期刊文献+

交感神经系统-肾上腺素能受体对骨改建的调节作用 被引量:5

Regulatory role of sympathetic nervous system–adrenergic receptor on bone remodeling
下载PDF
导出
摘要 骨组织终生处于改建中,交感神经系统(SNS)对骨组织和骨细胞的神经支配是其调控骨代谢的组织学基础。肾上腺素能受体与其对应的配体结合后,激活多条信号转导通路,完成其对成骨细胞和破骨细胞的调控,调节骨代谢。对于成骨细胞,SNS既可以通过激活α1受体促进骨形成,也可以通过激活β2受体抑制骨形成;对于破骨细胞,SNS既可直接作用于破骨前体细胞,促进其分化成熟,还可以通过调节成骨细胞分泌促破骨因子核因子-κB受体活化因子配体,间接促进破骨细胞活性。在骨生理病理改建方面,SNS通过调控破骨活动参与牙槽骨在力学刺激下的骨改建。SNS与骨质疏松症的发生发展密切相关,阻断SNS信号对预防骨质疏松等以病理性骨量丢失为特征的疾病具有重要的临床意义。 The sympathetic nervous system(SNS) of reconstructed bone tissues and bone cell innervation is the basis in regulating bone metabolism in histological studies. The binding of adrenergic receptor and its corresponding ligands can activate multiple signal transduction pathways, complete the regulation of osteoblast and osteoclast cells, and regulate bone metabolism. For osteoblasts, SNS can be activated by ct1 receptors to promote bone formation but can also be activated by 132 receptor to inhibit bone formation. For osteoclasts, SNS can directly affect osteoclast precursor cells and promote their differentiation. SNS can also be adjusted with a pro-osteoclastic factor nuclear factor kappa B receptor to activate secretion of bone cells, and thus, indirectly promote the activity of osteoclasts. In the physiology and pathology of bone remodeling, SNS regulates osteoclast activity in the alveolar bones under mechanical stimulation. In addition to the occurrence and development of SNS and osteoporosis, blocking SNS signals to prevent osteoporosis with pathological bone loss has important clinical implications to characterize the disease.
出处 《国际口腔医学杂志》 CAS 北大核心 2015年第3期348-351,共4页 International Journal of Stomatology
基金 国家自然科学基金(81300898) 军队青年培育项目(13-QNP138)
关键词 交感神经系统 肾上腺素能受体 成骨细胞 破骨细胞 生物力 sympathetic nervous system adrenergic receptor osteoblast osteoclast mechanical loading
  • 相关文献

参考文献19

  • 1Serre CM, Farlay D, Delmas PD, et al. Evidence for a dense and intimate innervation of the bone tissue, including glutamate-containing fibers[J]. Bone, 1999, 25(6):623-629.
  • 2Duncan CP, Shim SS. J. Edouard Samson Address: the autonomic nerve supply of bone. An experi- mental study of the intraosseous adrenergic nervi vasorum in the rabbit[J]. J Bone Joint Surg Br, 1977, 59(3):323-330.
  • 3Bonnet N, Pierroz DD, Ferrari SL. Adrenergic control of bone remodeling and its implications for the treatment of osteoporosis[J]. J Musculoskelet Neuronal Interact, 2008, 8(2):94-104.
  • 4Cottingham C, Chen Y, Jiao K, et al. The antide- pressant desipramine is an arrestin-biased ligand at the α(2A)-adrenergic receptor driving receptor down-regulation in vitro and in vivo[J]. J Biol Chem, 2011,286(41):36063-36075.
  • 5Cottingham C, Jones A, Wang Q. Desipramine selectively potentiates norepinephfine-elicited ERK1/2 activation through the α2A adrenergic receptor[J]. Bioehem Biophys Res Commun, 2012, 420(1):161- 165.
  • 6Wang Q, Lu R, Zhao J, et al. Arrestin serves as a molecular switch, linking endogenous alpha2-adre- nergic receptor to SRC-dependent, but not SRC- independent, ERK activation[J]. J Biol Chem, 2006, 281(36):25948-25955.
  • 7Elefteriou F, Campbell P, Ma Y. Control of bone remodeling by the peripheral sympathetic nervous system[J]. Calcif Tissue Int, 2014, 94(1): 140- 151.
  • 8Huang HH, Brennan TC, Muir MM, et al. Functional alphal, and beta2-adrenergic receptors in human osteoblasts[J]. J Cell Physiol, 2009, 220(1):267-275.
  • 9Suzuki A, Palmer G, Bonjour JP, et al. Catechola- mines stimulate the proliferation and alkaline phosphatase activity of MC3T3-E1 osteoblast-like cells[J]. Bone, 1998, 23(3): 197-203.
  • 10Suzuki A, Palmer G, Bonjour JP, et al. Regulation of alkaline phosphatase activity by p38 MAP kinase in response to activation of Gi protein-coupled receptors by epinephrine in osteoblast-like cells[J]. Endocri- nology, 1999, 140(7):3177-3182.

同被引文献57

引证文献5

二级引证文献16

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部