Neuromorphological and Neuroendocrine Research Laboratory, Department of Anatomy, Histology and Embryology, Hungarian Academy of Sciences and Semmelweis University, Budapest H-1094, Hungary.
J Comp Neurol. 2010 Sep 15;518(18):3752-70. doi: 10.1002/cne.22422.
Transforming growth factors-beta1 (TGF-beta1), -2, and -3 form a small group of related proteins involved in the regulation of proliferation, differentiation, and survival of various cell types. Recently, TGF-betas were also demonstrated to be neuroprotective. In the present study, we investigated their distribution in the rat brain as well as their expression following middle cerebral artery occlusion. Probes were produced for all types of TGF-betas, and in situ hybridization was performed. We demonstrated high TGF-beta1 expression in cerebral cortex, hippocampus, central amygdaloid nucleus, medial preoptic area, hypothalamic paraventricular nucleus, substantia nigra, brainstem reticular formation and motoneurons, and area postrema. In contrast, TGF-beta2 was abundantly expressed in deep cortical layers, dentate gyrus, midline thalamic nuclei, posterior hypothalamic area and mamillary body, superior olive, areas of monoaminergic neurons, spinal trigeminal nucleus, dorsal vagal complex, cerebellum, and choroid plexus, and a high level of TGF-beta3 mRNA was found in cerebral cortex, hippocampus, basal amygdaloid nuclei, lateral septal nucleus, several thalamic nuclei, arcuate and supramamillary nuclei, superior colliculus, superior olive, brainstem reticular formation and motoneurons, area postrema, and inferior olive. Focal brain ischemia induced TGF-betas with markedly different expression patterns. TGF-beta1 was induced in the penumbral region of cortex and striatum, whereas TGF-beta2 and -beta3 were induced in different layers of the ipsilateral cortex. The expression of the subtypes of TGF-betas in different brain regions suggests that they are involved in the regulation of different neurons and bind to different latent TGF-beta binding proteins. Furthermore, they might have subtype-specific functions following ischemic attack.
转化生长因子-β1（TGF-β1）、-2 和 -3 形成了一小组相关蛋白，参与调节各种细胞类型的增殖、分化和存活。最近，TGF-βs 也被证明具有神经保护作用。在本研究中，我们研究了它们在大鼠脑中的分布以及在大脑中动脉闭塞后的表达。为所有类型的 TGF-βs 生成了探针，并进行了原位杂交。我们证明了 TGF-β1 在大脑皮层、海马体、中央杏仁核、内侧视前区、下丘脑室旁核、黑质、脑干网状结构和运动神经元以及最后区有高表达。相比之下，TGF-β2 在皮质深层、齿状回、中线丘脑核、下丘脑后区和乳头体、上橄榄核、单胺能神经元区域、三叉神经脊核、迷走神经复合体、小脑和脉络丛中大量表达，而 TGF-β3 mRNA 的高水平则在大脑皮层、海马体、基底杏仁核、外侧隔核、几个丘脑核、弓状核和穹窿上核、上丘、上橄榄核、脑干网状结构和运动神经元、最后区和下橄榄核中发现。局灶性脑缺血诱导了具有明显不同表达模式的 TGF-βs。TGF-β1 在皮质和纹状体的半影区诱导，而 TGF-β2 和 -β3 在同侧皮质的不同层诱导。TGF-βs 亚型在不同脑区的表达表明它们参与了不同神经元的调节，并与不同的潜伏 TGF-β 结合蛋白结合。此外，它们在缺血攻击后可能具有亚型特异性功能。
