Differential neurodegenerative phenotypes are associated with heterogeneous voiding dysfunction in a coronavirus-induced model of multiple sclerosis.
Identifieur interne : 000596 ( PubMed/Checkpoint ); précédent : 000595; suivant : 000597Differential neurodegenerative phenotypes are associated with heterogeneous voiding dysfunction in a coronavirus-induced model of multiple sclerosis.
Auteurs : Sanghee Lee [États-Unis] ; Balachandar Nedumaran [États-Unis] ; Joseph Hypolite [États-Unis] ; Brian Caldwell [États-Unis] ; Michael C. Rudolph [États-Unis] ; Anna P. Malykhina [États-Unis]Source :
- Scientific reports [ 2045-2322 ] ; 2019.
Abstract
Patients with multiple sclerosis (MS) develop a variety of lower urinary tract symptoms (LUTS). We previously characterized a murine model of neurogenic bladder dysfunction induced by a neurotropic strain of a coronavirus. In the present study, we further study the role of long-lasting neurodegeneration on the development of neurogenic bladder dysfunction in mice with corona-virus induced encephalitis (CIE). Long-term follow up study revealed three phenotypes of neurodegenerative symptom development: recovery (REC group), chronic progression (C-PRO group) and chronic disease with relapsing-remitting episodes (C-RELAP group). The levels of IL-1β in REC group, IL-10 in C-RELAP group, and IL-1β, IL-6, IL-10 and TNF-α in C-PRO group were diminished in the brain. The levels of TNF-α in REC group and INF-γ, IL-2, TGF-β and TNF-α in the C-PRO group were also diminished in the urinary bladder. Mice in C-RELAP group showed a delayed recovery of voiding function. In vitro contractility studies determined a decreased basal detrusor tone and reduced amplitude of nerve-mediated contractions in C-RELAP group, whereas C-PRO group had elevated muscle-mediated contractions. In conclusion, mice with CIE developed three phenotypes of neurologic impairment mimicking different types of MS progression in humans and showed differential mechanisms driving neurogenic bladder dysfunction.
DOI: 10.1038/s41598-019-47407-x
PubMed: 31350464
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Rudolph</name><affiliation wicri:level="1"><nlm:affiliation>Division of Endocrinology, Metabolism & Diabetes, University of Colorado Denver, Aurora, Co, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Endocrinology, Metabolism & Diabetes, University of Colorado Denver, Aurora, Co</wicri:regionArea><wicri:noRegion>Co</wicri:noRegion></affiliation></author><author><name sortKey="Malykhina, Anna P" sort="Malykhina, Anna P" uniqKey="Malykhina A" first="Anna P" last="Malykhina">Anna P. Malykhina</name><affiliation wicri:level="1"><nlm:affiliation>Division of Urology, Department of Surgery, University of Colorado Denver, Aurora, Co, USA. Anna.Malykhina@ucdenver.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Urology, Department of Surgery, University of Colorado Denver, Aurora, Co</wicri:regionArea><wicri:noRegion>Co</wicri:noRegion></affiliation></author></analytic><series><title level="j">Scientific reports</title><idno type="eISSN">2045-2322</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Patients with multiple sclerosis (MS) develop a variety of lower urinary tract symptoms (LUTS). We previously characterized a murine model of neurogenic bladder dysfunction induced by a neurotropic strain of a coronavirus. In the present study, we further study the role of long-lasting neurodegeneration on the development of neurogenic bladder dysfunction in mice with corona-virus induced encephalitis (CIE). Long-term follow up study revealed three phenotypes of neurodegenerative symptom development: recovery (REC group), chronic progression (C-PRO group) and chronic disease with relapsing-remitting episodes (C-RELAP group). The levels of IL-1β in REC group, IL-10 in C-RELAP group, and IL-1β, IL-6, IL-10 and TNF-α in C-PRO group were diminished in the brain. The levels of TNF-α in REC group and INF-γ, IL-2, TGF-β and TNF-α in the C-PRO group were also diminished in the urinary bladder. Mice in C-RELAP group showed a delayed recovery of voiding function. In vitro contractility studies determined a decreased basal detrusor tone and reduced amplitude of nerve-mediated contractions in C-RELAP group, whereas C-PRO group had elevated muscle-mediated contractions. In conclusion, mice with CIE developed three phenotypes of neurologic impairment mimicking different types of MS progression in humans and showed differential mechanisms driving neurogenic bladder dysfunction.</div></front></TEI><pubmed><MedlineCitation Status="In-Data-Review" Owner="NLM"><PMID Version="1">31350464</PMID><DateRevised><Year>2020</Year><Month>03</Month><Day>06</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2045-2322</ISSN><JournalIssue CitedMedium="Internet"><Volume>9</Volume><Issue>1</Issue><PubDate><Year>2019</Year><Month>Jul</Month><Day>26</Day></PubDate></JournalIssue><Title>Scientific reports</Title><ISOAbbreviation>Sci Rep</ISOAbbreviation></Journal><ArticleTitle>Differential neurodegenerative phenotypes are associated with heterogeneous voiding dysfunction in a coronavirus-induced model of multiple sclerosis.</ArticleTitle><Pagination><MedlinePgn>10869</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/s41598-019-47407-x</ELocationID><Abstract><AbstractText>Patients with multiple sclerosis (MS) develop a variety of lower urinary tract symptoms (LUTS). We previously characterized a murine model of neurogenic bladder dysfunction induced by a neurotropic strain of a coronavirus. In the present study, we further study the role of long-lasting neurodegeneration on the development of neurogenic bladder dysfunction in mice with corona-virus induced encephalitis (CIE). Long-term follow up study revealed three phenotypes of neurodegenerative symptom development: recovery (REC group), chronic progression (C-PRO group) and chronic disease with relapsing-remitting episodes (C-RELAP group). The levels of IL-1β in REC group, IL-10 in C-RELAP group, and IL-1β, IL-6, IL-10 and TNF-α in C-PRO group were diminished in the brain. The levels of TNF-α in REC group and INF-γ, IL-2, TGF-β and TNF-α in the C-PRO group were also diminished in the urinary bladder. Mice in C-RELAP group showed a delayed recovery of voiding function. In vitro contractility studies determined a decreased basal detrusor tone and reduced amplitude of nerve-mediated contractions in C-RELAP group, whereas C-PRO group had elevated muscle-mediated contractions. In conclusion, mice with CIE developed three phenotypes of neurologic impairment mimicking different types of MS progression in humans and showed differential mechanisms driving neurogenic bladder dysfunction.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Sanghee</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Urology, University of California San Diego, La Jolla, California, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nedumaran</LastName><ForeName>Balachandar</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Division of Urology, Department of Surgery, University of Colorado Denver, Aurora, Co, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hypolite</LastName><ForeName>Joseph</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Division of Urology, Department of Surgery, University of Colorado Denver, Aurora, Co, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Caldwell</LastName><ForeName>Brian</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Division of Urology, Department of Surgery, University of Colorado Denver, Aurora, Co, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rudolph</LastName><ForeName>Michael C</ForeName><Initials>MC</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-6147-212X</Identifier><AffiliationInfo><Affiliation>Division of Endocrinology, Metabolism & Diabetes, University of Colorado Denver, Aurora, Co, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>NORC Metabolic and Cellular Analysis Core Center for Women's Health Research, University of Colorado Denver, Aurora, Co, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Malykhina</LastName><ForeName>Anna P</ForeName><Initials>AP</Initials><AffiliationInfo><Affiliation>Division of Urology, Department of Surgery, University of Colorado Denver, Aurora, Co, USA. 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last="Lee">Sanghee Lee</name></region><name sortKey="Caldwell, Brian" sort="Caldwell, Brian" uniqKey="Caldwell B" first="Brian" last="Caldwell">Brian Caldwell</name><name sortKey="Hypolite, Joseph" sort="Hypolite, Joseph" uniqKey="Hypolite J" first="Joseph" last="Hypolite">Joseph Hypolite</name><name sortKey="Malykhina, Anna P" sort="Malykhina, Anna P" uniqKey="Malykhina A" first="Anna P" last="Malykhina">Anna P. Malykhina</name><name sortKey="Nedumaran, Balachandar" sort="Nedumaran, Balachandar" uniqKey="Nedumaran B" first="Balachandar" last="Nedumaran">Balachandar Nedumaran</name><name sortKey="Rudolph, Michael C" sort="Rudolph, Michael C" uniqKey="Rudolph M" first="Michael C" last="Rudolph">Michael C. Rudolph</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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