Department of Stomatology, Affiliated Hospital of Qingdao University, College of Stomatology, Qingdao University, 16 Jiangsu Road, Qingdao, 266003, Shandong, China.
Department of Burn and Plastic Surgery, Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Arch Oral Biol. 2019 Feb;98:92-98. doi: 10.1016/j.archoralbio.2018.11.007. Epub 2018 Nov 14.
To examine the effects of gingival mesenchymal stem cells (GMSCs) on inflammatory macrophages upon oxidized low-density lipoprotein (ox-LDL) stimulation and evaluate therapeutic potential of GMSCs on mouse model of periodontitis associated with hyperlipidemia.
in vitro, GMSCs were co-cultured with macrophages for 48 h in the absence or presence of M1 polarizing conditions and oxidized low-density lipoprotein in the transwell system. The supernatants were collected for ELISA. M1 and M2 markers of macrophages were analyzed by flow cytometry and PCR, and lipid accumulation was assessed by oil red O staining. in vivo, eighteen mice were divided into three groups (n = 6): Group A (periodontally healthy mice as control), Group B (periodontitis mice with hyperlipidemia), Group C (periodontitis mice with hyperlipidemia with the transplantation of GMSCs). The serum levels of cholesterol and inflammatory factors were measured by automatic analyzer. Bone regeneration was evaluated by Masson staining.
When co-cultured with GMSCs, the M1 markers of Tumor Necrosis Factor (TNF) -α, Interleukin (IL) -6, Interleukin (IL) -1β, CD86, and Human Leukocyte Antigen (HLA) -DR were significantly reduced. In contrast, M2 markers such as Interleukin(IL) -10 and CD206 were moderately increased. Similar results were obtained in the cell culture supernatants. In animal experiment, GMSCs suppressed the expression of sterol regulatory element binding transcription factor 1c (SREBP-1c) and elevated the levels of peroxisome proliferator-activated receptor alpha (PPARα) and peroxisome proliferator activator receptor- coactivator 1(PGC-1α) in the liver, attenuated cholesterol dysfunction via the downregulation of low-density lipoprotein (LDL) and total cholesterol (TC), and the upregulation of high-density lipoprotein (HDL), and decreased the levels of TNF-α and IL-6. Moreover, GMSC treatment improved bone regeneration.
GMSCs inhibit the activation of M1 macrophages, regulate lipid metabolism and reduce inflammatory response, and promote bone regeneration in mouse model of periodontitis associated with hyperlipidemia.
探讨氧化型低密度脂蛋白(ox-LDL)刺激牙龈间充质干细胞(GMSCs)对炎性巨噬细胞的影响,并评估 GMSCs 对高脂血症相关牙周炎小鼠模型的治疗潜力。
体外,将 GMSCs 与巨噬细胞在无或存在 M1 极化条件和转染小室系统中的氧化型低密度脂蛋白的情况下共培养 48 小时。收集上清液进行 ELISA 分析。通过流式细胞术和 PCR 分析巨噬细胞的 M1 和 M2 标志物,并用油红 O 染色评估脂质蓄积。体内,将 18 只小鼠分为三组(n=6):A 组(牙周健康小鼠作为对照)、B 组(高脂血症性牙周炎小鼠)、C 组(高脂血症性牙周炎伴 GMSCs 移植小鼠)。自动分析仪测量血清胆固醇和炎症因子水平。Masson 染色评估骨再生。
与 GMSCs 共培养时,肿瘤坏死因子(TNF)-α、白细胞介素(IL)-6、白细胞介素(IL)-1β、CD86 和人类白细胞抗原(HLA)-DR 的 M1 标志物明显降低。相反,IL-10 和 CD206 等 M2 标志物中度增加。细胞培养上清液也得到了类似的结果。在动物实验中,GMSCs 抑制固醇调节元件结合转录因子 1c(SREBP-1c)的表达,升高过氧化物酶体增殖物激活受体α(PPARα)和过氧化物酶体增殖物激活受体共激活因子 1(PGC-1α)的水平,通过下调低密度脂蛋白(LDL)和总胆固醇(TC),上调高密度脂蛋白(HDL),降低 TNF-α 和 IL-6 水平,减轻胆固醇功能障碍。此外,GMSC 治疗改善了骨再生。
GMSCs 抑制 M1 巨噬细胞的激活,调节脂代谢,减轻炎症反应,促进高脂血症相关牙周炎小鼠模型的骨再生。