Dorsomedial Ventromedial Hypothalamic Nucleus Growth Hormone-Releasing Hormone Neuron Steroidogenic Factor-1 Gene Targets in Female Rat.

IF 3.9 4区 医学 Q2 NEUROSCIENCES ASN NEURO Pub Date : 2024-01-01 Epub Date: 2024-10-14 DOI:10.1080/17590914.2024.2403345
Subash Sapkota, Sagor C Roy, Karen P Briski
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引用次数: 0

Abstract

The prospect that the ventromedial hypothalamic nucleus (VMN) transcription factor steroidogenic factor-1/NR5A1 (SF-1) may exert sex-dimorphic control of glucose counterregulation is unresolved. Recent studies in male rats show that SF-1 regulates transcription of co-expressed hypoglycemia-sensitive neurochemicals in dorsomedial VMN growth hormone-releasing hormone (Ghrh) neurons. Gene knockdown and laser-catapult-microdissection/single-cell multiplex qPCR techniques were used here in a female rat model to determine if SF-1 control of Ghrh neuron transmitter marker, energy sensor, and estrogen receptor (ER) variant mRNAs varies according to sex. Data show that in females, hypoglycemia elicits a gain of SF-1 inhibitory control of VMNdm Ghrh neuron Ghrh and Ghrh-receptor gene profiles and loss of augmentation of glutaminase transcription; SF-1 gene silencing diminished eu- and hypoglycemic patterns of neuronal nitric oxide gene transcription. SF-1 imposes divergent control of baseline and hypoglycemic glutamate decarboxylase65 (GAD)-1 (stimulatory) versus GAD2 (inhibitory) mRNAs in that sex. SF-1 stimulates baseline VMNdm Ghrh neuron PRKAA1/AMPKα1 and PRKAA2/AMPKα2 gene expression, yet causes opposite changes in these gene profiles during hypoglycemia. SF-1 exerts glucose-dependent control of ER-alpha and G-protein-coupled ER-1 transcription, but blunts ER-beta gene profiles during eu- and hypoglycemia. In females, SF-1 knockdown did not affect hypercorticosteronemia or hyperglucagonemia, but blunted hypoglycemic suppression of growth hormone secretion. Results show that SF-1 expression is critical for female rat VMNdm Ghrh neuron counterregulatory neurochemical, AMPK catalytic subunit, and ER gene transcription responses to hypoglycemia. Sex differences in direction of SF-1 control of distinctive gene profiles may result in observed disparities in SF-1 regulation of counterregulatory hormone secretion between sexes.

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雌性大鼠下丘脑背内侧核生长激素释放激素神经元类固醇生成因子-1的基因靶点
腹内侧下丘脑核(VMN)转录因子类固醇生成因子-1/NR5A1(SF-1)可能对葡萄糖反调节具有性别二态性控制,这一前景尚未得到解决。最近在雄性大鼠身上进行的研究表明,SF-1 可调节背内侧 VMN 生长激素释放激素(Ghrh)神经元中共同表达的对低血糖敏感的神经化学物质的转录。本文在雌性大鼠模型中使用了基因敲除和激光弹弓微切片/单细胞多重 qPCR 技术,以确定 SF-1 对 Ghrh 神经元递质标记、能量传感器和雌激素受体(ER)变体 mRNA 的控制是否因性别而异。数据显示,在雌性大鼠中,低血糖会增强 SF-1 对 VMNdm Ghrh 神经元 Ghrh 和 Ghrh 受体基因图谱的抑制性控制,并丧失对谷氨酰胺酶转录的增强作用;SF-1 基因沉默会减少神经元一氧化氮基因转录的 eu- 和低血糖模式。SF-1对基线和低血糖谷氨酸脱羧酶65(GAD)-1(刺激性)与GAD2(抑制性)mRNA的控制存在差异。SF-1 可刺激基线 VMNdm Ghrh 神经元 PRKAA1/AMPKα1 和 PRKAA2/AMPKα2 基因的表达,但在低血糖时会导致这些基因发生相反的变化。SF-1对ER-α和G蛋白偶联的ER-1转录进行葡萄糖依赖性控制,但在优血症和低血糖时会减弱ER-β基因的表达。在女性中,SF-1基因敲除不会影响高皮质酮血症或高胰高血糖素血症,但会减弱低血糖对生长激素分泌的抑制。结果表明,SF-1的表达对雌性大鼠VMNdm Ghrh神经元反调节神经化学物质、AMPK催化亚基和ER基因转录对低血糖的反应至关重要。SF-1对不同基因的控制方向存在性别差异,这可能导致观察到的SF-1对不同性别间反调节激素分泌的调控存在差异。
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来源期刊
ASN NEURO
ASN NEURO NEUROSCIENCES-
CiteScore
7.70
自引率
4.30%
发文量
35
审稿时长
>12 weeks
期刊介绍: ASN NEURO is an open access, peer-reviewed journal uniquely positioned to provide investigators with the most recent advances across the breadth of the cellular and molecular neurosciences. The official journal of the American Society for Neurochemistry, ASN NEURO is dedicated to the promotion, support, and facilitation of communication among cellular and molecular neuroscientists of all specializations.
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