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dc.contributor.authorTee, Jing Yang
dc.contributor.authorSutharsan, Ratneswary
dc.contributor.authorFan, Yongjun
dc.contributor.authorMackay-Sim, Alan
dc.date.accessioned2017-07-25T12:31:05Z
dc.date.available2017-07-25T12:31:05Z
dc.date.issued2017
dc.identifier.issn1044-7431
dc.identifier.doi10.1016/j.mcn.2017.03.005
dc.identifier.urihttp://hdl.handle.net/10072/342066
dc.description.abstractSchizophrenia is a highly heritable psychiatric disorder linked to a large number of risk genes. The function of these genes in disease etiology is not fully understood but pathway analyses of genomic data suggest developmental dysregulation of cellular processes such as neuronal migration and axon guidance. Previous studies of patient-derived olfactory cells show them to be more motile than control-derived cells when grown on a fibronectin substrate, motility that is dependent on focal adhesion kinase signaling. The aim of this study was to investigate whether schizophrenia patient-derived cells are responsive to other extracellular matrix (ECM) proteins that bind integrin receptors. Olfactory neurosphere-derived cells from nine patients and nine matched controls were grown on ECM protein substrates at increasing concentrations and their movement was tracked for 24 h using automated high-throughput imaging. Control-derived cells increased their motility as the ECM substrate concentration increased, whereas patient-derived cell motility was little affected by ECM proteins. Patient and control cells had appropriate integrin receptors for these ECM substrates and detected them as shown by increases in focal adhesion number and size in response to ECM proteins, which also induced changes in cell morphology and cytoskeleton. These observations indicate that patient cells failed to translate the detection of ECM proteins into appropriate changes in cell motility. In a sense, patient cells act like a moving car whose accelerator is jammed, moving at the same speed without regard to the external environment. This focuses attention on cell motility regulation rather than speed as key to impairment of neuronal migration in the developing brain in schizophrenia.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherElsevier
dc.relation.ispartofpagefrom111
dc.relation.ispartofpageto122
dc.relation.ispartofjournalMolecular and Cellular Neuroscience
dc.relation.ispartofvolume80
dc.subject.fieldofresearchNeurosciences not elsewhere classified
dc.subject.fieldofresearchNeurosciences
dc.subject.fieldofresearchPsychology
dc.subject.fieldofresearchCognitive Sciences
dc.subject.fieldofresearchcode110999
dc.subject.fieldofresearchcode1109
dc.subject.fieldofresearchcode1701
dc.subject.fieldofresearchcode1702
dc.titleCell migration in schizophrenia: Patient-derived cells do not regulate motility in response to extracellular matrix
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
dcterms.licensehttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.description.versionVersion of Record (VoR)
gro.facultyGriffith Sciences, Griffith Institute for Drug Discovery
gro.rights.copyright© 2017 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, providing that the work is properly cited.
gro.hasfulltextFull Text
gro.griffith.authorMackay-Sim, Alan
gro.griffith.authorSutharsan, Ratneswary
gro.griffith.authorFan, Yongjun
gro.griffith.authorTee, Bernard


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