Human cellular differences in cAMP - CREB signaling correlate with light-dependent melatonin suppression and bipolar disorder
Various lines of evidence suggest a mechanistic role for altered cAMP‐CREB (cAMP response element ‐ binding protein) signaling in depressive and affective disorders. However, the establishment and validation of human inter‐individual differences in this and other major signaling pathways has proven...
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| Published in | The European journal of neuroscience Vol. 40; no. 1; pp. 2206 - 2215 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford
Blackwell Publishing Ltd
01.07.2014
Blackwell |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Various lines of evidence suggest a mechanistic role for altered cAMP‐CREB (cAMP response element ‐ binding protein) signaling in depressive and affective disorders. However, the establishment and validation of human inter‐individual differences in this and other major signaling pathways has proven difficult. Here, we describe a novel lentiviral methodology to investigate signaling variation over long periods of time directly in human primary fibroblasts. On a cellular level, this method showed surprisingly large inter‐individual differences in three major signaling pathways in human subjects that nevertheless correlated with cellular measures of genome‐wide transcription and drug toxicity. We next validated this method by establishing a likely role for cAMP‐mediated signaling in a human neuroendocrine response to light – the light‐dependent suppression of the circadian hormone melatonin – that shows wide inter‐individual differences of unknown origin in vivo. Finally, we show an overall greater magnitude of cellular CREB signaling in individuals with bipolar disorder, suggesting a possible role for this signaling pathway in susceptibility to mental disease. Overall, our results suggest that genetic differences in major signaling pathways can be reliably detected with sensitive viral‐based reporter profiling, and that these differences can be conserved across tissues and be predictive of physiology and disease susceptibility.
Alterations in cAMP/CREB and circadian signaling pathways have been implicated previously in bipolar disorder. In this paper, we use a novel lentiviral methodology to investigate signaling variation over long periods of time directly in human primary fibroblasts taken from bipolar and healthy subjects. Our results show that fibroblast cAMP/CREB signaling amplitude correlates with both light‐dependent melatonin suppression and susceptibility to bipolar disorder. More generally, our data suggest that genetic differences in major signaling pathways can be reliably unearthed by sensitive viral‐based reporter profiling, and that these differences can be conserved across tissues and predictive of neurophysiology and disease susceptibility. |
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| AbstractList | Various lines of evidence suggest a mechanistic role for altered cAMP-CREB (cAMP response element - binding protein) signaling in depressive and affective disorders. However, the establishment and validation of human inter-individual differences in this and other major signaling pathways has proven difficult. Here, we describe a novel lentiviral methodology to investigate signaling variation over long periods of time directly in human primary fibroblasts. On a cellular level, this method showed surprisingly large inter-individual differences in three major signaling pathways in human subjects that nevertheless correlated with cellular measures of genome-wide transcription and drug toxicity. We next validated this method by establishing a likely role for cAMP-mediated signaling in a human neuroendocrine response to light - the light-dependent suppression of the circadian hormone melatonin - that shows wide inter-individual differences of unknown origin in vivo. Finally, we show an overall greater magnitude of cellular CREB signaling in individuals with bipolar disorder, suggesting a possible role for this signaling pathway in susceptibility to mental disease. Overall, our results suggest that genetic differences in major signaling pathways can be reliably detected with sensitive viral-based reporter profiling, and that these differences can be conserved across tissues and be predictive of physiology and disease susceptibility.Various lines of evidence suggest a mechanistic role for altered cAMP-CREB (cAMP response element - binding protein) signaling in depressive and affective disorders. However, the establishment and validation of human inter-individual differences in this and other major signaling pathways has proven difficult. Here, we describe a novel lentiviral methodology to investigate signaling variation over long periods of time directly in human primary fibroblasts. On a cellular level, this method showed surprisingly large inter-individual differences in three major signaling pathways in human subjects that nevertheless correlated with cellular measures of genome-wide transcription and drug toxicity. We next validated this method by establishing a likely role for cAMP-mediated signaling in a human neuroendocrine response to light - the light-dependent suppression of the circadian hormone melatonin - that shows wide inter-individual differences of unknown origin in vivo. Finally, we show an overall greater magnitude of cellular CREB signaling in individuals with bipolar disorder, suggesting a possible role for this signaling pathway in susceptibility to mental disease. Overall, our results suggest that genetic differences in major signaling pathways can be reliably detected with sensitive viral-based reporter profiling, and that these differences can be conserved across tissues and be predictive of physiology and disease susceptibility. Various lines of evidence suggest a mechanistic role for altered cAMP-CREB (cAMP response element - binding protein) signaling in depressive and affective disorders. However, the establishment and validation of human inter-individual differences in this and other major signaling pathways has proven difficult. Here, we describe a novel lentiviral methodology to investigate signaling variation over long periods of time directly in human primary fibroblasts. On a cellular level, this method showed surprisingly large inter-individual differences in three major signaling pathways in human subjects that nevertheless correlated with cellular measures of genome-wide transcription and drug toxicity. We next validated this method by establishing a likely role for cAMP-mediated signaling in a human neuroendocrine response to light - the light-dependent suppression of the circadian hormone melatonin - that shows wide inter-individual differences of unknown origin in vivo. Finally, we show an overall greater magnitude of cellular CREB signaling in individuals with bipolar disorder, suggesting a possible role for this signaling pathway in susceptibility to mental disease. Overall, our results suggest that genetic differences in major signaling pathways can be reliably detected with sensitive viral-based reporter profiling, and that these differences can be conserved across tissues and be predictive of physiology and disease susceptibility. Alterations in cAMP/CREB and circadian signaling pathways have been implicated previously in bipolar disorder. In this paper, we use a novel lentiviral methodology to investigate signaling variation over long periods of time directly in human primary fibroblasts taken from bipolar and healthy subjects. Our results show that fibroblast cAMP/CREB signaling amplitude correlates with both light-dependent melatonin suppression and susceptibility to bipolar disorder. More generally, our data suggest that genetic differences in major signaling pathways can be reliably unearthed by sensitive viral-based reporter profiling, and that these differences can be conserved across tissues and predictive of neurophysiology and disease susceptibility. Various lines of evidence suggest a mechanistic role for altered cAMP-CREB (cAMP response element - binding protein) signaling in depressive and affective disorders. However, the establishment and validation of human inter-individual differences in this and other major signaling pathways has proven difficult. Here, we describe a novel lentiviral methodology to investigate signaling variation over long periods of time directly in human primary fibroblasts. On a cellular level, this method showed surprisingly large inter-individual differences in three major signaling pathways in human subjects that nevertheless correlated with cellular measures of genome-wide transcription and drug toxicity. We next validated this method by establishing a likely role for cAMP-mediated signaling in a human neuroendocrine response to light - the light-dependent suppression of the circadian hormone melatonin - that shows wide inter-individual differences of unknown origin in vivo. Finally, we show an overall greater magnitude of cellular CREB signaling in individuals with bipolar disorder, suggesting a possible role for this signaling pathway in susceptibility to mental disease. Overall, our results suggest that genetic differences in major signaling pathways can be reliably detected with sensitive viral-based reporter profiling, and that these differences can be conserved across tissues and be predictive of physiology and disease susceptibility. Various lines of evidence suggest a mechanistic role for altered cAMP‐CREB (cAMP response element ‐ binding protein) signaling in depressive and affective disorders. However, the establishment and validation of human inter‐individual differences in this and other major signaling pathways has proven difficult. Here, we describe a novel lentiviral methodology to investigate signaling variation over long periods of time directly in human primary fibroblasts. On a cellular level, this method showed surprisingly large inter‐individual differences in three major signaling pathways in human subjects that nevertheless correlated with cellular measures of genome‐wide transcription and drug toxicity. We next validated this method by establishing a likely role for cAMP ‐mediated signaling in a human neuroendocrine response to light – the light‐dependent suppression of the circadian hormone melatonin – that shows wide inter‐individual differences of unknown origin in vivo . Finally, we show an overall greater magnitude of cellular CREB signaling in individuals with bipolar disorder, suggesting a possible role for this signaling pathway in susceptibility to mental disease. Overall, our results suggest that genetic differences in major signaling pathways can be reliably detected with sensitive viral‐based reporter profiling, and that these differences can be conserved across tissues and be predictive of physiology and disease susceptibility. Various lines of evidence suggest a mechanistic role for altered cAMP‐CREB (cAMP response element ‐ binding protein) signaling in depressive and affective disorders. However, the establishment and validation of human inter‐individual differences in this and other major signaling pathways has proven difficult. Here, we describe a novel lentiviral methodology to investigate signaling variation over long periods of time directly in human primary fibroblasts. On a cellular level, this method showed surprisingly large inter‐individual differences in three major signaling pathways in human subjects that nevertheless correlated with cellular measures of genome‐wide transcription and drug toxicity. We next validated this method by establishing a likely role for cAMP‐mediated signaling in a human neuroendocrine response to light – the light‐dependent suppression of the circadian hormone melatonin – that shows wide inter‐individual differences of unknown origin in vivo. Finally, we show an overall greater magnitude of cellular CREB signaling in individuals with bipolar disorder, suggesting a possible role for this signaling pathway in susceptibility to mental disease. Overall, our results suggest that genetic differences in major signaling pathways can be reliably detected with sensitive viral‐based reporter profiling, and that these differences can be conserved across tissues and be predictive of physiology and disease susceptibility. Alterations in cAMP/CREB and circadian signaling pathways have been implicated previously in bipolar disorder. In this paper, we use a novel lentiviral methodology to investigate signaling variation over long periods of time directly in human primary fibroblasts taken from bipolar and healthy subjects. Our results show that fibroblast cAMP/CREB signaling amplitude correlates with both light‐dependent melatonin suppression and susceptibility to bipolar disorder. More generally, our data suggest that genetic differences in major signaling pathways can be reliably unearthed by sensitive viral‐based reporter profiling, and that these differences can be conserved across tissues and predictive of neurophysiology and disease susceptibility. |
| Author | Gaspar, Ludmila Gordijn, Marijke C. M. Moriggi, Ermanno Johansson, Anne-Sophie Owe-Larsson, Björn Brown, Steven A. van de Werken, Maan Kocks, Janwillem W. H. Lundkvist, Gabriella B. |
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| Copyright | 2014 Federation of European Neuroscience Societies and John Wiley & Sons Ltd 2015 INIST-CNRS 2014 Federation of European Neuroscience Societies and John Wiley & Sons Ltd. |
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| Keywords | Mood disorder Human Melatonin Cyclic AMP Bipolar disorder Biological rhythm Circadian rhythm Signal transduction circadian inter-individual differences cAMP-CREB Transcription factor CREB Fibroblast Pineal hormone bipolar disorder fibroblast melatonin |
| Language | English |
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| Notes | Swiss National Science Foundation ArticleID:EJN12602 istex:C0B840F8F836E6995BD6481DD6AFD428136DE3A2 ark:/67375/WNG-J8C58DW6-S Fig. S1. Response of CREB, ELK1 and CHOP pathway profiling reporters is dose-responsive. Fig. S2. Pathway profile values are robust to experimental variation. Fig. S3. Intersubject differences in pathway expression are conserved regardless of differences in viral titer, cellular confluence, and passage number. Fig. S4. Reporter - based variations in measured signaling pathways are robust. Table S1. Fold-activation of CREB target genes by forskolin. Table S2. Fold-activation of ELK1 target genes by PMA. Table S3. Fold-activation of CHOP target genes by MMS. Table S4. genego pathway analysis of the differences between subject 1 and subject 10 in response to forskolin treatment. Table S5. genego pathway analysis of the differences between subject 6 and subject 8 in response to PMA treatment. Table S6. genego pathway analysis of the differences between subject 7 and subject 6 in response to MMS treatment. Table S7. Cohort of 10 patients with bipolar disorder type I [Cohort 2/recruited in Sweden/bipolar patients (Cohort 2/SW/BIPO)]. Velux Foundation 6th European Framework project EUCLOCK - No. 018741 University of Zurich Clinical Research Priority Program 'Sleep and Health' ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Article-2 ObjectType-Feature-1 |
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| Snippet | Various lines of evidence suggest a mechanistic role for altered cAMP‐CREB (cAMP response element ‐ binding protein) signaling in depressive and affective... Various lines of evidence suggest a mechanistic role for altered cAMP-CREB (cAMP response element - binding protein) signaling in depressive and affective... |
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| SubjectTerms | Adult Adult and adolescent clinical studies Biological and medical sciences bipolar disorder Bipolar Disorder - metabolism Bipolar disorders cAMP-CREB Cells, Cultured Chronobiology circadian Cohort Studies Cyclic AMP - metabolism Cyclic AMP Response Element-Binding Protein - metabolism European Continental Ancestry Group Female fibroblast Fibroblasts - metabolism Fundamental and applied biological sciences. Psychology Genetic Vectors Humans inter-individual differences Lentivirus - genetics Light Male Medical sciences melatonin Melatonin - metabolism Middle Aged Mood disorders Photic Stimulation Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Signal Transduction Vertebrates: anatomy and physiology, studies on body, several organs or systems Young Adult |
| Title | Human cellular differences in cAMP - CREB signaling correlate with light-dependent melatonin suppression and bipolar disorder |
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