Park Sun H, Peters Megan, Aguayo Caleb, Farris Michael K, Hughes Ryan T, Moore Joseph, Munley Michael T, Reno Kaitlyn E, Gardin Jean, Cline J Mark, Peters Christopher M, Willey Jeffrey S
Wake Forest University School of Medicine.
Res Sq. 2024 Jul 1:rs.3.rs-4534694. doi: 10.21203/rs.3.rs-4534694/v1.
Stereotactic Body Radiation Therapy for lung tumors near the chest wall often causes significant chest wall pain (CWP), negatively impacting patients' quality of life. The mechanisms behind SBRT-induced CWP remain unclear and may involve multiple factors. We investigated the potential crosstalk between radiation-activated osteoclasts and sensory neurons, focusing on osteoclast-derived factors in CWP. Using the murine pre-osteoclast cell line Raw264.7, we induced differentiation with RANKL, followed by 10Gy gamma-irradiation. Conditioned media from these irradiated osteoclasts was used to treat sensory neuronal cultures from mouse dorsal root ganglia. Neuronal cultures were also directly exposed to 10Gy radiation, with and without osteoclast co-culture. Analysis of osteoclast markers and pain-associated neuropeptides was conducted using RT-qPCR and histochemical staining. Osteoclast differentiation and activity were inhibited using Osteoprotegerin and risedronate. Results showed that high-dose radiation significantly increased osteoclast size, resorption pit size, and activity biomarkers. Neurons treated with CM from irradiated osteoclasts showed increased expression of pain-associated neuropeptides CGRP and Substance P, which was mitigated by osteoprotegerin and risedronate. This study suggests that high-dose radiation enhances osteoclast activity, upregulating pain-associated neuropeptides in sensory neurons, and that inhibitors like osteoprotegerin and risedronate may offer therapeutic strategies for managing radiation-induced pain.
立体定向体部放射治疗用于治疗靠近胸壁的肺部肿瘤时,常常会引发显著的胸壁疼痛(CWP),对患者的生活质量产生负面影响。立体定向体部放射治疗(SBRT)诱发胸壁疼痛背后的机制尚不清楚,可能涉及多种因素。我们研究了辐射激活的破骨细胞与感觉神经元之间潜在的相互作用,重点关注破骨细胞衍生因子在胸壁疼痛中的作用。我们使用小鼠破骨细胞前体细胞系Raw264.7,用RANKL诱导其分化,然后进行10Gy的γ射线照射。将这些经照射的破骨细胞的条件培养基用于处理来自小鼠背根神经节的感觉神经元培养物。感觉神经元培养物也直接接受10Gy的辐射,有或没有破骨细胞共培养。使用RT-qPCR和组织化学染色对破骨细胞标志物和疼痛相关神经肽进行分析。使用骨保护素和利塞膦酸盐抑制破骨细胞的分化和活性。结果表明,高剂量辐射显著增加了破骨细胞大小、吸收陷窝大小和活性生物标志物。用经照射的破骨细胞的条件培养基处理的神经元显示出疼痛相关神经肽降钙素基因相关肽(CGRP)和P物质的表达增加,而骨保护素和利塞膦酸盐可减轻这种增加。这项研究表明,高剂量辐射增强了破骨细胞活性,上调了感觉神经元中与疼痛相关的神经肽,并且骨保护素和利塞膦酸盐等抑制剂可能为管理辐射诱导的疼痛提供治疗策略。