Basis of progesterone protection in spinal cord neurodegeneration

Progesterone neuroprotection has been reported in experimental brain, peripheral nerve and spinal cord injury. To investigate for a similar role in neurodegeneration, we studied progesterone effects in the Wobbler mouse, a mutant presenting severe motoneuron degeneration and astrogliosis of the spin...

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Publicado: 2002
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Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_09600760_v83_n1-5_p199_GonzalezDeniselle
http://hdl.handle.net/20.500.12110/paper_09600760_v83_n1-5_p199_GonzalezDeniselle
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spelling paper:paper_09600760_v83_n1-5_p199_GonzalezDeniselle2023-06-08T15:57:27Z Basis of progesterone protection in spinal cord neurodegeneration Neurodegeneration Progesterone Spinal cord Wobbler mouse adenosine triphosphatase (potassium sodium) glial fibrillary acidic protein messenger RNA neuromodulin progesterone adenosine triphosphatase cation transport protein glial fibrillary acidic protein messenger RNA neuromodulin potassium transporting ATPase progesterone alpha chain astrocytosis beta chain brain mitochondrion cell organelle cell ultrastructure cell vacuole conference paper drug implant drug pellet grip strength hormonal regulation hormonal therapy hormone action immunohistochemistry morphological trait mouse strain nerve degeneration neuropathology neuroprotection nonhuman observation progesterone synthesis protein blood level protein determination protein expression species comparison spinal cord motoneuron survival time animal apoptosis article astrocyte cell nucleus chromatin degenerative disease electron microscopy in situ hybridization metabolism mouse nerve cell pathology spinal cord ultrastructure Animalia Adenosine Triphosphatases Animals Apoptosis Astrocytes Cation Transport Proteins Cell Nucleus Chromatin GAP-43 Protein Glial Fibrillary Acidic Protein In Situ Hybridization Mice Microscopy, Electron Neurodegenerative Diseases Neurons Progesterone RNA, Messenger Spinal Cord Progesterone neuroprotection has been reported in experimental brain, peripheral nerve and spinal cord injury. To investigate for a similar role in neurodegeneration, we studied progesterone effects in the Wobbler mouse, a mutant presenting severe motoneuron degeneration and astrogliosis of the spinal cord. Implant of a single progesterone pellet (20mg) during 15 days produced substantial changes in Wobbler mice spinal cord. Morphologically, motoneurons of untreated Wobbler mice showed severe vacuolation of intracellular organelles including mitochondria. In contrast, neuropathology was less pronounced in Wobbler mice receiving progesterone, together with a reduction of vacuolated cells and preservation of mitochondrial ultrastructure. Determination of mRNAs for the α3 and β1 subunits of neuronal Na, K-ATPase, showed that mRNA levels in untreated mice were significantly reduced, whereas progesterone therapy re-established the expression of both subunits. Additionally, progesterone treatment of Wobbler mice attenuated the aberrant expression of the growth-associated protein (GAP-43) mRNA which otherwise occurred in motoneurons of untreated animals. The hormone, however, was without effect on astrocytosis of Wobbler mice, determined by glial fibrillary acidic protein (GFAP)-immunostaining. Lastly, progesterone treatment of Wobbler mice enhanced grip strength and prolonged survival at the end of the 15-day observation period. Recovery of morphology and molecular motoneuron parameters of Wobbler mice receiving progesterone, suggest a new and important role for this hormone in the prevention of spinal cord neurodegenerative disorders. © 2003 Elsevier Science Ltd. All rights reserved. 2002 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_09600760_v83_n1-5_p199_GonzalezDeniselle http://hdl.handle.net/20.500.12110/paper_09600760_v83_n1-5_p199_GonzalezDeniselle
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic Neurodegeneration
Progesterone
Spinal cord
Wobbler mouse
adenosine triphosphatase (potassium sodium)
glial fibrillary acidic protein
messenger RNA
neuromodulin
progesterone
adenosine triphosphatase
cation transport protein
glial fibrillary acidic protein
messenger RNA
neuromodulin
potassium transporting ATPase
progesterone
alpha chain
astrocytosis
beta chain
brain mitochondrion
cell organelle
cell ultrastructure
cell vacuole
conference paper
drug implant
drug pellet
grip strength
hormonal regulation
hormonal therapy
hormone action
immunohistochemistry
morphological trait
mouse strain
nerve degeneration
neuropathology
neuroprotection
nonhuman
observation
progesterone synthesis
protein blood level
protein determination
protein expression
species comparison
spinal cord motoneuron
survival time
animal
apoptosis
article
astrocyte
cell nucleus
chromatin
degenerative disease
electron microscopy
in situ hybridization
metabolism
mouse
nerve cell
pathology
spinal cord
ultrastructure
Animalia
Adenosine Triphosphatases
Animals
Apoptosis
Astrocytes
Cation Transport Proteins
Cell Nucleus
Chromatin
GAP-43 Protein
Glial Fibrillary Acidic Protein
In Situ Hybridization
Mice
Microscopy, Electron
Neurodegenerative Diseases
Neurons
Progesterone
RNA, Messenger
Spinal Cord
spellingShingle Neurodegeneration
Progesterone
Spinal cord
Wobbler mouse
adenosine triphosphatase (potassium sodium)
glial fibrillary acidic protein
messenger RNA
neuromodulin
progesterone
adenosine triphosphatase
cation transport protein
glial fibrillary acidic protein
messenger RNA
neuromodulin
potassium transporting ATPase
progesterone
alpha chain
astrocytosis
beta chain
brain mitochondrion
cell organelle
cell ultrastructure
cell vacuole
conference paper
drug implant
drug pellet
grip strength
hormonal regulation
hormonal therapy
hormone action
immunohistochemistry
morphological trait
mouse strain
nerve degeneration
neuropathology
neuroprotection
nonhuman
observation
progesterone synthesis
protein blood level
protein determination
protein expression
species comparison
spinal cord motoneuron
survival time
animal
apoptosis
article
astrocyte
cell nucleus
chromatin
degenerative disease
electron microscopy
in situ hybridization
metabolism
mouse
nerve cell
pathology
spinal cord
ultrastructure
Animalia
Adenosine Triphosphatases
Animals
Apoptosis
Astrocytes
Cation Transport Proteins
Cell Nucleus
Chromatin
GAP-43 Protein
Glial Fibrillary Acidic Protein
In Situ Hybridization
Mice
Microscopy, Electron
Neurodegenerative Diseases
Neurons
Progesterone
RNA, Messenger
Spinal Cord
Basis of progesterone protection in spinal cord neurodegeneration
topic_facet Neurodegeneration
Progesterone
Spinal cord
Wobbler mouse
adenosine triphosphatase (potassium sodium)
glial fibrillary acidic protein
messenger RNA
neuromodulin
progesterone
adenosine triphosphatase
cation transport protein
glial fibrillary acidic protein
messenger RNA
neuromodulin
potassium transporting ATPase
progesterone
alpha chain
astrocytosis
beta chain
brain mitochondrion
cell organelle
cell ultrastructure
cell vacuole
conference paper
drug implant
drug pellet
grip strength
hormonal regulation
hormonal therapy
hormone action
immunohistochemistry
morphological trait
mouse strain
nerve degeneration
neuropathology
neuroprotection
nonhuman
observation
progesterone synthesis
protein blood level
protein determination
protein expression
species comparison
spinal cord motoneuron
survival time
animal
apoptosis
article
astrocyte
cell nucleus
chromatin
degenerative disease
electron microscopy
in situ hybridization
metabolism
mouse
nerve cell
pathology
spinal cord
ultrastructure
Animalia
Adenosine Triphosphatases
Animals
Apoptosis
Astrocytes
Cation Transport Proteins
Cell Nucleus
Chromatin
GAP-43 Protein
Glial Fibrillary Acidic Protein
In Situ Hybridization
Mice
Microscopy, Electron
Neurodegenerative Diseases
Neurons
Progesterone
RNA, Messenger
Spinal Cord
description Progesterone neuroprotection has been reported in experimental brain, peripheral nerve and spinal cord injury. To investigate for a similar role in neurodegeneration, we studied progesterone effects in the Wobbler mouse, a mutant presenting severe motoneuron degeneration and astrogliosis of the spinal cord. Implant of a single progesterone pellet (20mg) during 15 days produced substantial changes in Wobbler mice spinal cord. Morphologically, motoneurons of untreated Wobbler mice showed severe vacuolation of intracellular organelles including mitochondria. In contrast, neuropathology was less pronounced in Wobbler mice receiving progesterone, together with a reduction of vacuolated cells and preservation of mitochondrial ultrastructure. Determination of mRNAs for the α3 and β1 subunits of neuronal Na, K-ATPase, showed that mRNA levels in untreated mice were significantly reduced, whereas progesterone therapy re-established the expression of both subunits. Additionally, progesterone treatment of Wobbler mice attenuated the aberrant expression of the growth-associated protein (GAP-43) mRNA which otherwise occurred in motoneurons of untreated animals. The hormone, however, was without effect on astrocytosis of Wobbler mice, determined by glial fibrillary acidic protein (GFAP)-immunostaining. Lastly, progesterone treatment of Wobbler mice enhanced grip strength and prolonged survival at the end of the 15-day observation period. Recovery of morphology and molecular motoneuron parameters of Wobbler mice receiving progesterone, suggest a new and important role for this hormone in the prevention of spinal cord neurodegenerative disorders. © 2003 Elsevier Science Ltd. All rights reserved.
title Basis of progesterone protection in spinal cord neurodegeneration
title_short Basis of progesterone protection in spinal cord neurodegeneration
title_full Basis of progesterone protection in spinal cord neurodegeneration
title_fullStr Basis of progesterone protection in spinal cord neurodegeneration
title_full_unstemmed Basis of progesterone protection in spinal cord neurodegeneration
title_sort basis of progesterone protection in spinal cord neurodegeneration
publishDate 2002
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_09600760_v83_n1-5_p199_GonzalezDeniselle
http://hdl.handle.net/20.500.12110/paper_09600760_v83_n1-5_p199_GonzalezDeniselle
_version_ 1768544374612819968