Expression of vesicular glutamate transporter-2 in gonadotrope and thyrotrope cells of the rat pituitary.: Regulation by estrogen and thyroid hormone status
Expression of vesicular glutamate transporter-2 in gonadotrope and thyrotrope cells of the rat pituitary.: Regulation by estrogen and thyroid hormone status
复制标题
DOI：
10.1210/en.2005-1229
复制
发表时间：
2006-08-01
期刊：
影响因子：
4.8
通讯作者：
Liposits, Zsolt
中科院分区：
文献类型：
--
作者：
Hrabovszky, Erik;Kallo, Imre;Liposits, Zsolt
大鼠腺垂体的免疫细胞化学研究确定了一个细胞群，表现出免疫反应性的2型囊泡谷氨酸转运蛋白（VGLUT 2），一个标志物的谷氨酸能神经元表型。原位杂交检测VGLUT 2 mRNA在腺垂体细胞中的表达，证实VGLUT 2免疫反应性是由于真实的VGLUT 2的局部合成。雄性大鼠垂体的双重免疫荧光研究显示，VGLUT 2在LH（93.3 +/- 1.3%）-、FSH（44.7 +/- 3.9%）-和TSH（70.0 +/- 5.6%）-免疫反应性细胞中的百分比较高，在催乳素、GH和ACTH表型细胞中的发生率较低。定量原位杂交研究已经确定，单剂量的17-β-雌二醇（20 μ g/kg; sc）给卵巢切除大鼠注射后16 h，腺垂体中VGLUT 2 mRNA显著升高。通过比较甲状腺功能减退和甲状腺功能亢进动物模型与甲状腺功能正常对照动物模型的杂交信号，研究VGLUT 2表达的甲状腺激素依赖性。虽然甲状腺功能亢进对VGLUT 2 mRNA没有影响，但甲状腺功能减退会增加腺垂体VGLUT 2 mRNA水平。这与VGLUT 2免疫反应性TSH细胞的比例降低相一致，被认为是分泌增强的标志。在促性腺细胞和促甲状腺细胞中存在谷氨酸标记物VGLUT 2，以及其受雌激素或甲状腺功能减退的上调，解决了腺垂体内分泌细胞可能以雌激素和甲状腺状态调节的方式与肽激素共同分泌谷氨酸的可能性。主要在促性腺激素细胞和促甲状腺激素细胞中观察到的内源性谷氨酸的确切作用，包括其假定参与自分泌/旁分泌调节机制，将需要澄清。
Immunocytochemical studies of the rat adenohypophysis identified a cell population that exhibits immunoreactivity for type-2 vesicular glutamate transporter (VGLUT2), a marker for glutamatergic neuronal phenotype. The in situ hybridization detection of VGLUT2 mRNA expression in adenohypophysial cells verified that VGLUT2 immunoreactivity is due to local synthesis of authentic VGLUT2. Dual-immunofluorescent studies of the hypophyses from male rats showed the presence of VGLUT2 in high percentages of LH (93.3 +/- 1.3%)-, FSH (44.7 +/- 3.9%)-, and TSH (70.0 +/- 5.6%)- immunoreactive cells and its much lower incidence in cells of the prolactin, GH, and ACTH phenotypes. Quantitative in situ hybridization studies have established that the administration of a single dose of 17-beta-estradiol (20 mu g/kg; sc) to ovariectomized rats significantly elevated VGLUT2 mRNA in the adenohypophysis 16 h postinjection. Thyroid hormone dependence of VGLUT2 expression was addressed by the comparison of hybridization signals in animal models of hypo- and hyperthyroidism to those in euthyroid controls. Although hyperthyroidism had no effect on VGLUT2 mRNA, hypothyroidism increased adenohypophysial VGLUT2 mRNA levels. This coincided with a decreased ratio of VGLUT2-immunoreactive TSH cells, regarded as a sign of enhanced secretion. The presence of the glutamate marker VGLUT2 in gonadotrope and thyrotrope cells, and its up-regulation by estrogen or hypothyroidism, address the possibility that endocrine cells of the adenohypophysis may cosecrete glutamate with peptide hormones in an estrogen- and thyroid status-regulated manner. The exact roles of endogenous glutamate observed primarily in gonadotropes and thyrotropes, including its putative involvement in autocrine/paracrine regulatory mechanisms, will require clarification.