载脂蛋白E
医学
骨重建
内科学
骨吸收
炎症
内分泌学
骨质疏松症
骨保护素
促炎细胞因子
兰克尔
病理
受体
激活剂(遗传学)
疾病
作者
Diana Carmona-Fernandes,Renata I. Casimiro,Augusto Silva,Antti Koskela,Mikko Finnilä,María José Santos,Helena Canhão,João Eurico Fonseca
出处
期刊:Clinical and Experimental Rheumatology
日期:2022-07-01
被引量:1
标识
DOI:10.55563/clinexprheumatol/ydmqjl
摘要
Epidemiological evidence supports a link between atherosclerosis and osteoporosis. These conditions might share common pathophysiological mechanisms, with inflammation being one of the hypotheses.Apolipoprotein E deficient mice (ApoE-/-) develop atherosclerotic lesions spontaneously, further aggravated by a high-fat diet. Their bone remodelling is also disturbed. We hypothesised that a proinflammatory state could be a common contributive factor for vessel and bone disturbances observed in this animal model.We evaluated vessels and bones of ApoE-/- and control C57BL/6 (B6) female mice fed a high-fat diet in five time-points (8, 16, 20, 24 and 28 weeks of age) and quantified the development of atherosclerotic lesions, analysed gene expression of inflammatory and bone remodelling proteins (IL-1β, IL-6, IL-17A, TNF, RANKL, and OPG), measured serum bone turnover markers (P1NP and CTX-I), performed bone (L3-L4 vertebras) histomorphometric analysis and evaluated biomechanical properties of bones.We compared the outcomes of B6 and ApoE-/- groups at each time-point and, within each group, over time. Atherosclerotic lesions developed as previously described for ApoE-/- mice, but no significant differences were found in bone histomorphometry or biomechanical properties between ApoE-/- and B6 mice. Also, gene expression (either in bones or aortas) and serum biomarkers were similar in both groups. When considering over time evaluations we found that bone histomorphometry changes were similar between ApoE-/- and B6 mice, but CTX-I/P1NP ratio was significantly increased (meaning higher resorption than bone formation) in ApoE-/- as compared to B6 mice.Our study suggests that inflammation is not the principal driver for atherosclerosis progression and bone disturbances in this animal model.
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