相关实验视频

Updated: Jun 10, 2025

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness

Published on: March 18, 2022

叉头盒子C1通过Piezo1/YAP轴促进了骨底骨骨质细胞中骨关节炎的病理

Zhengyuan Li¹, Lin Hao¹, Shenghong Chen¹

¹Department of Orthopedics, The First Affiliated Hospital of Anhui Medical University, 218 JiXi Road, Hefei 230022, Anhui, China; Anhui Province Key Laboratory of Zoonoses, Anhui Medical University, Anhui, China.

Cellular signalling

|October 13, 2024

概括

叉头盒子C1 (FoxC1) 通过激活Piezo1和YAP信号,驱动骨关节炎 (OA) 和骨硬化. 抑制这种途径减少了OA病变,为骨关节炎提供了潜在的治疗点.

科学领域:

整形外科整形外科整形外科
分子生物学分子生物学
病理学病理学病理学

背景情况:

底骨硬化是骨关节炎 (OA) 的一个标志.
叉头盒 C1 (FoxC1) 涉及OA突性炎症,但其在子冠状腺骨中的作用尚不清楚.
了解FoxC1在OA下丘脑骨中的功能对于开发新疗法至关重要.

研究的目的:

为了研究FoxC1在骨关节炎中所扮演的角色.
阐明在OA中FoxC1的功能背后的分子机制.
根据FoxC1信号来确定OA的潜在治疗点.

主要方法:

分析了OA中FoxC1和Piezo1表达的分析.
在OA骨质细胞中对FoxC1和Piezo1的过度表达研究.
双 luciferase 试验验证 FoxC1 的结合和 Piezo1 的激活.
条件淘汰赛小鼠模型 (FoxC1-CKO和Piezo1-CKO) 来评估体内效应.

主要成果:

在OA中观察到FoxC1和Piezo1表达的升高.
过度表达FoxC1/Piezo1会增加骨质母细胞的增殖,骨质原生标记物的表达,以及促炎因素的分泌.
FoxC1通过Piezo1激活和下游YAP信号作用,影响ALP,COL1A1,RUNX2,骨质素,MMP3和MMP9.
抑制Piezo1可以逆转FoxC1的作用.
在小鼠模型中,FoxC1和Piezo1的缺乏减少了亚冠状腺骨质硬化和微血管生成.

结论:

通过Piezo1/YAP信号通路,FoxC1显著促进了骨关节炎的亚冠状腺骨病理.
准FoxC1-Piezo1-YAP轴为骨关节炎提供了一个新的治疗策略.
这项研究提供了关键的洞察力,了解驱动OA下丘脑骨变化的分子机制.

关键词:

在FoxC1C1中使用.骨关节炎是一种骨关节炎.骨质母细胞是骨质母细胞.这是一个Piezo1.哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈

更多相关视频

A Reproducible Cartilage Impact Model to Generate Post-Traumatic Osteoarthritis in the Rabbit

A Reproducible Cartilage Impact Model to Generate Post-Traumatic Osteoarthritis in the Rabbit

Published on: November 21, 2023

Micro-Computed Tomography Analysis of the Knee in Aged Dunkin-Hartley Guinea Pigs after Intra Articular Injection

Micro-Computed Tomography Analysis of the Knee in Aged Dunkin-Hartley Guinea Pigs after Intra Articular Injection

Published on: August 2, 2024

相关概念视频

The JAK-STAT Signaling Pathway

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...

Osteoclasts in Bone Remodeling

Osteoclasts in Bone Remodeling

Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...

NF-κB-dependent Signaling Pathway

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...