Bone disturbances and progression of atherosclerosis in ApoE knockout mice

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 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.

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
大幅提高文件上传限制,最高150M (2024-4-1)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
2秒前
淙淙柔水完成签到,获得积分0
2秒前
fox199753206完成签到,获得积分10
3秒前
3秒前
爆米花应助fpbovo采纳,获得10
3秒前
4秒前
lemon完成签到,获得积分10
5秒前
酷酷发布了新的文献求助10
5秒前
6秒前
ding应助曾经厉采纳,获得10
6秒前
7秒前
碎碎念发布了新的文献求助30
7秒前
13134发布了新的文献求助10
8秒前
Akim应助我是張寜啊采纳,获得10
8秒前
丘比特应助顺心绮兰采纳,获得30
9秒前
木木完成签到,获得积分10
9秒前
Yuciyy完成签到,获得积分10
9秒前
脑洞疼应助HHTTY采纳,获得10
9秒前
Kabutack完成签到,获得积分10
10秒前
元谷雪应助横A采纳,获得10
10秒前
自知完成签到,获得积分10
10秒前
万能图书馆应助酷酷采纳,获得10
13秒前
自知发布了新的文献求助10
14秒前
15秒前
15秒前
16秒前
vic完成签到,获得积分10
17秒前
木白四发布了新的文献求助10
18秒前
zhangnan发布了新的文献求助10
18秒前
小樱没有魔法阵应助李伟采纳,获得10
19秒前
19秒前
丘比特应助mumu采纳,获得20
21秒前
HHTTY发布了新的文献求助10
21秒前
HEROTREE完成签到 ,获得积分10
23秒前
cleva完成签到,获得积分10
24秒前
Daisy完成签到,获得积分10
26秒前
科研通AI2S应助飞兰采纳,获得10
26秒前
开朗万恶发布了新的文献求助10
26秒前
zhao完成签到 ,获得积分10
27秒前
Leviathan完成签到 ,获得积分10
27秒前
高分求助中
The Oxford Handbook of Social Cognition (Second Edition, 2024) 1050
Kinetics of the Esterification Between 2-[(4-hydroxybutoxy)carbonyl] Benzoic Acid with 1,4-Butanediol: Tetrabutyl Orthotitanate as Catalyst 1000
The Young builders of New china : the visit of the delegation of the WFDY to the Chinese People's Republic 1000
юрские динозавры восточного забайкалья 800
English Wealden Fossils 700
Handbook of Qualitative Cross-Cultural Research Methods 600
Chen Hansheng: China’s Last Romantic Revolutionary 500
热门求助领域 (近24小时)
化学 医学 生物 材料科学 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 基因 遗传学 催化作用 物理化学 免疫学 量子力学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 3139963
求助须知:如何正确求助?哪些是违规求助? 2790878
关于积分的说明 7796853
捐赠科研通 2447242
什么是DOI,文献DOI怎么找? 1301754
科研通“疑难数据库(出版商)”最低求助积分说明 626336
版权声明 601194