<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Filice, Federica</dc:creator>
  <dc:creator>Celio, Marco R.</dc:creator>
  <dc:creator>Babalian, Alexandre</dc:creator>
  <dc:creator>Blum, Walter</dc:creator>
  <dc:creator>Szabolcsi, Viktoria</dc:creator>
  <dc:date>2017-10-15</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">Aging-associated ependymal-cell pathologies can manifest as ventricular gliosis,  ventricle enlargement, or ventricle stenosis. Ventricle stenosis and fusion of the lateral  ventricle (LV) walls is associated with a massive decline of the proliferative capacities  of the stem cell niche in the affected subventricular zone (SVZ) in aging mice. We  examined the brains of adult C57BL/6 mice and found that ependymal cells located in  the adhesions of the medial and lateral walls of the rostral LVs upregulated  parvalbumin (PV) and displayed reactive phenotype, similarly to injury-reactive  ependymal cells. However, PV+ ependymal cells in the LV-wall adhesions, unlike  injury-reactive ones, did not express glial fibrillary acidic protein. S100B+/PV+  ependymal cells found in younger mice diminished in the LV-wall adhesions  throughout aging. We found that periventricular PV-immunofluorescence showed  positive correlation to the grade of LV stenosis in nonaged mice (&lt;10-month-old), and  that the extent of LV-wall adhesions and LV stenosis was significantly lower in mid- aged (&gt;10-month-old) PV-knock out (PV-KO) mice. This suggests an involvement of  PV+ ependymal cells in aging-associated ventricle stenosis. Additionally, we observed  a time-shift in microglial activation in the LV-wall adhesions between age-grouped PV- KO and wild-type mice, suggesting a delay in microglial activation when PV is absent  from ependymal cells. Our findings implicate that compromised ependymal cells of the  adhering ependymal layers upregulate PV and display phenotype shift to “reactive”  ependymal cells in aging-related ventricle stenosis; moreover, they also contribute to  the progression of LV-wall fusion associated with a decline of the affected SVZ-stem  cell niche in aged mice.</dc:description>
  <dc:format>application/pdf</dc:format>
  <dc:identifier>https://folia.unifr.ch/global/documents/305989</dc:identifier>
  <dc:identifier>https://folia.unifr.ch/documents/305989/files/cel_pee.pdf</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.1002/cne.24276</dc:relation>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:rights>License undefined</dc:rights>
  <dc:source>Journal of Comparative Neurology. - 2017, vol. 525, no. 15, p. 3266–3285</dc:source>
  <dc:subject xmlns:ns1="xml" ns1:lang="en">Aging</dc:subject>
  <dc:subject xmlns:ns2="xml" ns2:lang="en">Ependymal cell</dc:subject>
  <dc:subject xmlns:ns3="xml" ns3:lang="en">Lateral ventricle</dc:subject>
  <dc:subject xmlns:ns4="xml" ns4:lang="en">Parvalbumin</dc:subject>
  <dc:subject xmlns:ns5="xml" ns5:lang="en">Ventricle stenosis</dc:subject>
  <dc:subject xmlns:ns6="xml" ns6:lang="en">RRID:AB_10000344</dc:subject>
  <dc:subject xmlns:ns7="xml" ns7:lang="en">RRID:AB_2665495</dc:subject>
  <dc:subject xmlns:ns8="xml" ns8:lang="en">RRID:AB_2315304</dc:subject>
  <dc:subject xmlns:ns9="xml" ns9:lang="en">RRID:AB_2620025</dc:subject>
  <dc:subject xmlns:ns10="xml" ns10:lang="en">RRID:AB_1555288</dc:subject>
  <dc:subject xmlns:ns11="xml" ns11:lang="en">RRID:AB_221569</dc:subject>
  <dc:subject xmlns:ns12="xml" ns12:lang="en">RRII</dc:subject>
  <dc:subject>info:eu-repo/classification/udc/57</dc:subject>
  <dc:title xmlns:ns13="xml" ns13:lang="en">Parvalbumin-expressing ependymal cells in rostral lateral ventricle wall adhesions contribute to aging-related ventricle stenosis in mice</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>
