RT Conference Proceedings
T1 Multiciliated ependyma recovery through a sequential cell therapy in posthemorrhagic hydrocephalus.
A1 López-de-San-Sebastián, Javier
A1 Rodríguez-Pérez, Luis Manuel
A1 González-García, Marcos
A1 Páez-González, Patricia
A1 Jiménez-Lara, Antonio Jesús
K1 Hidrocefalia - Tratamiento
K1 Terapia celular - Ensayos
AB Posthemorrhagic hydrocephalus (PHH) is a significant cause for premature children’s morbidity, mortality, andperi/postnatal neurodevelopmental impairment. PHH is mainly triggered by germinal matrix hemorrhages (GMH)and causes germinal matrix and ependyma disfunction. Ependyma constitutes a relevant tissue barrier with roles incerebrospinal fluid homeostasis, circulation, and neurogenesis, hence situating ependyma as a main target whentreating PHH. Clinical treatments are directed to eliminate immediate inflammatory condition triggered by thebleeding, to drain excess of CSF if needed, but not to treat or recover ependyma structure. Ependymal progenitorswere obtained from P0 mice. Cells were cultured under specific conditions to enhance either ependymalproliferation or differentiation status. Different GMH/IVH neuroinflammatory conditions were mimed in theependyma cultures, different stem cell therapies tested and effect on the ependymal differentiation measured.Additionally, ventricular wall explants from mice with induced PHH were obtained and cultured as ex-vivo system ofPHH. A combination of stem cells was applied on the tissue to probe its regenerative capabilities on themulticiliated ependyma. All samples were analyzed through immunofluorescence and laser confocal microscopyand quantified. Results show that (i) ependymal progenitors’ maturation is hindered under neuroinflammatoryconditions, showing no multiciliated ependyma and (ii) the tested stem cell combination promotes ependymalprogenitors’ survival albeit does not alter the differentiation of the selfsame. In summary, it can be stated that thefinal differentiation of the ependyma is disrupted by the molecular conditions triggered by GMH/IVH, which ourproposed cell therapy is able to counteract through increased survival and differentiation in a murine model ofexperimental PHH
YR 2023
FD 2023
LK https://hdl.handle.net/10630/27738
UL https://hdl.handle.net/10630/27738
LA eng
NO Junta de Andalucia (UMA18-FEDERJA-277) and Instituto de Salud Carlos III(PI19/00778), Spain; co-financed by FEDER funds from the European Union, Spain. Also, II-PPITD, Universidad deMalaga, Spain (to JL-dSS); and I-PPITD, Universidad de Málaga, Spain (to LMR-P)Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech.
DS RIUMA. Repositorio Institucional de la Universidad de Málaga
RD 3 mar 2026