mental Health, University of Melbourne, Parkville 3052, Australia
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– name: 1 Institute for Innovation in Physical and Mental Health and Clinical Translation, School of Medicine, Deakin University, IMPACT, Geelong 3220, Australia; b.panizzuttiparry@deakin.edu.au (B.P.); chiara.b@deakin.edu.au (C.C.B.); briana.spolding@deakin.edu.au (B.S.); srisaiyini.kidnapillai@med.lu.se (S.K.); timothy.connor@deakin.edu.au (T.C.); truongtra@deakin.edu.au (T.T.T.T.); zoe.liu@deakin.edu.au (Z.S.J.L.); activatedmicroglia@gmail.com (G.M.); l.gray@deakin.edu.au (L.G.); jee.kim@deakin.edu.au (J.H.K.); o.dean@deakin.edu.au (O.M.D.); michael.berk@deakin.edu.au (M.B.)
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Keywords bipolar disorder
Hippo pathway
drug repurposing
inflammation
neuroscience
connectivity map
psychiatry
schizophrenia
psychotropic drugs
Language English
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SSID ssj0023259
Score 2.424551
Snippet Recent reports suggest a link between positive regulation of the Hippo pathway with bipolar disorder (BD), and the Hippo pathway is known to interact with...
SourceID pubmedcentral
proquest
pubmed
crossref
SourceType Open Access Repository
Aggregation Database
Index Database
Enrichment Source
StartPage 7164
SubjectTerms Alzheimer's disease
Apoptosis
Bipolar disorder
Bipolar Disorder - drug therapy
Cell Line, Tumor
Drugs
Gene Expression Regulation - drug effects
Hippo Signaling Pathway
Humans
Insects
Nervous system
Pathophysiology
Protein Serine-Threonine Kinases - genetics
Protein Serine-Threonine Kinases - metabolism
Psychotropic drugs
Psychotropic Drugs - pharmacology
Psychotropic Drugs - therapeutic use
Schizophrenia
Schizophrenia - drug therapy
Signal Transduction - drug effects
Transcription factors
Transcription Factors - metabolism
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Title Transcriptional Modulation of the Hippo Signaling Pathway by Drugs Used to Treat Bipolar Disorder and Schizophrenia
URI https://www.ncbi.nlm.nih.gov/pubmed/34281223
https://www.proquest.com/docview/2549411870
https://www.proquest.com/docview/2553521809
https://pubmed.ncbi.nlm.nih.gov/PMC8268913
Volume 22
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