在骨质疏松症小鼠模型中,Vitronectin 可调节破骨细胞生成和骨重塑。

IF 1.4 Q3 ANATOMY & MORPHOLOGY Anatomy & Cell Biology Pub Date : 2024-04-05 DOI:10.5115/acb.23.251
Mari Nakashima, Akiko Suzuki, K. Hashimoto, Mayu Yamashita, Yoko Fujiwara, Yasunori Miyamoto
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引用次数: 0

摘要

Vitronectin(VN)是一种细胞外基质蛋白,在调节骨重塑中起着至关重要的作用。本研究旨在探讨卵巢切除术(OVX)诱导的骨质疏松症小鼠模型中缺乏 VN 的影响。研究结果表明,缺乏 VN 会导致卵巢切除术小鼠血浆中破骨细胞的标志物--抗酒石酸磷酸酶(TRAP)的活性增加。TRAP染色进一步表明,VN缺乏会导致OVX手术小鼠股骨中破骨细胞数量增加。OVX 术后小鼠股骨的 X 射线显微计算机断层扫描分析表明,VN 缺乏可显著抑制 OVX 引起的骨髓面积和骨总量的增加。此外,我们还评估了作为骨质疏松症指数的结构模型指数(SMI)和各向异性程度(DA)。结果表明,VN的缺乏有效地减轻了OVX诱导的OVX手术小鼠SMI和DA的增加。总之,我们的研究证明了 VN 在骨质疏松症小鼠模型中调节破骨细胞生成和骨重塑的重要作用。
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Vitronectin regulates osteoclastogenesis and bone remodeling in a mouse model of osteoporosis.
Vitronectin (VN) is an extracellular matrix protein with a crucial role in regulating bone remodeling. In this study, we aimed to investigate the effect of VN deficiency in a mouse model of osteoporosis induced by ovariectomy (OVX). The findings revealed that the absence of VN led to an increase in the activity of tartrate-resistant acid phosphatase (TRAP), a marker for osteoclasts, in the plasma of OVX-operated mice. TRAP staining further demonstrated that VN deficiency resulted in a higher number of osteoclasts within the femurs of OVX-operated mice. X-ray micro-computed tomography analysis of the femurs in OVX-operated mice indicated that VN deficiency significantly suppressed the OVX-induced increase of marrow area and total volume of bone. Additionally, we assessed structural model index (SMI) and degree of anisotropy (DA) as indices of osteoporosis. The results showed that VN deficiency effectively attenuated the OVX-induced increase in SMI and DA among OVX-operated mice. In summary, our study demonstrates the vital role of VN in regulating osteoclastogenesis and bone remodeling in the mouse model of osteoporosis.
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来源期刊
Anatomy & Cell Biology
Anatomy & Cell Biology ANATOMY & MORPHOLOGY-
CiteScore
1.80
自引率
9.10%
发文量
75
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