ORCID Profile
0000-0002-0401-0615
Current Organisation
University of Cambridge
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Publisher: No publisher found
Date: 2020
Publisher: Wiley
Date: 08-04-2022
DOI: 10.1111/ANS.17684
Publisher: MDPI AG
Date: 12-2015
Publisher: BioInsights Publishing, Ltd.
Date: 10-12-2015
Publisher: Cold Spring Harbor Laboratory
Date: 31-12-2019
DOI: 10.1101/2019.12.31.891804
Abstract: Little is known about the origin of the inductive signal that translates the utation stress into a cooperative cellular response. By studying the process underlying the reformation of lost body parts in the anthozoan cnidarian Nematostella vectensis , we identified a regeneration-inducing structure that, via a tissue crosstalk, is responsible for the initiation of the repair program. We further revealed for the first time in anthozoan cnidarians, that fast and slow-cycling/quiescent stem cells respond to the utation stress and actively participate in the reformation of lost body parts. Importantly, a synergic interaction of both stem cell populations is required to complete the regeneration process. Our findings suggest that the emergence/loss of structure complexity/compartmentalization influences the proprieties of tissue plasticity, changes the competence of a tissue to reprogram and, in the context of regeneration, the capacity of the tissue to emit or respond to a regeneration-inducing signal.
Publisher: Elsevier BV
Date: 2005
Publisher: Wiley
Date: 14-04-2021
DOI: 10.1111/EJN.14726
Abstract: Myelin and axon losses are associated with cognitive decline in healthy ageing but are worse in people diagnosed with tauopathy. To determine whether tauopathy is also associated with enhanced myelin plasticity, we evaluated the behaviour of OPCs in mice that expressed a human pathological variant of microtubule‐associated protein tau ( MAPT P301S ). By 6 months of age (P180), MAPT P301S mice overexpressed hyperphosphorylated tau and had developed reactive gliosis in the hippoc us but had not developed overt locomotor or memory impairment. By performing cre‐lox lineage tracing of adult OPCs, we determined that the number of newborn oligodendrocytes added to the hippoc us, entorhinal cortex and fimbria was equivalent in control and MAPT P301S mice prior to P150. However, between P150 and P180, significantly more new oligodendrocytes were added to these regions in the MAPT P301S mouse brain. This large increase in new oligodendrocyte number was not the result of increased OPC proliferation, nor did it alter oligodendrocyte density in the hippoc us, entorhinal cortex or fimbria, which was equivalent in P180 wild‐type and MAPT P301S mice. Furthermore, the proportion of hippoc al and fimbria axons with myelin was unaffected by tauopathy. However, the proportion of myelinated axons that were ensheathed by immature myelin internodes was significantly increased in the hippoc us and fimbria of P180 MAPT P301S mice, when compared with their wild‐type littermates. These data suggest that MAPT P301S transgenic mice experience significant oligodendrocyte turnover, with newborn oligodendrocytes compensating for myelin loss early in the development of tauopathy.
Publisher: Wiley
Date: 18-06-2020
DOI: 10.1002/JNR.24672
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Solène Ferreira.