Progesterone down-regulates spinal cord inflammatory mediators and increases myelination in experimental autoimmune encephalomyelitis
In mice with experimental autoimmune encephalomyelitis (EAE) pretreatment with progesterone improves clinical signs and decreases the loss of myelin basic protein (MBP) and proteolipid protein (PLP) measured by immunohistochemistry and in situ hybridization. Presently, we analyzed if progesterone ef...
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2012
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_03064522_v226_n_p40_Garay http://hdl.handle.net/20.500.12110/paper_03064522_v226_n_p40_Garay |
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paper:paper_03064522_v226_n_p40_Garay2025-07-30T18:08:48Z Progesterone down-regulates spinal cord inflammatory mediators and increases myelination in experimental autoimmune encephalomyelitis Experimental autoimmune encephalomyelitis Myelin proteins Neuroprotection Progesterone Proinflammatory mediators Transcription factors autacoid CD11b antigen glial fibrillary acidic protein messenger RNA myelin basic protein progesterone protein Olig1 proteolipid protein toll like receptor 4 transcription factor transcription factor Nkx2.2 tumor necrosis factor alpha tumor necrosis factor receptor 1 unclassified drug allergic encephalomyelitis animal cell animal experiment animal model animal tissue article astrocyte confocal microscopy controlled study down regulation drug mechanism female immunocytochemistry immunohistochemistry in situ hybridization microglia mouse myelination nonhuman nucleotide sequence oligodendroglia pharmacological blocking priority journal protein localization real time polymerase chain reaction spinal cord Animals Calcium-Binding Proteins Down-Regulation Encephalomyelitis, Autoimmune, Experimental Female Immunohistochemistry Inflammation Mediators Mice Mice, Inbred C57BL Microfilament Proteins Microglia Microscopy, Confocal Myelin Proteins Myelin Sheath Oligodendroglia Progesterone Real-Time Polymerase Chain Reaction RNA, Messenger Spinal Cord Transcription Factors In mice with experimental autoimmune encephalomyelitis (EAE) pretreatment with progesterone improves clinical signs and decreases the loss of myelin basic protein (MBP) and proteolipid protein (PLP) measured by immunohistochemistry and in situ hybridization. Presently, we analyzed if progesterone effects in the spinal cord of EAE mice involved the decreased transcription of local inflammatory mediators and the increased transcription of myelin proteins and myelin transcription factors. C57Bl/6 female mice were divided into controls, EAE and EAE receiving progesterone (100. mg implant) 7. days before EAE induction. Tissues were collected on day 17 post-immunization. Real time PCR technology demonstrated that progesterone blocked the EAE-induced increase of the proinflammatory mediators tumor necrosis factor alpha (TNFα) and its receptor TNFR1, the microglial marker CD11b and toll-like receptor 4 (TLR4) mRNAs, and increased mRNA expression of PLP and MBP, the myelin transcription factors NKx2.2 and Olig1 and enhanced CC1. +. oligodendrocyte density respect of untreated EAE mice. Immunocytochemistry demonstrated decreased Iba1. +. microglial cells. Confocal microscopy demonstrated that TNFα colocalized with glial-fibrillary acidic protein. +. astrocytes and OX-42. +. microglial cells. Therefore, progesterone treatment improved the clinical signs of EAE, decreased inflammatory glial reactivity and increased myelination. Data suggest that progesterone neuroprotection involves the modulation of transcriptional events in the spinal cord of EAE mice. © 2012 IBRO. 2012 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_03064522_v226_n_p40_Garay http://hdl.handle.net/20.500.12110/paper_03064522_v226_n_p40_Garay |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
Experimental autoimmune encephalomyelitis Myelin proteins Neuroprotection Progesterone Proinflammatory mediators Transcription factors autacoid CD11b antigen glial fibrillary acidic protein messenger RNA myelin basic protein progesterone protein Olig1 proteolipid protein toll like receptor 4 transcription factor transcription factor Nkx2.2 tumor necrosis factor alpha tumor necrosis factor receptor 1 unclassified drug allergic encephalomyelitis animal cell animal experiment animal model animal tissue article astrocyte confocal microscopy controlled study down regulation drug mechanism female immunocytochemistry immunohistochemistry in situ hybridization microglia mouse myelination nonhuman nucleotide sequence oligodendroglia pharmacological blocking priority journal protein localization real time polymerase chain reaction spinal cord Animals Calcium-Binding Proteins Down-Regulation Encephalomyelitis, Autoimmune, Experimental Female Immunohistochemistry Inflammation Mediators Mice Mice, Inbred C57BL Microfilament Proteins Microglia Microscopy, Confocal Myelin Proteins Myelin Sheath Oligodendroglia Progesterone Real-Time Polymerase Chain Reaction RNA, Messenger Spinal Cord Transcription Factors |
| spellingShingle |
Experimental autoimmune encephalomyelitis Myelin proteins Neuroprotection Progesterone Proinflammatory mediators Transcription factors autacoid CD11b antigen glial fibrillary acidic protein messenger RNA myelin basic protein progesterone protein Olig1 proteolipid protein toll like receptor 4 transcription factor transcription factor Nkx2.2 tumor necrosis factor alpha tumor necrosis factor receptor 1 unclassified drug allergic encephalomyelitis animal cell animal experiment animal model animal tissue article astrocyte confocal microscopy controlled study down regulation drug mechanism female immunocytochemistry immunohistochemistry in situ hybridization microglia mouse myelination nonhuman nucleotide sequence oligodendroglia pharmacological blocking priority journal protein localization real time polymerase chain reaction spinal cord Animals Calcium-Binding Proteins Down-Regulation Encephalomyelitis, Autoimmune, Experimental Female Immunohistochemistry Inflammation Mediators Mice Mice, Inbred C57BL Microfilament Proteins Microglia Microscopy, Confocal Myelin Proteins Myelin Sheath Oligodendroglia Progesterone Real-Time Polymerase Chain Reaction RNA, Messenger Spinal Cord Transcription Factors Progesterone down-regulates spinal cord inflammatory mediators and increases myelination in experimental autoimmune encephalomyelitis |
| topic_facet |
Experimental autoimmune encephalomyelitis Myelin proteins Neuroprotection Progesterone Proinflammatory mediators Transcription factors autacoid CD11b antigen glial fibrillary acidic protein messenger RNA myelin basic protein progesterone protein Olig1 proteolipid protein toll like receptor 4 transcription factor transcription factor Nkx2.2 tumor necrosis factor alpha tumor necrosis factor receptor 1 unclassified drug allergic encephalomyelitis animal cell animal experiment animal model animal tissue article astrocyte confocal microscopy controlled study down regulation drug mechanism female immunocytochemistry immunohistochemistry in situ hybridization microglia mouse myelination nonhuman nucleotide sequence oligodendroglia pharmacological blocking priority journal protein localization real time polymerase chain reaction spinal cord Animals Calcium-Binding Proteins Down-Regulation Encephalomyelitis, Autoimmune, Experimental Female Immunohistochemistry Inflammation Mediators Mice Mice, Inbred C57BL Microfilament Proteins Microglia Microscopy, Confocal Myelin Proteins Myelin Sheath Oligodendroglia Progesterone Real-Time Polymerase Chain Reaction RNA, Messenger Spinal Cord Transcription Factors |
| description |
In mice with experimental autoimmune encephalomyelitis (EAE) pretreatment with progesterone improves clinical signs and decreases the loss of myelin basic protein (MBP) and proteolipid protein (PLP) measured by immunohistochemistry and in situ hybridization. Presently, we analyzed if progesterone effects in the spinal cord of EAE mice involved the decreased transcription of local inflammatory mediators and the increased transcription of myelin proteins and myelin transcription factors. C57Bl/6 female mice were divided into controls, EAE and EAE receiving progesterone (100. mg implant) 7. days before EAE induction. Tissues were collected on day 17 post-immunization. Real time PCR technology demonstrated that progesterone blocked the EAE-induced increase of the proinflammatory mediators tumor necrosis factor alpha (TNFα) and its receptor TNFR1, the microglial marker CD11b and toll-like receptor 4 (TLR4) mRNAs, and increased mRNA expression of PLP and MBP, the myelin transcription factors NKx2.2 and Olig1 and enhanced CC1. +. oligodendrocyte density respect of untreated EAE mice. Immunocytochemistry demonstrated decreased Iba1. +. microglial cells. Confocal microscopy demonstrated that TNFα colocalized with glial-fibrillary acidic protein. +. astrocytes and OX-42. +. microglial cells. Therefore, progesterone treatment improved the clinical signs of EAE, decreased inflammatory glial reactivity and increased myelination. Data suggest that progesterone neuroprotection involves the modulation of transcriptional events in the spinal cord of EAE mice. © 2012 IBRO. |
| title |
Progesterone down-regulates spinal cord inflammatory mediators and increases myelination in experimental autoimmune encephalomyelitis |
| title_short |
Progesterone down-regulates spinal cord inflammatory mediators and increases myelination in experimental autoimmune encephalomyelitis |
| title_full |
Progesterone down-regulates spinal cord inflammatory mediators and increases myelination in experimental autoimmune encephalomyelitis |
| title_fullStr |
Progesterone down-regulates spinal cord inflammatory mediators and increases myelination in experimental autoimmune encephalomyelitis |
| title_full_unstemmed |
Progesterone down-regulates spinal cord inflammatory mediators and increases myelination in experimental autoimmune encephalomyelitis |
| title_sort |
progesterone down-regulates spinal cord inflammatory mediators and increases myelination in experimental autoimmune encephalomyelitis |
| publishDate |
2012 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_03064522_v226_n_p40_Garay http://hdl.handle.net/20.500.12110/paper_03064522_v226_n_p40_Garay |
| _version_ |
1840323656667889664 |