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首页> 外文期刊>Progress in brain research >The role of NT-3 signaling in Merkel cell development.
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The role of NT-3 signaling in Merkel cell development.

机译：NT-3信号在默克尔细胞发育中的作用。

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Merkel cells originate from the neural crest. They are located in hairy and glabrous skin and have neuroendocrine characteristics. Together with A beta afferents, Merkel cells form a slowly adapting mechanoreceptor, the Merkel nerve ending, which transduces steady skin indentation. Neurotphin-3 (NT-3) plays important roles in neural crest cell development. We thus sought to determine whether neurotrophin signaling is essential for Merkel cell development in the whisker pad of the mouse. Our data indicate that at embryonic day 16.5 (E 16.5), NT-3 and its receptors, p75 neurotrophin receptor (p75NTR) and tyrosine kinase receptor, TrkC are not expressed at detectable levels in Merkel cells. After a perinatal switch, however, Merkel cells in whiskers of newborn mice are immunoreactive for p75NTR, TrkC and NT-3. Immunoreactivity of all three markers persists into adulthood. By contrast, innervating fibers are intensely p75NTR-immunoreactive in E16.5 whiskers, but no TrkC immunoreactivity is detected. At birth, and at 6 weeks of age, afferent fibers are intensely immunoreactive for both p75NTR and TrkC. In TrkC null whiskers, numerous Merkel cells are present at E16.5, and they are innervated. We draw three major conclusions from these observations: (i) NT-3 signaling through p75NTR or TrkC is not required for the development and prenatal survival of either a major subset or of all Merkel cells, (ii) the postnatal survival of Merkel cells is supported by autocrine or paracrine NT-3, rather than by neuron-derived NT-3, and (iii) Merkel cell-derived NT-3 is not a chemoattractant for innervating A beta fibers, but is likely to be involved in maintaining Merkel cell innervation postnatally.
机译：默克尔细胞起源于神经c。它们位于多毛和无毛的皮肤中，并具有神经内分泌特征。默克尔细胞与Aβ传入分子一起形成缓慢适应的机械感受器，即默克尔神经末梢，可转导稳定的皮肤压痕。 Neurotphin-3（NT-3）在神经c细胞发育中起重要作用。因此，我们寻求确定神经营养蛋白信号传导对于小鼠晶须垫中的默克尔细胞发育是否必不可少。我们的数据表明，在胚胎第16.5天（E 16.5），NT-3及其受体，p75神经营养蛋白受体（p75NTR）和酪氨酸激酶受体，TrkC在默克尔细胞中未以可检测的水平表达。但是，在围产期转换后，新生小鼠晶须中的默克尔细胞对p75NTR，TrkC和NT-3具有免疫反应性。所有这三种标记物的免疫反应性一直持续到成年期。相比之下，支配神经纤维在E16.5晶须中具有强烈的p75NTR免疫反应性，但未检测到TrkC免疫反应性。出生时和6周大时，传入纤维对p75NTR和TrkC都具有强烈的免疫反应性。在TrkC空须晶中，E16.5存在大量默克尔细胞，它们被神经支配。我们从这些观察中得出三个主要结论：（i）主要子集或所有默克尔细胞的发育和产前存活不需要通过p75NTR或TrkC的NT-3信号传导;（ii）默克尔细胞的产后存活时间是由自分泌或旁分泌的NT-3支持，而不是由神经元衍生的NT-3支持;（iii）默克尔细胞衍生的NT-3并不是神经支配Aβ纤维的趋化因子，但可能与维持默克尔细胞有关产后神经支配。

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