Li Dong, Li Kaihua, Chen Gang, Xia Jianlong, Yang Ting, Cai Ping, Yao Chen, Yang Yongjiang, Yan Shichang, Zhang Rihua, Chen Hui
Department of Orthopedics, Jiangsu Province Hospital of TCM, Affiliated Hospital of Nanjing University of TCM, Nanjing, Jiangsu 210029, P.R. China.
Department of Orthopedics, Benq Hospital, Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210019, P.R. China.
Mol Med Rep. 2016 Oct;14(4):3878-86. doi: 10.3892/mmr.2016.5697. Epub 2016 Sep 1.
S100 calcium-binding protein B (S100B) is expressed and released by adipocytes, and is positively correlated with body mass index, however, the direct effects of S100B on adipocytes remain unclear. Bone marrow‑derived mesenchymal stem cells have the capacity to differentiate into osteoblasts and adipocytes, which is important for bone metabolism. The current study aimed to determine the effect of S100B on adipogenesis and osteogenesis. The mouse embryo cell line C3H/10T1/2 was used to build cell models with varying levels of S100B protein expression. Western blot analysis was performed to assess the expression of various marker proteins. Oil red O staining and alizarin red S staining were used to detect adipogenesis and osteogenesis, respectively. S100B overexpression was associated with a significant increase in oil red O staining and a significant reduction in alizarin red S staining. Runt‑related transcription factor‑2 and bone morphogenetic protein 2 expression levels were significantly increased in the S100B underexpression group, however not in the S100B overexpression group. By contrast, the expression levels of the adipogenesis markers peroxisome proliferator‑activated receptor γ and CCAAT‑enhancer‑binding protein α was significantly increased in the S100B overexpression group, however not in the S100B underexpression group. Osteogenesis stimulation increased extracellular signal‑regulated kinase (ERK) phosphorylation, and adipogenesis stimulation increased c‑Jun N‑terminal kinase (JNK) phosphorylation. The results suggest that S100B inhibits osteogenesis, however stimulates adipogenesis. The ERK pathway is involved in the regulation of osteogenesis, whereas the JNK pathway is involved in the regulation of adipogenesis.
S100钙结合蛋白B(S100B)由脂肪细胞表达并释放,且与体重指数呈正相关,然而,S100B对脂肪细胞的直接作用仍不清楚。骨髓来源的间充质干细胞具有分化为成骨细胞和脂肪细胞的能力,这对骨代谢很重要。当前研究旨在确定S100B对脂肪生成和成骨的影响。使用小鼠胚胎细胞系C3H/10T1/2构建具有不同水平S100B蛋白表达的细胞模型。进行蛋白质免疫印迹分析以评估各种标记蛋白的表达。分别使用油红O染色和茜素红S染色来检测脂肪生成和成骨。S100B过表达与油红O染色显著增加和茜素红S染色显著减少相关。在S100B低表达组中,与 runt相关转录因子2和骨形态发生蛋白2的表达水平显著增加,然而在S100B过表达组中并非如此。相比之下,在S100B过表达组中,脂肪生成标记物过氧化物酶体增殖物激活受体γ和CCAAT增强子结合蛋白α的表达水平显著增加,然而在S100B低表达组中并非如此。成骨刺激增加细胞外信号调节激酶(ERK)磷酸化,脂肪生成刺激增加c-Jun氨基末端激酶(JNK)磷酸化。结果表明,S100B抑制成骨,但刺激脂肪生成。ERK通路参与成骨的调节,而JNK通路参与脂肪生成的调节。