牙周炎
川地31
免疫组织化学
病态的
血管生成
髓过氧化物酶
病理
医学
渗透(HVAC)
下调和上调
接收机工作特性
炎症
免疫学
内科学
生物
物理
热力学
生物化学
基因
作者
Wenxin Jiang,Weijun Yu,Shucheng Hu,Yuan-jie Shi,Lu Lin,Ruhan Yang,Jiaqi Tang,Yuting Gu,Yuhua Gong,Min Jin,Eryi Lu
摘要
Abstract Aims This study aimed to elucidate the alterations in Follistatin‐like protein 1 (FSTL1) and its association with the pathological process of periodontitis. Methods This study included 48 patients with periodontitis and 42 healthy controls. The expression level of FSTL1 in the gingiva was determined by RT‐qPCR, validated using the dataset GSE16134, and subsequently examined by western blotting. Bioinformatics analysis revealed a single‐cell distribution of FSTL1, characteristic of angiogenesis and immune cell infiltration. The expression and distribution of FSTL1, vascular endothelial marker protein CD31 and myeloperoxidase (MPO), the indicator of neutrophil activity, were determined by immunohistochemistry (IHC). A series of correlation analyses was performed to determine the associations between FSTL1 and clinical parameters, including probing depth (PD) and clinical attachment loss (CAL), and their potential role in angiogenesis (CD31) and neutrophil infiltration (MPO). Results FSTL1 was significantly upregulated in the gingiva of patients with periodontitis compared to their healthy counterparts. In addition, FSTL1 was positively correlated with the clinical parameters PD ( r = .5971, p = .0005) and CAL ( r = .6078, p = .0004). Bioinformatic analysis and IHC indicated that high FSTL1 expression was significantly correlated with angiogenesis and neutrophil infiltration in periodontitis. Moreover, receiver operating characteristic (ROC) analysis demonstrated that FSTL1 could serve as an independent indicator for evaluating the severity of periodontitis (area under the curve [AUC] = 0.9011, p < .0001). Conclusion This study demonstrated FSTL1 upregulation in periodontitis and its potential contribution to the disease via angiogenesis and neutrophil infiltration.
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