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背根神经节植入电刺激通过降钙素基因相关肽加速骨质疏松性骨折愈合。

Implantable Electrical Stimulation at Dorsal Root Ganglions Accelerates Osteoporotic Fracture Healing via Calcitonin Gene-Related Peptide.

机构信息

Musculoskeletal Research Laboratory, Department of Orthopedics & Traumatology, Innovative Orthopaedic Biomaterial and Drug Translational Research Laboratory, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, Hong Kong, 999077, China.

Shanghai Key Laboratory of Orthopaedic Implants, Department of Orthopaedics, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 639 Zhizaoju Road, Shanghai, 200011, People's Republic of China.

出版信息

Adv Sci (Weinh). 2022 Jan;9(1):e2103005. doi: 10.1002/advs.202103005. Epub 2021 Oct 28.

DOI:10.1002/advs.202103005
PMID:34708571
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8728818/
Abstract

The neuronal engagement of the peripheral nerve system plays a crucial role in regulating fracture healing, but how to modulate the neuronal activity to enhance fracture healing remains unexploited. Here it is shown that electrical stimulation (ES) directly promotes the biosynthesis and release of calcitonin gene-related peptide (CGRP) by activating Ca /CaMKII/CREB signaling pathway and action potential, respectively. To accelerate rat femoral osteoporotic fracture healing which presents with decline of CGRP, soft electrodes are engineered and they are implanted at L3 and L4 dorsal root ganglions (DRGs). ES delivered at DRGs for the first two weeks after fracture increases CGRP expression in both DRGs and fracture callus. It is also identified that CGRP is indispensable for type-H vessel formation, a biological event coupling angiogenesis and osteogenesis, contributing to ES-enhanced osteoporotic fracture healing. This proof-of-concept study shows for the first time that ES at lumbar DRGs can effectively promote femoral fracture healing, offering an innovative strategy using bioelectronic device to enhance bone regeneration.

摘要

外周神经系统的神经元参与在调节骨折愈合中起着至关重要的作用，但如何调节神经元活动以增强骨折愈合仍未被开发。在这里，研究表明电刺激（ES）通过分别激活钙/钙调蛋白激酶 II/CREB 信号通路和动作电位，直接促进降钙素基因相关肽（CGRP）的生物合成和释放。为了加速表现出 CGRP 下降的大鼠股骨骨质疏松性骨折愈合，设计了软电极，并将其植入 L3 和 L4 背根神经节（DRG）。骨折后前两周在 DRG 处施加 ES 可增加 DRG 和骨折骨痂中 CGRP 的表达。还确定 CGRP 对于 H 型血管形成是必不可少的，H 型血管形成是一种将血管生成和成骨偶联的生物学事件，有助于 ES 增强骨质疏松性骨折愈合。这项概念验证研究首次表明，腰椎 DRG 处的 ES 可有效促进股骨骨折愈合，为使用生物电子设备增强骨再生提供了一种创新策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4d5/8728818/12d66242a706/ADVS-9-2103005-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4d5/8728818/8565d85a290f/ADVS-9-2103005-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4d5/8728818/be95f9b2b989/ADVS-9-2103005-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4d5/8728818/03cf23161bcb/ADVS-9-2103005-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4d5/8728818/2ce0939a180c/ADVS-9-2103005-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4d5/8728818/66071905f9c4/ADVS-9-2103005-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4d5/8728818/12d66242a706/ADVS-9-2103005-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4d5/8728818/8565d85a290f/ADVS-9-2103005-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4d5/8728818/be95f9b2b989/ADVS-9-2103005-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4d5/8728818/03cf23161bcb/ADVS-9-2103005-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4d5/8728818/2ce0939a180c/ADVS-9-2103005-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4d5/8728818/66071905f9c4/ADVS-9-2103005-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4d5/8728818/12d66242a706/ADVS-9-2103005-g007.jpg

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