St John Hillary C, Meyer Mark B, Benkusky Nancy A, Carlson Alex H, Prideaux Mathew, Bonewald Lynda F, Pike J Wesley
Department of Biochemistry, University of Wisconsin-Madison, Madison, WI 53706, USA.
Department of Oral Biology, School of Dentistry, University of Missouri, Kansas City, MO 64110, USA.
Bone. 2015 Mar;72:81-91. doi: 10.1016/j.bone.2014.11.010. Epub 2014 Nov 22.
Although localized to the mineralized matrix of bone, osteocytes are able to respond to systemic factors such as the calciotropic hormones 1,25(OH)2D3 and PTH. In the present studies, we examined the transcriptomic response to PTH in an osteocyte cell model and found that this hormone regulated an extensive panel of genes. Surprisingly, PTH uniquely modulated two cohorts of genes, one that was expressed and associated with the osteoblast to osteocyte transition and the other a cohort that was expressed only in the mature osteocyte. Interestingly, PTH's effects were largely to oppose the expression of differentiation-related genes in the former cohort, while potentiating the expression of osteocyte-specific genes in the latter cohort. A comparison of the transcriptional effects of PTH with those obtained previously with 1,25(OH)2D3 revealed a subset of genes that was strongly overlapping. While 1,25(OH)2D3 potentiated the expression of osteocyte-specific genes similar to that seen with PTH, the overlap between the two hormones was more limited. Additional experiments identified the PKA-activated phospho-CREB (pCREB) cistrome, revealing that while many of the differentiation-related PTH regulated genes were apparent targets of a PKA-mediated signaling pathway, a reduction in pCREB binding at sites associated with osteocyte-specific PTH targets appeared to involve alternative PTH activation pathways. That pCREB binding activities positioned near important hormone-regulated gene cohorts were localized to control regions of genes was reinforced by the presence of epigenetic enhancer signatures exemplified by unique modifications at histones H3 and H4. These studies suggest that both PTH and 1,25(OH)2D3 may play important and perhaps cooperative roles in limiting osteocyte differentiation from its precursors while simultaneously exerting distinct roles in regulating mature osteocyte function. Our results provide new insight into transcription factor-associated mechanisms through which PTH and 1,25(OH)2D3 regulate a plethora of genes important to the osteoblast/osteocyte lineage.
尽管骨细胞局限于骨的矿化基质中,但它们能够对全身因素作出反应,如钙调节激素1,25(OH)₂D₃和甲状旁腺激素(PTH)。在本研究中,我们在骨细胞模型中检测了对PTH的转录组反应,发现该激素调节了大量基因。令人惊讶的是,PTH独特地调节了两组基因,一组是在成骨细胞向骨细胞转变过程中表达并与之相关的基因,另一组是仅在成熟骨细胞中表达的基因。有趣的是,PTH的作用主要是抑制前一组中与分化相关基因的表达,同时增强后一组中骨细胞特异性基因的表达。将PTH的转录作用与先前用1,25(OH)₂D₃获得的转录作用进行比较,发现有一部分基因存在强烈重叠。虽然1,25(OH)₂D₃增强骨细胞特异性基因表达的方式与PTH相似,但两种激素之间的重叠更为有限。进一步的实验确定了蛋白激酶A(PKA)激活的磷酸化环磷腺苷反应元件结合蛋白(pCREB)的顺反组,结果表明,虽然许多与分化相关的PTH调节基因显然是PKA介导信号通路的靶点,但与骨细胞特异性PTH靶点相关位点处pCREB结合的减少似乎涉及其他PTH激活途径。组蛋白H3和H4独特修饰所体现的表观遗传增强子特征表明,位于重要激素调节基因组附近的pCREB结合活性定位于基因的调控区域。这些研究表明,PTH和1,25(OH)₂D₃在限制骨细胞从其前体分化的过程中可能都发挥着重要且可能是协同的作用,同时在调节成熟骨细胞功能方面发挥着不同的作用。我们的研究结果为PTH和1,25(OH)₂D₃调节成骨细胞/骨细胞谱系中众多重要基因的转录因子相关机制提供了新的见解。