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PTH (1-34),PTHrP (1-36) 和阿巴洛帕拉提德对小鼠骨质细胞转录基因的差异影响

Michael J Mosca^1,2, Zhiming He¹, Florante R Ricarte¹

¹Department of Molecular Pathobiology, New York University College of Dentistry, New York, NY 10010, USA.

Journal of the Endocrine Society

|December 29, 2023

概括

特里巴拉提德,PTHrP和阿巴洛巴拉提德差异调节骨质细胞基因表达,影响骨质疏松症的治疗. 像Vdr和Wnt4这样的关键基因是由盐诱导性激酶和CRTCs调节的.

科学领域:

分子生物学分子生物学
基因组学就是基因组学.
药理学药理学是指药理学的学科.

背景情况:

用Teriparatide (PTH (1-34)),PTHrP (1-36) 和 abaloparatide (ABL) 治疗骨质疏松症的长期疗效有限.
这些在骨质母细胞中表现出不同的时间和剂量依赖的反应.
这表明它们对骨质细胞转录基因组的调制存在潜在的差异.

研究的目的:

为了比较PTH (1-34),PTHrP (1-36) 和ABL在骨质细胞转录组上的全球影响.
为了确定由这些骨质疏松症治疗诱导的共享和独特的基因表达模式.
研究盐诱导酶 (SIK) 和CREB调控的转录协活性剂 (CRTC) 在调解PTH效应中的作用 (1-34).

主要方法:

用1nM的PTH (1-34),PTHrP (1-36),或ABL4小时治疗小鼠骨质母细胞.
RNA测序以分析全球基因表达变化.
基因本体学分析以确定丰富的生物过程和分子功能.
小干扰RNA (siRNA) 的SIK1/2/3和CRTC1/2/3的淘汰,然后进行基因表达分析.

主要成果:

PTH (1-34) 调节了367个基因 (194个独特),PTHrP (1-36) 调节了117个基因 (15个独特),ABL调节了179个基因 (20个独特).
83个基因被这三种共同调节.
基因本体学揭示了Wnt信号传递,cAMP介导信号传递和骨化中的相似之处,但在形态发生和受体-连接体活性方面存在差异.
Vdr,Cited1和Pde10a的mRNA水平以PTH (1-34) > ABL > PTHrP (1-36) 的顺序增加.
SIK和CRTC的淘汰表明它们参与了PTH对Vdr和Wnt4的监管 (1-34).

结论:

PTH (1-34),PTHrP (1-36) 和ABL对骨质细胞转录组产生不同的影响.
共同的途径包括Wnt信号和骨化,而独特的途径突出显示不同的作用机制.
SIK和CRTC在调解Vdr和Wnt4对PTH的转录反应方面发挥着作用 (1-34).
这项研究为这些骨质疏松症疗法的差异效应背后的分子机制提供了新的见解.

关键词:

在RNA-Seqq.这就是阿巴洛帕拉提德.骨质母细胞的骨质母细胞.骨质疏松症是一种骨质疏松症.副甲状腺激素 (PTH) 是一种信号传导的信号传导.

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