Gene expression analysis suggests that 1,25-dihydroxyvitamin D3 reverses experimental autoimmune encephalomyelitis by stimulating inflammatory cell apoptosis
1 Department of Nutritional Sciences, University of Wisconsin-Madison, Madison, Wisconsin 53706 2 Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin 53706 3 Department of Horticulture and Statistics, University of Wisconsin-Madison, Madison, Wisconsin 53706 4 Department...
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| Veröffentlicht in: | Physiological genomics 2004-07, Vol.18 (2), p.141-151 |
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| creator | Spach, Karen M Pedersen, Laura B Nashold, Faye E Kayo, Tsuyoshi Yandell, Brian S Prolla, Tomas A Hayes, Colleen E |
| description | 1 Department of Nutritional Sciences, University of Wisconsin-Madison, Madison, Wisconsin 53706
2 Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin 53706
3 Department of Horticulture and Statistics, University of Wisconsin-Madison, Madison, Wisconsin 53706
4 Department of Genetics and Medical Genetics, University of Wisconsin-Madison, Madison, Wisconsin 53706
Multiple sclerosis (MS) is a debilitating autoimmune disease of the central nervous system (CNS) that develops in genetically susceptible individuals who are exposed to undefined environmental risk factors. Epidemiological, genetic, and biological evidence suggests that insufficient vitamin D may be an MS risk factor. However, little is known about how vitamin D might be protective in MS. We hypothesized that 1,25-dihydroxyvitamin D 3 [1,25-(OH) 2 D 3 ] might regulate gene expression patterns in a manner that would resolve inflammation. To test this hypothesis, experimental autoimmune encephalomyelitis (EAE) was induced in mice, 1,25-(OH) 2 D 3 or a placebo was administered, and 6 h later, DNA microarray hybridization was performed with spinal cord RNA to analyze the gene expression patterns. At this time, clinical, histopathological, and biological studies showed that the two groups did not differ in EAE disease, but changes in several 1,25-(OH) 2 D 3 -responsive genes indicated that the 1,25-(OH) 2 D 3 had reached the CNS. Compared with normal mice, placebo-treated mice with EAE showed increased expression of many immune system genes, confirming the acute inflammation. When 1,25-(OH) 2 D 3 was administered, several genes like glial fibrillary acidic protein and eukaryotic initiation factor 2 kinase 4, whose expression increased or decreased with EAE, returned to homeostatic levels. Also, two genes with pro-apoptotic functions, calpain-2 and caspase-8-associated protein, increased significantly. A terminal deoxynucleotidyl transferase-mediated dUTP nicked end labeling study detected increased nuclear fragmentation in the 1,25-(OH) 2 D 3 -treated samples, confirming increased apoptosis. Together, these results suggest that sensitization of inflammatory cells to apoptotic signals may be one mechanism by which the 1,25-(OH) 2 D 3 resolved EAE.
vitamin D; multiple sclerosis; autoimmune disease; DNA microarray |
| doi_str_mv | 10.1152/physiolgenomics.00003.2004 |
| format | Article |
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2 Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin 53706
3 Department of Horticulture and Statistics, University of Wisconsin-Madison, Madison, Wisconsin 53706
4 Department of Genetics and Medical Genetics, University of Wisconsin-Madison, Madison, Wisconsin 53706
Multiple sclerosis (MS) is a debilitating autoimmune disease of the central nervous system (CNS) that develops in genetically susceptible individuals who are exposed to undefined environmental risk factors. Epidemiological, genetic, and biological evidence suggests that insufficient vitamin D may be an MS risk factor. However, little is known about how vitamin D might be protective in MS. We hypothesized that 1,25-dihydroxyvitamin D 3 [1,25-(OH) 2 D 3 ] might regulate gene expression patterns in a manner that would resolve inflammation. To test this hypothesis, experimental autoimmune encephalomyelitis (EAE) was induced in mice, 1,25-(OH) 2 D 3 or a placebo was administered, and 6 h later, DNA microarray hybridization was performed with spinal cord RNA to analyze the gene expression patterns. At this time, clinical, histopathological, and biological studies showed that the two groups did not differ in EAE disease, but changes in several 1,25-(OH) 2 D 3 -responsive genes indicated that the 1,25-(OH) 2 D 3 had reached the CNS. Compared with normal mice, placebo-treated mice with EAE showed increased expression of many immune system genes, confirming the acute inflammation. When 1,25-(OH) 2 D 3 was administered, several genes like glial fibrillary acidic protein and eukaryotic initiation factor 2 kinase 4, whose expression increased or decreased with EAE, returned to homeostatic levels. Also, two genes with pro-apoptotic functions, calpain-2 and caspase-8-associated protein, increased significantly. A terminal deoxynucleotidyl transferase-mediated dUTP nicked end labeling study detected increased nuclear fragmentation in the 1,25-(OH) 2 D 3 -treated samples, confirming increased apoptosis. Together, these results suggest that sensitization of inflammatory cells to apoptotic signals may be one mechanism by which the 1,25-(OH) 2 D 3 resolved EAE.
vitamin D; multiple sclerosis; autoimmune disease; DNA microarray</description><identifier>ISSN: 1094-8341</identifier><identifier>EISSN: 1531-2267</identifier><identifier>DOI: 10.1152/physiolgenomics.00003.2004</identifier><identifier>PMID: 15138306</identifier><language>eng</language><publisher>United States: Am Physiological Soc</publisher><subject>Animals ; Apoptosis - physiology ; Astrocytes - chemistry ; Astrocytes - metabolism ; CD4-Positive T-Lymphocytes - chemistry ; CD4-Positive T-Lymphocytes - metabolism ; Central Nervous System - chemistry ; Central Nervous System - metabolism ; Central Nervous System - pathology ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental - genetics ; Encephalomyelitis, Autoimmune, Experimental - metabolism ; Encephalomyelitis, Autoimmune, Experimental - pathology ; Gene Expression Profiling - methods ; Gene Expression Regulation - genetics ; Gene Expression Regulation - physiology ; Lymphocytes - chemistry ; Lymphocytes - metabolism ; Lymphocytes - physiology ; Macrophages - chemistry ; Macrophages - metabolism ; Macrophages - physiology ; Male ; Mice ; Mice, Inbred C57BL ; Spinal Cord - pathology ; T-Lymphocyte Subsets - chemistry ; T-Lymphocyte Subsets - metabolism ; Vitamin D - analogs & derivatives ; Vitamin D - physiology</subject><ispartof>Physiological genomics, 2004-07, Vol.18 (2), p.141-151</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15138306$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Spach, Karen M</creatorcontrib><creatorcontrib>Pedersen, Laura B</creatorcontrib><creatorcontrib>Nashold, Faye E</creatorcontrib><creatorcontrib>Kayo, Tsuyoshi</creatorcontrib><creatorcontrib>Yandell, Brian S</creatorcontrib><creatorcontrib>Prolla, Tomas A</creatorcontrib><creatorcontrib>Hayes, Colleen E</creatorcontrib><title>Gene expression analysis suggests that 1,25-dihydroxyvitamin D3 reverses experimental autoimmune encephalomyelitis by stimulating inflammatory cell apoptosis</title><title>Physiological genomics</title><addtitle>Physiol Genomics</addtitle><description>1 Department of Nutritional Sciences, University of Wisconsin-Madison, Madison, Wisconsin 53706
2 Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin 53706
3 Department of Horticulture and Statistics, University of Wisconsin-Madison, Madison, Wisconsin 53706
4 Department of Genetics and Medical Genetics, University of Wisconsin-Madison, Madison, Wisconsin 53706
Multiple sclerosis (MS) is a debilitating autoimmune disease of the central nervous system (CNS) that develops in genetically susceptible individuals who are exposed to undefined environmental risk factors. Epidemiological, genetic, and biological evidence suggests that insufficient vitamin D may be an MS risk factor. However, little is known about how vitamin D might be protective in MS. We hypothesized that 1,25-dihydroxyvitamin D 3 [1,25-(OH) 2 D 3 ] might regulate gene expression patterns in a manner that would resolve inflammation. To test this hypothesis, experimental autoimmune encephalomyelitis (EAE) was induced in mice, 1,25-(OH) 2 D 3 or a placebo was administered, and 6 h later, DNA microarray hybridization was performed with spinal cord RNA to analyze the gene expression patterns. At this time, clinical, histopathological, and biological studies showed that the two groups did not differ in EAE disease, but changes in several 1,25-(OH) 2 D 3 -responsive genes indicated that the 1,25-(OH) 2 D 3 had reached the CNS. Compared with normal mice, placebo-treated mice with EAE showed increased expression of many immune system genes, confirming the acute inflammation. When 1,25-(OH) 2 D 3 was administered, several genes like glial fibrillary acidic protein and eukaryotic initiation factor 2 kinase 4, whose expression increased or decreased with EAE, returned to homeostatic levels. Also, two genes with pro-apoptotic functions, calpain-2 and caspase-8-associated protein, increased significantly. A terminal deoxynucleotidyl transferase-mediated dUTP nicked end labeling study detected increased nuclear fragmentation in the 1,25-(OH) 2 D 3 -treated samples, confirming increased apoptosis. Together, these results suggest that sensitization of inflammatory cells to apoptotic signals may be one mechanism by which the 1,25-(OH) 2 D 3 resolved EAE.
vitamin D; multiple sclerosis; autoimmune disease; DNA microarray</description><subject>Animals</subject><subject>Apoptosis - physiology</subject><subject>Astrocytes - chemistry</subject><subject>Astrocytes - metabolism</subject><subject>CD4-Positive T-Lymphocytes - chemistry</subject><subject>CD4-Positive T-Lymphocytes - metabolism</subject><subject>Central Nervous System - chemistry</subject><subject>Central Nervous System - metabolism</subject><subject>Central Nervous System - pathology</subject><subject>Disease Models, Animal</subject><subject>Encephalomyelitis, Autoimmune, Experimental - genetics</subject><subject>Encephalomyelitis, Autoimmune, Experimental - metabolism</subject><subject>Encephalomyelitis, Autoimmune, Experimental - pathology</subject><subject>Gene Expression Profiling - methods</subject><subject>Gene Expression Regulation - genetics</subject><subject>Gene Expression Regulation - physiology</subject><subject>Lymphocytes - chemistry</subject><subject>Lymphocytes - metabolism</subject><subject>Lymphocytes - physiology</subject><subject>Macrophages - chemistry</subject><subject>Macrophages - metabolism</subject><subject>Macrophages - physiology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Spinal Cord - pathology</subject><subject>T-Lymphocyte Subsets - chemistry</subject><subject>T-Lymphocyte Subsets - metabolism</subject><subject>Vitamin D - analogs & derivatives</subject><subject>Vitamin D - physiology</subject><issn>1094-8341</issn><issn>1531-2267</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc1u1TAQhSMEoqXwCshiwYpc_BPnOiuECm2RKrEpa8vXniRG_gmxU24ehnfFUW83lTqbmcU5n-bMVNUHgneEcPp5GtdkoxsgRG912uFSbEcxbl5U54QzUlPa7l-WGXdNLVhDzqo3Kf3GmDR7wV9XZ4QTJhhuz6t_1xAAwXGaIRVoQCooV_AJpWUYIOWE8qgyIp8or40dVzPH43pvs_I2oG8MzXAPc4K0MWC2HkJWDqklR-v9srGDhmlULvoVnM2FfFhRytYvTmUbBmRD75T3Ksd5RRpccU9xyrEs8bZ61SuX4N2pX1S_rr7fXd7Utz-vf1x-va1HSmmue3XQhhtWGnCxFwRMp0Az02kDvGkPWDeG7nvoG2Ci6Xretpp3pO8E01gTdlF9fOBOc_yzlNTS27StogLEJcm2bTsqxCZ8fxIuBw9GTiWxmlf5eNAiYA-C0Q7jXzuDPH0rDqt88jhJhKSSNBv2y_Ouq8W5Ozjmp_ZHt5xMz_4DRdyuvA</recordid><startdate>20040708</startdate><enddate>20040708</enddate><creator>Spach, Karen M</creator><creator>Pedersen, Laura B</creator><creator>Nashold, Faye E</creator><creator>Kayo, Tsuyoshi</creator><creator>Yandell, Brian S</creator><creator>Prolla, Tomas A</creator><creator>Hayes, Colleen E</creator><general>Am Physiological Soc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20040708</creationdate><title>Gene expression analysis suggests that 1,25-dihydroxyvitamin D3 reverses experimental autoimmune encephalomyelitis by stimulating inflammatory cell apoptosis</title><author>Spach, Karen M ; Pedersen, Laura B ; Nashold, Faye E ; Kayo, Tsuyoshi ; Yandell, Brian S ; Prolla, Tomas A ; Hayes, Colleen E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h222t-fabcd5d3abce58781ed9aec3d9cde546b0c4d27fef4e3849f566c591f983c0c13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Apoptosis - physiology</topic><topic>Astrocytes - chemistry</topic><topic>Astrocytes - metabolism</topic><topic>CD4-Positive T-Lymphocytes - chemistry</topic><topic>CD4-Positive T-Lymphocytes - metabolism</topic><topic>Central Nervous System - chemistry</topic><topic>Central Nervous System - metabolism</topic><topic>Central Nervous System - pathology</topic><topic>Disease Models, Animal</topic><topic>Encephalomyelitis, Autoimmune, Experimental - genetics</topic><topic>Encephalomyelitis, Autoimmune, Experimental - metabolism</topic><topic>Encephalomyelitis, Autoimmune, Experimental - pathology</topic><topic>Gene Expression Profiling - methods</topic><topic>Gene Expression Regulation - genetics</topic><topic>Gene Expression Regulation - physiology</topic><topic>Lymphocytes - chemistry</topic><topic>Lymphocytes - metabolism</topic><topic>Lymphocytes - physiology</topic><topic>Macrophages - chemistry</topic><topic>Macrophages - metabolism</topic><topic>Macrophages - physiology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Spinal Cord - pathology</topic><topic>T-Lymphocyte Subsets - chemistry</topic><topic>T-Lymphocyte Subsets - metabolism</topic><topic>Vitamin D - analogs & derivatives</topic><topic>Vitamin D - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Spach, Karen M</creatorcontrib><creatorcontrib>Pedersen, Laura B</creatorcontrib><creatorcontrib>Nashold, Faye E</creatorcontrib><creatorcontrib>Kayo, Tsuyoshi</creatorcontrib><creatorcontrib>Yandell, Brian S</creatorcontrib><creatorcontrib>Prolla, Tomas A</creatorcontrib><creatorcontrib>Hayes, Colleen E</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Physiological genomics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Spach, Karen M</au><au>Pedersen, Laura B</au><au>Nashold, Faye E</au><au>Kayo, Tsuyoshi</au><au>Yandell, Brian S</au><au>Prolla, Tomas A</au><au>Hayes, Colleen E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gene expression analysis suggests that 1,25-dihydroxyvitamin D3 reverses experimental autoimmune encephalomyelitis by stimulating inflammatory cell apoptosis</atitle><jtitle>Physiological genomics</jtitle><addtitle>Physiol Genomics</addtitle><date>2004-07-08</date><risdate>2004</risdate><volume>18</volume><issue>2</issue><spage>141</spage><epage>151</epage><pages>141-151</pages><issn>1094-8341</issn><eissn>1531-2267</eissn><abstract>1 Department of Nutritional Sciences, University of Wisconsin-Madison, Madison, Wisconsin 53706
2 Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin 53706
3 Department of Horticulture and Statistics, University of Wisconsin-Madison, Madison, Wisconsin 53706
4 Department of Genetics and Medical Genetics, University of Wisconsin-Madison, Madison, Wisconsin 53706
Multiple sclerosis (MS) is a debilitating autoimmune disease of the central nervous system (CNS) that develops in genetically susceptible individuals who are exposed to undefined environmental risk factors. Epidemiological, genetic, and biological evidence suggests that insufficient vitamin D may be an MS risk factor. However, little is known about how vitamin D might be protective in MS. We hypothesized that 1,25-dihydroxyvitamin D 3 [1,25-(OH) 2 D 3 ] might regulate gene expression patterns in a manner that would resolve inflammation. To test this hypothesis, experimental autoimmune encephalomyelitis (EAE) was induced in mice, 1,25-(OH) 2 D 3 or a placebo was administered, and 6 h later, DNA microarray hybridization was performed with spinal cord RNA to analyze the gene expression patterns. At this time, clinical, histopathological, and biological studies showed that the two groups did not differ in EAE disease, but changes in several 1,25-(OH) 2 D 3 -responsive genes indicated that the 1,25-(OH) 2 D 3 had reached the CNS. Compared with normal mice, placebo-treated mice with EAE showed increased expression of many immune system genes, confirming the acute inflammation. When 1,25-(OH) 2 D 3 was administered, several genes like glial fibrillary acidic protein and eukaryotic initiation factor 2 kinase 4, whose expression increased or decreased with EAE, returned to homeostatic levels. Also, two genes with pro-apoptotic functions, calpain-2 and caspase-8-associated protein, increased significantly. A terminal deoxynucleotidyl transferase-mediated dUTP nicked end labeling study detected increased nuclear fragmentation in the 1,25-(OH) 2 D 3 -treated samples, confirming increased apoptosis. Together, these results suggest that sensitization of inflammatory cells to apoptotic signals may be one mechanism by which the 1,25-(OH) 2 D 3 resolved EAE.
vitamin D; multiple sclerosis; autoimmune disease; DNA microarray</abstract><cop>United States</cop><pub>Am Physiological Soc</pub><pmid>15138306</pmid><doi>10.1152/physiolgenomics.00003.2004</doi><tpages>11</tpages></addata></record> |
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| source | MEDLINE; American Physiological Society; EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Apoptosis - physiology Astrocytes - chemistry Astrocytes - metabolism CD4-Positive T-Lymphocytes - chemistry CD4-Positive T-Lymphocytes - metabolism Central Nervous System - chemistry Central Nervous System - metabolism Central Nervous System - pathology Disease Models, Animal Encephalomyelitis, Autoimmune, Experimental - genetics Encephalomyelitis, Autoimmune, Experimental - metabolism Encephalomyelitis, Autoimmune, Experimental - pathology Gene Expression Profiling - methods Gene Expression Regulation - genetics Gene Expression Regulation - physiology Lymphocytes - chemistry Lymphocytes - metabolism Lymphocytes - physiology Macrophages - chemistry Macrophages - metabolism Macrophages - physiology Male Mice Mice, Inbred C57BL Spinal Cord - pathology T-Lymphocyte Subsets - chemistry T-Lymphocyte Subsets - metabolism Vitamin D - analogs & derivatives Vitamin D - physiology |
| title | Gene expression analysis suggests that 1,25-dihydroxyvitamin D3 reverses experimental autoimmune encephalomyelitis by stimulating inflammatory cell apoptosis |
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