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在退行性椎间盘细胞中使用Phorbol Myristate 乙酸表达蛋白激酶C和矩阵金属蛋白酶的表达

He Quan¹, Haksun Kim¹

¹Department of Orthopedic Surgery, Yonsei University College of Medicine, Seoul, Korea.

Clinics in orthopedic surgery

|October 4, 2024

概括

博胺基乙酸 (PMA) 激活了NP细胞中非正规的Wnt通路,但没有防止NP细胞退化. PMA增加矩阵金属蛋白酶 (MMP) 和炎症标记物,这表明它不会抑制衰老.

科学领域:

生物化学生物化学
细胞生物学细胞生物学
生物医学工程生物医学工程

背景情况:

细胞核 (NP) 细胞退化是一种与细胞衰老相关的复杂过程.
在NP细胞衰老中,Wnt/β-catenin信号通路和矩阵金属蛋白酶 (MMPs) 起着至关重要的作用.
醇酸 (PMA) 激活蛋白激酶C (PKC) 可能抑制NP细胞衰老,但这需要在人类细胞中进行研究.

研究的目的:

研究PMA对人类NP细胞中非正规和正规Wnt通路的影响.
为了确定PMA对人类NP细胞MMP表达的影响.
为了确定PMA是否抑制NP细胞衰老.

主要方法:

来自Pfirrmann等级1-2盘组织的人类NP细胞被培养并用PMA (400nM) 处理.
分离了蛋白质和RNA,以分析关键的Wnt途径中间体 (PKC-δ,β-catenin),MMPs (MMP1,MMP13),抑制剂 (TIMP1),其他蛋白酶 (ADAMTS5),炎症标记物 (IL-6,PGE2) 和TRPV4.4的表达.
评估了II型原和糖氨基甘氨酸 (GAG) 的信使RNA (mRNA) 水平.

主要成果:

PMA治疗增加了PKC-δ和β-catenin的表达,表明非正规和正规Wnt通路的激活.
二型原蛋白和GAG的mRNA水平增加,但蛋白质水平保持不变.
在PMA上调调节MMP1,TIMP1,ADAMTS5,IL-6,PGE2和TRPV4,而MMP13和NF-κB表达不受影响.

结论:

PMA通过PKC-δ激活非正规Wnt通路,但对正规Wnt通路的β-catenin的影响有限.
可能通过TRPV4的β-catenin激活导致通过NF-κB增加MMP1,ADAMTS5,IL-6和PGE2的表达.
PMA治疗没有防止NP细胞退化,这是MMP和炎症标志物增加的证据.

关键词:

椎间盘退化椎间盘退化矩阵金属蛋白质酶的结构.它的核心是脉的.博胺酸乙酸 (Phorbol myristate acetate) 是一种可以蛋白激酶C-delta是一种蛋白激酶.

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