Bladder dysfunction in a transgenic mouse model of multiple system atrophy.
Identifieur interne : 000A85 ( Main/Exploration ); précédent : 000A84; suivant : 000A86Bladder dysfunction in a transgenic mouse model of multiple system atrophy.
Auteurs : Mathieu Boudes [Belgique] ; Pieter Uvin ; Silvia Pinto ; Thomas Voets ; Clare J. Fowler ; Gregor K. Wenning ; Dirk De Ridder ; Nadia StefanovaSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2013.
English descriptors
- KwdEn :
- Acetylcholine (pharmacology), Age Factors, Animals, Brain (pathology), Disease Models, Animal, Disease Progression, Diuresis (drug effects), Diuresis (physiology), Female, Gene Expression Regulation (genetics), Humans, Image Cytometry, In Vitro Techniques, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Multiple System Atrophy (complications), Multiple System Atrophy (genetics), Myelin Proteolipid Protein (genetics), Urinary Bladder (drug effects), Urinary Bladder (metabolism), Urinary Bladder (physiopathology), Urinary Bladder Diseases (etiology), Urinary Bladder Diseases (genetics), Uterine Contraction (drug effects), Uterine Contraction (genetics), alpha-Synuclein (genetics).
- MESH :
- chemical , genetics : Myelin Proteolipid Protein, alpha-Synuclein.
- chemical , pharmacology : Acetylcholine.
- complications : Multiple System Atrophy.
- drug effects : Diuresis, Urinary Bladder, Uterine Contraction.
- etiology : Urinary Bladder Diseases.
- genetics : Gene Expression Regulation, Multiple System Atrophy, Urinary Bladder Diseases, Uterine Contraction.
- metabolism : Urinary Bladder.
- pathology : Brain.
- physiology : Diuresis.
- physiopathology : Urinary Bladder.
- Age Factors, Animals, Disease Models, Animal, Disease Progression, Female, Humans, Image Cytometry, In Vitro Techniques, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic.
Abstract
Multiple system atrophy (MSA) is an adult-onset neurodegenerative disorder presenting with motor impairment and autonomic dysfunction. Urological function is altered in the majority of MSA patients, and urological symptoms often precede the motor syndrome. To date, bladder function and structure have never been investigated in MSA models. We aimed to test bladder function in a transgenic MSA mouse featuring oligodendroglial α-synucleinopathy and define its applicability as a preclinical model to study urological failure in MSA. Experiments were performed in proteolipid protein (PLP)-human α-synuclein (hαSyn) transgenic and control wild-type mice. Diuresis, urodynamics, and detrusor strip contractility were assessed to characterize the urological phenotype. Bladder morphology and neuropathology of the lumbosacral intermediolateral column and the pontine micturition center (PMC) were analyzed in young and aged mice. Urodynamic analysis revealed a less efficient and unstable bladder in MSA mice with increased voiding contraction amplitude, higher frequency of nonvoiding contractions, and increased postvoid residual volume. MSA mice bladder walls showed early detrusor hypertrophy and age-related urothelium hypertrophy. Transgenic hαSyn expression was detected in Schwann cells ensheathing the local nerve fibers in the lamina propria and muscularis of MSA bladders. Early loss of parasympathetic outflow neurons and delayed degeneration of the PMC accompanied the urological deficits in MSA mice. PLP-hαSyn mice recapitulate major urological symptoms of human MSA that may be linked to αSyn-related central and peripheral neuropathology and can be further used as a preclinical model to decipher pathomechanisms of MSA.
DOI: 10.1002/mds.25336
PubMed: 23426727
Affiliations:
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Fowler</name></author><author><name sortKey="Wenning, Gregor K" sort="Wenning, Gregor K" uniqKey="Wenning G" first="Gregor K" last="Wenning">Gregor K. 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Fowler</name></author><author><name sortKey="Wenning, Gregor K" sort="Wenning, Gregor K" uniqKey="Wenning G" first="Gregor K" last="Wenning">Gregor K. Wenning</name></author><author><name sortKey="De Ridder, Dirk" sort="De Ridder, Dirk" uniqKey="De Ridder D" first="Dirk" last="De Ridder">Dirk De Ridder</name></author><author><name sortKey="Stefanova, Nadia" sort="Stefanova, Nadia" uniqKey="Stefanova N" first="Nadia" last="Stefanova">Nadia Stefanova</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acetylcholine (pharmacology)</term><term>Age Factors</term><term>Animals</term><term>Brain (pathology)</term><term>Disease Models, Animal</term><term>Disease Progression</term><term>Diuresis (drug effects)</term><term>Diuresis (physiology)</term><term>Female</term><term>Gene Expression Regulation (genetics)</term><term>Humans</term><term>Image Cytometry</term><term>In Vitro Techniques</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Transgenic</term><term>Multiple System Atrophy (complications)</term><term>Multiple System Atrophy (genetics)</term><term>Myelin Proteolipid Protein (genetics)</term><term>Urinary Bladder (drug effects)</term><term>Urinary Bladder (metabolism)</term><term>Urinary Bladder (physiopathology)</term><term>Urinary Bladder Diseases (etiology)</term><term>Urinary Bladder Diseases (genetics)</term><term>Uterine Contraction (drug effects)</term><term>Uterine Contraction (genetics)</term><term>alpha-Synuclein (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Myelin Proteolipid Protein</term><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Acetylcholine</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Multiple System Atrophy</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Diuresis</term><term>Urinary Bladder</term><term>Uterine Contraction</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Urinary Bladder Diseases</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Gene Expression Regulation</term><term>Multiple System Atrophy</term><term>Urinary Bladder Diseases</term><term>Uterine Contraction</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Urinary Bladder</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Diuresis</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Urinary Bladder</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Age Factors</term><term>Animals</term><term>Disease Models, Animal</term><term>Disease Progression</term><term>Female</term><term>Humans</term><term>Image Cytometry</term><term>In Vitro Techniques</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Transgenic</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Multiple system atrophy (MSA) is an adult-onset neurodegenerative disorder presenting with motor impairment and autonomic dysfunction. Urological function is altered in the majority of MSA patients, and urological symptoms often precede the motor syndrome. To date, bladder function and structure have never been investigated in MSA models. We aimed to test bladder function in a transgenic MSA mouse featuring oligodendroglial α-synucleinopathy and define its applicability as a preclinical model to study urological failure in MSA. Experiments were performed in proteolipid protein (PLP)-human α-synuclein (hαSyn) transgenic and control wild-type mice. Diuresis, urodynamics, and detrusor strip contractility were assessed to characterize the urological phenotype. Bladder morphology and neuropathology of the lumbosacral intermediolateral column and the pontine micturition center (PMC) were analyzed in young and aged mice. Urodynamic analysis revealed a less efficient and unstable bladder in MSA mice with increased voiding contraction amplitude, higher frequency of nonvoiding contractions, and increased postvoid residual volume. MSA mice bladder walls showed early detrusor hypertrophy and age-related urothelium hypertrophy. Transgenic hαSyn expression was detected in Schwann cells ensheathing the local nerve fibers in the lamina propria and muscularis of MSA bladders. Early loss of parasympathetic outflow neurons and delayed degeneration of the PMC accompanied the urological deficits in MSA mice. PLP-hαSyn mice recapitulate major urological symptoms of human MSA that may be linked to αSyn-related central and peripheral neuropathology and can be further used as a preclinical model to decipher pathomechanisms of MSA.</div></front></TEI><affiliations><list><country><li>Belgique</li></country></list><tree><noCountry><name sortKey="De Ridder, Dirk" sort="De Ridder, Dirk" uniqKey="De Ridder D" first="Dirk" last="De Ridder">Dirk De Ridder</name><name sortKey="Fowler, Clare J" sort="Fowler, Clare J" uniqKey="Fowler C" first="Clare J" last="Fowler">Clare J. Fowler</name><name sortKey="Pinto, Silvia" sort="Pinto, Silvia" uniqKey="Pinto S" first="Silvia" last="Pinto">Silvia Pinto</name><name sortKey="Stefanova, Nadia" sort="Stefanova, Nadia" uniqKey="Stefanova N" first="Nadia" last="Stefanova">Nadia Stefanova</name><name sortKey="Uvin, Pieter" sort="Uvin, Pieter" uniqKey="Uvin P" first="Pieter" last="Uvin">Pieter Uvin</name><name sortKey="Voets, Thomas" sort="Voets, Thomas" uniqKey="Voets T" first="Thomas" last="Voets">Thomas Voets</name><name sortKey="Wenning, Gregor K" sort="Wenning, Gregor K" uniqKey="Wenning G" first="Gregor K" last="Wenning">Gregor K. Wenning</name></noCountry><country name="Belgique"><noRegion><name sortKey="Boudes, Mathieu" sort="Boudes, Mathieu" uniqKey="Boudes M" first="Mathieu" last="Boudes">Mathieu Boudes</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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