Combined effects of transferrin and thyroid hormone during oligodendrogenesis <i>In vitro</i>

Marziali, Leandro N.; Correale, Jorge; Pasquini, Juana M.

doi:10.1002/glia.23029

Cited by 7 publications

(6 citation statements)

References 40 publications

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“…Specifically, OPC quantities increase three-fold in the presence of T3 [69]. This effect requires the presence of the glycoprotein transferrin, which increases TRα1 expression [70]. Similar effects on oligodendrogenesis are observed in adult-derived NSCs.…”

Section: Effects On Oligodendrogenesismentioning

confidence: 63%

Hormonal Regulation of Oligodendrogenesis I: Effects across the Lifespan

et al. 2021

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The brain’s capacity to respond to changing environments via hormonal signaling is critical to fine-tuned function. An emerging body of literature highlights a role for myelin plasticity as a prominent type of experience-dependent plasticity in the adult brain. Myelin plasticity is driven by oligodendrocytes (OLs) and their precursor cells (OPCs). OPC differentiation regulates the trajectory of myelin production throughout development, and importantly, OPCs maintain the ability to proliferate and generate new OLs throughout adulthood. The process of oligodendrogenesis, the creation of new OLs, can be dramatically influenced during early development and in adulthood by internal and environmental conditions such as hormones. Here, we review the current literature describing hormonal regulation of oligodendrogenesis within physiological conditions, focusing on several classes of hormones: steroid, peptide, and thyroid hormones. We discuss hormonal regulation at each stage of oligodendrogenesis and describe mechanisms of action, where known. Overall, the majority of hormones enhance oligodendrogenesis, increasing OPC differentiation and inducing maturation and myelin production in OLs. The mechanisms underlying these processes vary for each hormone but may ultimately converge upon common signaling pathways, mediated by specific receptors expressed across the OL lineage. However, not all of the mechanisms have been fully elucidated, and here, we note the remaining gaps in the literature, including the complex interactions between hormonal systems and with the immune system. In the companion manuscript in this issue, we discuss the implications of hormonal regulation of oligodendrogenesis for neurological and psychiatric disorders characterized by white matter loss. Ultimately, a better understanding of the fundamental mechanisms of hormonal regulation of oligodendrogenesis across the entire lifespan, especially in vivo, will progress both basic and translational research.

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Section: Effects On Oligodendrogenesismentioning

confidence: 63%

Hormonal Regulation of Oligodendrogenesis I: Effects across the Lifespan

et al. 2021

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“…High concentration of apo-Tf in the culture media of OPCs isolated from iron-deficient pups also promotes the maturation of these cells to control levels ( Badaracco et al., 2008 ). Interestingly, apo-Tf enhances the effect of the thyroid hormone on OPC maturation and in turn, the thyroid hormone promotes the synthesis of apo-Tf in OPCs ( Marziali et al., 2015 , 2016 ). The effects of apo-Tf on oligodendrocyte maturation and myelination were found to be mediated by several signaling pathways.…”

Section: Iron Homeostasis In Oligodendrocyte Developmentmentioning

confidence: 99%

Iron Metabolism in Oligodendrocytes and Astrocytes, Implications for Myelination and Remyelination

et al. 2020

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Iron is a key nutrient for normal central nervous system (CNS) development and function; thus, iron deficiency as well as iron excess may result in harmful effects in the CNS. Oligodendrocytes and astrocytes are crucial players in brain iron equilibrium. However, the mechanisms of iron uptake, storage, and efflux in oligodendrocytes and astrocytes during CNS development or under pathological situations such as demyelination are not completely understood. In the CNS, iron is directly required for myelin production as a cofactor for enzymes involved in ATP, cholesterol and lipid synthesis, and oligodendrocytes are the cells with the highest iron levels in the brain which is linked to their elevated metabolic needs associated with the process of myelination. Unlike oligodendrocytes, astrocytes do not have a high metabolic requirement for iron. However, these cells are in close contact with blood vessel and have a strong iron transport capacity. In several pathological situations, changes in iron homoeostasis result in altered cellular iron distribution and accumulation and oxidative stress. In inflammatory demyelinating diseases such as multiple sclerosis, reactive astrocytes accumulate iron and upregulate iron efflux and influx molecules, which suggest that they are outfitted to take up and safely recycle iron. In this review, we will discuss the participation of oligodendrocytes and astrocytes in CNS iron homeostasis. Understanding the molecular mechanisms of iron uptake, storage, and efflux in oligodendrocytes and astrocytes is necessary for planning effective strategies for iron management during CNS development as well as for the treatment of demyelinating diseases.

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“…Following the recapitulation hypothesis, which postulates that remyelination recapitulates developmental myelination (Franklin & Hinks, 1999), we postulate that, in being two well‐known factors which promote myelination (Ahlgren, Wallace, Bishop, Neophytou, & Raff, 1997; Barres, Lazar, & Raff, 1994; Escobar Cabrera et al, 1994; Escobar Cabrera, Zakin, Soto, & Pasquini, 1997) by acting coordinately at different stages of OLG differentiation (Marziali et al, 2015; Marziali, Correale, Garcia, & Pasquini, 2016), T3 and aTf concomitantly administered might show increased efficiency in favoring remyelination when compared with single treatments (Adamo et al, 2006; Franco et al,Franco et al, 2008). In testing this hypothesis, our current studies using the CPZ‐induced demyelination model proved that combined aTf + T3 treatment yielded higher MBP expression and more mature CC1+ OLG in the CC.…”

Section: Discussionmentioning

confidence: 99%

“…Further studies by our group showed that, during myelination, THRα expression is independent of T3 modulation and regulated by aTf, while THRβ expression appears to respond exclusively to T3 stimulus. THRα1 emerged as the aTf‐regulated THR isoform, (Marziali et al, 2015, 2016).…”

Section: Discussionmentioning

confidence: 99%