白细胞介素-1β抑制颞下颌关节中的转化生长因子β。
IL-1beta inhibits TGFbeta in the temporomandibular joint.
作者信息
Lim W H, Toothman J, Miller J H, Tallents R H, Brouxhon S M, Olschowka M E, Kyrkanides S
机构信息
Department of Orthodontics, School of Dentistry, Dental Research Institute, Seoul National University, Seoul, Korea.
出版信息
J Dent Res. 2009 Jun;88(6):557-62. doi: 10.1177/0022034509336823.
Similarly to humans, healthy, wild-type mice develop osteoarthritis, including of the temporomandibular joint (TMJ), as a result of aging. Pro-inflammatory cytokines, such as IL-1beta, IL-6, and TNFalpha, are known to contribute to the development of osteoarthritis, whereas TGFbeta has been associated with articular regeneration. We hypothesized that a balance between IL-1beta and TGFbeta underlies the development of TMJ osteoarthritis, whereby IL-1beta signaling down-regulates TGFbeta expression as part of disease pathology. Our studies in wild-type mice, as well as the Col1-IL1beta(XAT) mouse model of osteoarthritis, demonstrated an inverse correlation between IL-1beta and TGFbeta expression in the TMJ. IL-1beta etiologically correlated with joint pathology, whereas TGFbeta expression associated with IL-1beta down-regulation and improvement of articular pathology. Better understanding of the underlying inflammatory processes during disease will potentially enable us to harness inflammation for orofacial tissue regeneration.
与人类相似，健康的野生型小鼠会随着年龄增长而患上骨关节炎，包括颞下颌关节（TMJ）骨关节炎。已知促炎细胞因子，如白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNFα），会促进骨关节炎的发展，而转化生长因子-β（TGFβ）则与关节再生有关。我们假设IL-1β和TGFβ之间的平衡是TMJ骨关节炎发展的基础，其中IL-1β信号传导会下调TGFβ表达，作为疾病病理的一部分。我们对野生型小鼠以及骨关节炎的Col1-IL1β(XAT)小鼠模型的研究表明，TMJ中IL-1β和TGFβ表达呈负相关。IL-1β与关节病理在病因上相关，而TGFβ表达与IL-1β下调和关节病理改善相关。更好地了解疾病期间潜在的炎症过程可能会使我们能够利用炎症促进口腔面部组织再生。
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