White Matter Plasticity and Enhanced Remyelination in the Maternal CNS

Gregg, Christopher; Shikar, Viktor; Larsen, Peter H.; Mak, Gloria; Chojnacki, Andrew; Yong, V. Wee; Weiss, Samuel

doi:10.1523/jneurosci.4441-06.2007

Cited by 222 publications

(195 citation statements)

References 74 publications

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“…Moreover, PRL has been shown to regulate oligodendrocyte precursor proliferation and mimic the regenerative effects of pregnancy. PRL's striking ability to repair demyelination identifies it as a potential therapeutic agent in multiple sclerosis (48). There could be some potential side effects of higher levels of PRL.…”

Section: Figurementioning

confidence: 99%

Prolactin increases SMN expression and survival in a mouse model of severe spinal muscular atrophy via the STAT5 pathway

Farooq

Molina²,

Hadwen³

et al. 2011

J. Clin. Invest.

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Section: Figurementioning

confidence: 99%

Prolactin increases SMN expression and survival in a mouse model of severe spinal muscular atrophy via the STAT5 pathway

Farooq

Molina²,

Hadwen³

et al. 2011

J. Clin. Invest.

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“…In the MS field, PRL has gained renewed interest in recent years, because two studies showed that exclusive breastfeeding (a hyperprolactinemic physiologic condition) reduces the risk for postpartum relapses (35,36), albeit other articles reported discordant results (5,37,38). Further, another article has demonstrated that PRL mediates proliferation of oligodendrocyte progenitor cells during pregnancy and promotes myelin repair in a spontaneously remyelinating model of chemical (lysolecithin)-induced focal demyelination, suggesting PRL as a potential therapeutic agent for MS (39). By studying EAE, an immune-mediated model of demyelination, in PRLR-and PRL-deficient mice, we had the possibility to evaluate the net effect of PRL on disease development between the potential immune-stimulating (detrimental) and myelinogenic (beneficial) properties of this hormone.…”

Section: Discussionmentioning

confidence: 99%

Prolactin Is Not Required for the Development of Severe Chronic Experimental Autoimmune Encephalomyelitis

Costanza

Musio

Abou-Hamdan

et al. 2013

The Journal of Immunology

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Predominance of multiple sclerosis (MS) in women, reductions of disease flares during pregnancy, and their increase in the postpartum period have suggested a hormonal influence on MS activity. The hormone prolactin (PRL) has long been debated as a potential immune-stimulating factor in several autoimmune disorders, including MS and its animal model experimental autoimmune encephalomyelitis (EAE). However, to date, no data clearly ascribe a pathogenic role to PRL in these diseases. Using PRL receptor–deficient (Prlr−/−) and PRL-deficient (Prl−/−) mice, we show that PRL plays a redundant role in the development of chronic EAE. In Prlr−/− and Prl−/− mice, EAE developed with a delayed onset compared with littermate control mice, but with full clinical severity. In line with the clinical outcome, T cell proliferation and production of IFN-γ, IL-17A, and IL-6 induced by myelin Ag were delayed in Prlr−/− and Prl−/− mice. Ag-specific IgG Ab responses were not affected by PRLR or PRL deficiency. We also show that mouse lymph node cells and purified CD4+ T cells express transcript for Prlr, but not for Prl. These results reveal that PRL does not play a central role in the development of chronic EAE and optimal Th1 and Th17 responses against myelin. Moreover, they also rule out a possible contribution of PRL secreted by immune cells to the modulation of autoreactive T cell response in this model.

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“…9 In addition to its primary roles in mammary gland development, as well as the initiation and maintenance of lactation, PRL is believed to be involved in a number of physiological roles, including immune system modulation, cell proliferation and neuroregeneration. [8][9][10][11][12] For example, PRL possesses both pro-and anti-inflammatory properties. High levels of circulating PRL can enhance Th1 cellular activity and antigen-specific T-lymphocyte function in mice.…”

Section: Introductionmentioning

confidence: 99%

Prolactin in multiple sclerosis

et al. 2012

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Multiple sclerosis (MS) is more common among women than men. MS often goes into remission during pregnancy, when prolactin (PRL) levels are known to be high. In an animal model of demyelination, PRL promoted myelin repair, suggesting it has potential as a remyelinating therapy in MS. In this systematic review, we examined the known associations between PRL and MS, in order to elucidate its potential role in the pathophysiology and treatment of MS. A systematic search was performed in the electronic databases PubMed and EMBASE, using the keywords "prolactin" AND "multiple sclerosis." The inclusion criteria were met by 23 studies. These studies suggested to us that elevated PRL may be more common in MS patients than in controls. Hyperprolactinemia may also be associated with clinical relapse in MS, especially among patients with hypothalamic lesions or optic neuritis; however, it is unknown if this is a cause or consequence of a relapse. Overall, most people with MS have normal PRL levels. The impact of PRL on MS outcomes remains unclear.

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White Matter Plasticity and Enhanced Remyelination in the Maternal CNS

Cited by 222 publications

References 74 publications

Prolactin increases SMN expression and survival in a mouse model of severe spinal muscular atrophy via the STAT5 pathway

Prolactin increases SMN expression and survival in a mouse model of severe spinal muscular atrophy via the STAT5 pathway

Prolactin Is Not Required for the Development of Severe Chronic Experimental Autoimmune Encephalomyelitis

Prolactin in multiple sclerosis

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