Oligodendrocytes maturation and metabolic profile upon iron deficiency.

GUITART ME; ROSATO-SIRI V; MARTINO ADAMI PV; VERSTRATEN S; MORELLI L; PASQUINI, J.M.

Congreso; Reunion de Sociedades Conjuntas; 2017

Iron deficiency (ID) represents one of the most prevalent nutritionaldeficits, affecting almost two billion people worldwide. Gestationaliron deprivation as an experimental model is a useful tool to describespecific oligodendrocyte (OL) requirements for progressionto a mature and myelinating state. Previous work demonstrated thatID-OL appear to exhibit intrinsic alterations in terms of proliferation,migration and maturation.To better understand OL maturation, we explore the hypothesisthat ID constrains OL maturation by impairing metabolic pathways.In vivo and in vitro studies were conducted to evaluate: a) OL lineage composition along ontogenetic myelination; b) OL lineage cell number regulation; c) Glial cell metabolic profiles. We used an eGFP::CNPase transgenic mouse which renders the whole OL-lineage-committed cells as green-fluorescent (CNPase-positive cells). Pregnant mice were fed an ID diet (4mg/g/kg) as from gestational day 5. Postnatal development of myelination was evaluated 15 and 30 days after birth (PND15 and 30). At PND15, ID-OL lineage exhibited an increase in CNPase-positive cells but this redundancy failed to attain complexity and maturity (p≤ 0.01). At PND30, the number of CNPase-positive cells decreased, through an increase in cell death (p≤ 0.01). To further describe ID effects, the correlation was explored between maturational stage and ID metabolic signature.