Comparison of Necroptosis With Apoptosis for OVX-Induced Osteoporosis

坏死性下垂 骨细胞 细胞凋亡 程序性细胞死亡 骨质疏松症 内科学 化学 内分泌学 骨吸收 医学 细胞生物学 癌症研究 生物 成骨细胞 生物化学 体外
作者
Bin He,Yongjun Zhu,Hongwang Cui,Bo Sun,Tian Su,Peng Wen
出处
期刊:Frontiers in Molecular Biosciences [Frontiers Media SA]
卷期号:8 被引量:3
标识
DOI:10.3389/fmolb.2021.790613
摘要

As one common kind of osteoporosis, postmenopausal osteoporosis (PMOP) is associated with the death and excessive loss of osteocytes. Estrogen deficiency of PMOP can cause osteocyte death by regulating necroptosis and apoptosis, but their roles in POMP have not been compared. In the present study, ovariectomy (OVX)-induced rat and murine long bone osteocyte Y4 (MLO-Y4) cells were used to compare the influence of necroptosis and apoptosis on osteocyte death and bone loss. Benzyloxycarbonyl-Val-Ala-Asp (zVAD) and necrostatin-1 (Nec-1) were used to specifically block cell apoptosis and necroptosis, respectively. OVX rats and MLO-Y4 cells were divided into zVAD group, Nec-1 group, zVAD + Nec-1 group, vehicle, and control group. The tibial plateaus of the rat model were harvested at 8 weeks after OVX and were analyzed by micro–computed tomography, transmission electron microscopy (TEM), the transferase dUTP nick end labeling assay, and western blot. The death of MLO-Y4 was stimulated by TNF-α and was measured by flow cytometry and TEM. The results found that necroptosis and apoptosis were both responsible for the death and excessive loss of osteocytes, as well as bone loss in OVX-induced osteoporosis, and furthermore necroptosis may generate greater impact on the death of osteocytes than apoptosis. Necroptotic death of osteocytes was mainly regulated by the receptor-interacting protein kinase 3 signaling pathway. Collectively, inhibition of necroptosis may produce better efficacy in reducing osteocyte loss than that of apoptosis, and combined blockade of necroptosis and apoptosis provide new insights into preventing and treating PMOP.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI

祝大家在新的一年里科研腾飞
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
~。~完成签到,获得积分20
1秒前
1秒前
领导范儿应助合适的楷瑞采纳,获得10
1秒前
六月初八夜完成签到,获得积分10
2秒前
2秒前
3秒前
legaldie完成签到,获得积分10
3秒前
黄嵩发布了新的文献求助10
5秒前
豆的的的的豆完成签到,获得积分20
7秒前
黎某发布了新的文献求助10
7秒前
调研昵称发布了新的文献求助10
7秒前
曾经曼梅关注了科研通微信公众号
9秒前
sugar完成签到,获得积分10
10秒前
李健应助淡然的宛秋采纳,获得10
10秒前
11秒前
12秒前
12秒前
Zero完成签到,获得积分10
14秒前
14秒前
上官若男应助尖头叉子采纳,获得10
16秒前
17秒前
18秒前
18秒前
夕瑶完成签到,获得积分10
19秒前
20秒前
奋斗完成签到,获得积分10
20秒前
CodeCraft应助舒适的秋尽采纳,获得30
21秒前
21秒前
六等于三二一完成签到 ,获得积分10
21秒前
Shadow发布了新的文献求助10
22秒前
大虎关注了科研通微信公众号
23秒前
24秒前
灿烂千阳发布了新的文献求助10
24秒前
甜甜若血发布了新的文献求助10
24秒前
25秒前
hhh发布了新的文献求助10
25秒前
25秒前
芋泥小天才完成签到 ,获得积分10
25秒前
JamesPei应助Rabbit采纳,获得10
28秒前
28秒前
高分求助中
Востребованный временем 2500
The Three Stars Each: The Astrolabes and Related Texts 1500
Classics in Total Synthesis IV: New Targets, Strategies, Methods 1000
Les Mantodea de Guyane 800
Mantids of the euro-mediterranean area 700
The Oxford Handbook of Educational Psychology 600
有EBL数据库的大佬进 Matrix Mathematics 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 内科学 物理 纳米技术 计算机科学 遗传学 化学工程 基因 复合材料 免疫学 物理化学 细胞生物学 催化作用 病理
热门帖子
关注 科研通微信公众号,转发送积分 3412792
求助须知:如何正确求助?哪些是违规求助? 3015318
关于积分的说明 8869950
捐赠科研通 2703064
什么是DOI,文献DOI怎么找? 1482033
科研通“疑难数据库(出版商)”最低求助积分说明 685108
邀请新用户注册赠送积分活动 679789