Reelin signaling is impaired in autism
Autism is a severe neurodevelopmental disorder with genetic and environmental etiologies. Recent genetic linkage studies implicate Reelin glycoprotein in causation of autism. To further investigate these studies, brain levels of Reelin protein and mRNA and mRNAs for VLDLR, Dab-1, and GSK3 were inves...
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| Veröffentlicht in: | Biological psychiatry (1969) 2005-04, Vol.57 (7), p.777-787 |
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| container_title | Biological psychiatry (1969) |
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| creator | Fatemi, S. Hossein Snow, Anne V. Stary, Joel M. Araghi-Niknam, Mohsen Reutiman, Teri J. Lee, Suzanne Brooks, Andrew I. Pearce, David A. |
| description | Autism is a severe neurodevelopmental disorder with genetic and environmental etiologies. Recent genetic linkage studies implicate Reelin glycoprotein in causation of autism. To further investigate these studies, brain levels of Reelin protein and mRNA and mRNAs for VLDLR, Dab-1, and GSK3 were investigated.
Postmortem superior frontal, parietal, and cerebellar cortices of age, gender, and postmortem interval-matched autistic and control subjects were subjected to SDS-PAGE and Western blotting of Reelin protein. Quantitative reverse transcriptase polymerase chain reaction analysis of Reelin, VLDL-R, Dab-1, and GSK3 mRNA species in superior frontal and cerebellar cortices of autistic and control subjects were also performed.
Reelin 410, 330, and 180 kDa/β-actin values were reduced significantly in frontal and cerebellar, and nonsignificantly in parietal, areas of autistic brains versus control subjects, respectively. The mRNAs for Reln and Dab-1 were reduced significantly whereas the mRNA for Reln receptor VLDLR was elevated significantly in superior frontal and cerebellar areas of autistic brains versus control brains, respectively.
Reductions in Reelin protein and mRNA and Dab 1 mRNA and elevations in Reln receptor VLDLR mRNA demonstrate impairments in the Reelin signaling system in autism, accounting for some of the brain structural and cognitive deficits observed in the disorder. |
| doi_str_mv | 10.1016/j.biopsych.2004.12.018 |
| format | Article |
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Postmortem superior frontal, parietal, and cerebellar cortices of age, gender, and postmortem interval-matched autistic and control subjects were subjected to SDS-PAGE and Western blotting of Reelin protein. Quantitative reverse transcriptase polymerase chain reaction analysis of Reelin, VLDL-R, Dab-1, and GSK3 mRNA species in superior frontal and cerebellar cortices of autistic and control subjects were also performed.
Reelin 410, 330, and 180 kDa/β-actin values were reduced significantly in frontal and cerebellar, and nonsignificantly in parietal, areas of autistic brains versus control subjects, respectively. The mRNAs for Reln and Dab-1 were reduced significantly whereas the mRNA for Reln receptor VLDLR was elevated significantly in superior frontal and cerebellar areas of autistic brains versus control brains, respectively.
Reductions in Reelin protein and mRNA and Dab 1 mRNA and elevations in Reln receptor VLDLR mRNA demonstrate impairments in the Reelin signaling system in autism, accounting for some of the brain structural and cognitive deficits observed in the disorder.</description><identifier>ISSN: 0006-3223</identifier><identifier>EISSN: 1873-2402</identifier><identifier>DOI: 10.1016/j.biopsych.2004.12.018</identifier><identifier>PMID: 15820235</identifier><identifier>CODEN: BIPCBF</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Actins - metabolism ; Adaptor Proteins, Signal Transducing ; Adult ; Adult and adolescent clinical studies ; Age Factors ; autism ; Autistic Disorder - genetics ; Autistic Disorder - metabolism ; Biological and medical sciences ; bipolar disorder ; Blotting, Western - methods ; Case-Control Studies ; Cell Adhesion Molecules, Neuronal - genetics ; Cell Adhesion Molecules, Neuronal - metabolism ; cerebellum ; Cerebral Cortex - metabolism ; Cerebral Cortex - pathology ; Dab-1 ; Electrophoretic Mobility Shift Assay - methods ; Extracellular Matrix Proteins - genetics ; Extracellular Matrix Proteins - metabolism ; Female ; Glycogen Synthase Kinase 3 - genetics ; Glycogen Synthase Kinase 3 - metabolism ; GSK-3β ; Humans ; Male ; Medical sciences ; Miscellaneous ; Models, Biological ; mRNA ; Nerve Tissue Proteins - genetics ; Nerve Tissue Proteins - metabolism ; parietal cortex ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; QPCR ; Receptors, LDL - genetics ; Receptors, LDL - metabolism ; Reelin ; Reverse Transcriptase Polymerase Chain Reaction - methods ; RNA, Messenger - biosynthesis ; schizophrenia ; Serine Endopeptidases - genetics ; Serine Endopeptidases - metabolism ; Sex Factors ; Signal Transduction - physiology ; superior frontal cortex ; VLDLR ; Western blotting ; β-actin</subject><ispartof>Biological psychiatry (1969), 2005-04, Vol.57 (7), p.777-787</ispartof><rights>2005 Society of Biological Psychiatry</rights><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c427t-a55454d191059dcb9e32d053d1f94724026b6b7d1d2348cfe99df60e917c32b43</citedby><cites>FETCH-LOGICAL-c427t-a55454d191059dcb9e32d053d1f94724026b6b7d1d2348cfe99df60e917c32b43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006322304013228$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16733218$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15820235$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fatemi, S. Hossein</creatorcontrib><creatorcontrib>Snow, Anne V.</creatorcontrib><creatorcontrib>Stary, Joel M.</creatorcontrib><creatorcontrib>Araghi-Niknam, Mohsen</creatorcontrib><creatorcontrib>Reutiman, Teri J.</creatorcontrib><creatorcontrib>Lee, Suzanne</creatorcontrib><creatorcontrib>Brooks, Andrew I.</creatorcontrib><creatorcontrib>Pearce, David A.</creatorcontrib><title>Reelin signaling is impaired in autism</title><title>Biological psychiatry (1969)</title><addtitle>Biol Psychiatry</addtitle><description>Autism is a severe neurodevelopmental disorder with genetic and environmental etiologies. Recent genetic linkage studies implicate Reelin glycoprotein in causation of autism. To further investigate these studies, brain levels of Reelin protein and mRNA and mRNAs for VLDLR, Dab-1, and GSK3 were investigated.
Postmortem superior frontal, parietal, and cerebellar cortices of age, gender, and postmortem interval-matched autistic and control subjects were subjected to SDS-PAGE and Western blotting of Reelin protein. Quantitative reverse transcriptase polymerase chain reaction analysis of Reelin, VLDL-R, Dab-1, and GSK3 mRNA species in superior frontal and cerebellar cortices of autistic and control subjects were also performed.
Reelin 410, 330, and 180 kDa/β-actin values were reduced significantly in frontal and cerebellar, and nonsignificantly in parietal, areas of autistic brains versus control subjects, respectively. The mRNAs for Reln and Dab-1 were reduced significantly whereas the mRNA for Reln receptor VLDLR was elevated significantly in superior frontal and cerebellar areas of autistic brains versus control brains, respectively.
Reductions in Reelin protein and mRNA and Dab 1 mRNA and elevations in Reln receptor VLDLR mRNA demonstrate impairments in the Reelin signaling system in autism, accounting for some of the brain structural and cognitive deficits observed in the disorder.</description><subject>Actins - metabolism</subject><subject>Adaptor Proteins, Signal Transducing</subject><subject>Adult</subject><subject>Adult and adolescent clinical studies</subject><subject>Age Factors</subject><subject>autism</subject><subject>Autistic Disorder - genetics</subject><subject>Autistic Disorder - metabolism</subject><subject>Biological and medical sciences</subject><subject>bipolar disorder</subject><subject>Blotting, Western - methods</subject><subject>Case-Control Studies</subject><subject>Cell Adhesion Molecules, Neuronal - genetics</subject><subject>Cell Adhesion Molecules, Neuronal - metabolism</subject><subject>cerebellum</subject><subject>Cerebral Cortex - metabolism</subject><subject>Cerebral Cortex - pathology</subject><subject>Dab-1</subject><subject>Electrophoretic Mobility Shift Assay - methods</subject><subject>Extracellular Matrix Proteins - genetics</subject><subject>Extracellular Matrix Proteins - metabolism</subject><subject>Female</subject><subject>Glycogen Synthase Kinase 3 - genetics</subject><subject>Glycogen Synthase Kinase 3 - metabolism</subject><subject>GSK-3β</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Miscellaneous</subject><subject>Models, Biological</subject><subject>mRNA</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>parietal cortex</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>QPCR</subject><subject>Receptors, LDL - genetics</subject><subject>Receptors, LDL - metabolism</subject><subject>Reelin</subject><subject>Reverse Transcriptase Polymerase Chain Reaction - methods</subject><subject>RNA, Messenger - biosynthesis</subject><subject>schizophrenia</subject><subject>Serine Endopeptidases - genetics</subject><subject>Serine Endopeptidases - metabolism</subject><subject>Sex Factors</subject><subject>Signal Transduction - physiology</subject><subject>superior frontal cortex</subject><subject>VLDLR</subject><subject>Western blotting</subject><subject>β-actin</subject><issn>0006-3223</issn><issn>1873-2402</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkF1LwzAUhoMobk7_wuiNu2vNSdqkvVOGXzAQRK9DmqQzox8zaYX9ezNX2eWuTg55zjkvD0JzwAlgYHebpLTd1u_UV0IwThMgCYb8DE0h5zQmKSbnaIoxZjElhE7Qlfeb0HJC4BJNIMsJJjSbosW7MbVtI2_XrQyPdWR9ZJuttM7oKHzIobe-uUYXlay9uRnrDH0-PX4sX-LV2_Pr8mEVq5TwPpZZlmaphgJwVmhVFoYSjTOqoSpSvk_FSlZyDZrQNFeVKQpdMWwK4IqSMqUztDjs3bruezC-F431ytS1bE03eMF42MIwPgkCpwRymgWQHUDlOu-dqcTW2Ua6nQAs9irFRvyrFHuVAogIKsPgfLwwlI3Rx7HRXQBuR0B6JevKyVZZf-QYp38ZZuj-wJkg7scaJ7yyplVGB8eqF7qzp7L8Asx1kuM</recordid><startdate>20050401</startdate><enddate>20050401</enddate><creator>Fatemi, S. Hossein</creator><creator>Snow, Anne V.</creator><creator>Stary, Joel M.</creator><creator>Araghi-Niknam, Mohsen</creator><creator>Reutiman, Teri J.</creator><creator>Lee, Suzanne</creator><creator>Brooks, Andrew I.</creator><creator>Pearce, David A.</creator><general>Elsevier Inc</general><general>Elsevier Science</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>20050401</creationdate><title>Reelin signaling is impaired in autism</title><author>Fatemi, S. Hossein ; Snow, Anne V. ; Stary, Joel M. ; Araghi-Niknam, Mohsen ; Reutiman, Teri J. ; Lee, Suzanne ; Brooks, Andrew I. ; Pearce, David A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c427t-a55454d191059dcb9e32d053d1f94724026b6b7d1d2348cfe99df60e917c32b43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Actins - metabolism</topic><topic>Adaptor Proteins, Signal Transducing</topic><topic>Adult</topic><topic>Adult and adolescent clinical studies</topic><topic>Age Factors</topic><topic>autism</topic><topic>Autistic Disorder - genetics</topic><topic>Autistic Disorder - metabolism</topic><topic>Biological and medical sciences</topic><topic>bipolar disorder</topic><topic>Blotting, Western - methods</topic><topic>Case-Control Studies</topic><topic>Cell Adhesion Molecules, Neuronal - genetics</topic><topic>Cell Adhesion Molecules, Neuronal - metabolism</topic><topic>cerebellum</topic><topic>Cerebral Cortex - metabolism</topic><topic>Cerebral Cortex - pathology</topic><topic>Dab-1</topic><topic>Electrophoretic Mobility Shift Assay - methods</topic><topic>Extracellular Matrix Proteins - genetics</topic><topic>Extracellular Matrix Proteins - metabolism</topic><topic>Female</topic><topic>Glycogen Synthase Kinase 3 - genetics</topic><topic>Glycogen Synthase Kinase 3 - metabolism</topic><topic>GSK-3β</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Miscellaneous</topic><topic>Models, Biological</topic><topic>mRNA</topic><topic>Nerve Tissue Proteins - genetics</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>parietal cortex</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>QPCR</topic><topic>Receptors, LDL - genetics</topic><topic>Receptors, LDL - metabolism</topic><topic>Reelin</topic><topic>Reverse Transcriptase Polymerase Chain Reaction - methods</topic><topic>RNA, Messenger - biosynthesis</topic><topic>schizophrenia</topic><topic>Serine Endopeptidases - genetics</topic><topic>Serine Endopeptidases - metabolism</topic><topic>Sex Factors</topic><topic>Signal Transduction - physiology</topic><topic>superior frontal cortex</topic><topic>VLDLR</topic><topic>Western blotting</topic><topic>β-actin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fatemi, S. Hossein</creatorcontrib><creatorcontrib>Snow, Anne V.</creatorcontrib><creatorcontrib>Stary, Joel M.</creatorcontrib><creatorcontrib>Araghi-Niknam, Mohsen</creatorcontrib><creatorcontrib>Reutiman, Teri J.</creatorcontrib><creatorcontrib>Lee, Suzanne</creatorcontrib><creatorcontrib>Brooks, Andrew I.</creatorcontrib><creatorcontrib>Pearce, David A.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biological psychiatry (1969)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fatemi, S. Hossein</au><au>Snow, Anne V.</au><au>Stary, Joel M.</au><au>Araghi-Niknam, Mohsen</au><au>Reutiman, Teri J.</au><au>Lee, Suzanne</au><au>Brooks, Andrew I.</au><au>Pearce, David A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reelin signaling is impaired in autism</atitle><jtitle>Biological psychiatry (1969)</jtitle><addtitle>Biol Psychiatry</addtitle><date>2005-04-01</date><risdate>2005</risdate><volume>57</volume><issue>7</issue><spage>777</spage><epage>787</epage><pages>777-787</pages><issn>0006-3223</issn><eissn>1873-2402</eissn><coden>BIPCBF</coden><abstract>Autism is a severe neurodevelopmental disorder with genetic and environmental etiologies. Recent genetic linkage studies implicate Reelin glycoprotein in causation of autism. To further investigate these studies, brain levels of Reelin protein and mRNA and mRNAs for VLDLR, Dab-1, and GSK3 were investigated.
Postmortem superior frontal, parietal, and cerebellar cortices of age, gender, and postmortem interval-matched autistic and control subjects were subjected to SDS-PAGE and Western blotting of Reelin protein. Quantitative reverse transcriptase polymerase chain reaction analysis of Reelin, VLDL-R, Dab-1, and GSK3 mRNA species in superior frontal and cerebellar cortices of autistic and control subjects were also performed.
Reelin 410, 330, and 180 kDa/β-actin values were reduced significantly in frontal and cerebellar, and nonsignificantly in parietal, areas of autistic brains versus control subjects, respectively. The mRNAs for Reln and Dab-1 were reduced significantly whereas the mRNA for Reln receptor VLDLR was elevated significantly in superior frontal and cerebellar areas of autistic brains versus control brains, respectively.
Reductions in Reelin protein and mRNA and Dab 1 mRNA and elevations in Reln receptor VLDLR mRNA demonstrate impairments in the Reelin signaling system in autism, accounting for some of the brain structural and cognitive deficits observed in the disorder.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>15820235</pmid><doi>10.1016/j.biopsych.2004.12.018</doi><tpages>11</tpages></addata></record> |
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| subjects | Actins - metabolism Adaptor Proteins, Signal Transducing Adult Adult and adolescent clinical studies Age Factors autism Autistic Disorder - genetics Autistic Disorder - metabolism Biological and medical sciences bipolar disorder Blotting, Western - methods Case-Control Studies Cell Adhesion Molecules, Neuronal - genetics Cell Adhesion Molecules, Neuronal - metabolism cerebellum Cerebral Cortex - metabolism Cerebral Cortex - pathology Dab-1 Electrophoretic Mobility Shift Assay - methods Extracellular Matrix Proteins - genetics Extracellular Matrix Proteins - metabolism Female Glycogen Synthase Kinase 3 - genetics Glycogen Synthase Kinase 3 - metabolism GSK-3β Humans Male Medical sciences Miscellaneous Models, Biological mRNA Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism parietal cortex Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry QPCR Receptors, LDL - genetics Receptors, LDL - metabolism Reelin Reverse Transcriptase Polymerase Chain Reaction - methods RNA, Messenger - biosynthesis schizophrenia Serine Endopeptidases - genetics Serine Endopeptidases - metabolism Sex Factors Signal Transduction - physiology superior frontal cortex VLDLR Western blotting β-actin |
| title | Reelin signaling is impaired in autism |
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