The pathophysiological changes in cartilage are a crucial feature of lumbar facet joint (LFJ) degeneration and arthritis. However, the molecular mechanism of human LFJ degeneration remains largely defined. This study aimed to examine the changes in chondrocytes at different stages of degenerative LFJ using hematoxylin and eosin and Safranin O staining. The significant loss of chondrocytes in grades 2 and 3 of LFJs was observed. The expression levels of CCAAT enhancer binding protein β (C/EBPβ), Runt-related transcription factor 2 (RUNX2), and matrix metalloproteinase 13 (MMP13) also increased with the aggravation of degeneration (4.89, 5.77, and 6.3 times by Western blot). In vitro, chondrocytes scraped from the LFJs during surgery were stimulated by interleukin (IL)-1β to establish the injury model. The association of C/EBPβ and RUNX2 with active caspase-3 on chondrocytes was analyzed. The high expression level of C/EBPβ, RUNX2, and MMP13 was consistent with that of caspase-3, which reached a peak after 36 h of stimulation. Immunofluorescence suggested that C/EBPβ, RUNX2, and MMP13 co-labeled with active caspase-3. Moreover, immunoprecipitation data prompted that C/EBPβ was able to interact with RUNX2. The knockdown of C/EBPβ significantly decreased the expression levels of MMP13 and active caspase-3 (2.48 and 2.89 times as detected by Western blot analysis) and inhibited chondrocyte apoptosis, which was further demonstrated using flow cytometry. Taken together, the findings of this study uncovered that C/EBPβ could interact with RUNX2 to induce chondrocyte apoptosis in human LFJ degeneration by regulating the expression of MMP13.

中文翻译：

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C/EBPβ 和 RUNX2 之间的相互作用促进人腰椎小关节退变过程中软骨细胞的凋亡。

软骨的病理生理变化是腰椎小关节 (LFJ) 退变和关节炎的重要特征。然而，人类 LFJ 退化的分子机制在很大程度上仍未明确。本研究旨在使用苏木精和曙红以及番红 O 染色检查软骨细胞在退行性 LFJ 不同阶段的变化。观察到 2 级和 3 级 LFJ 中软骨细胞的显着损失。CCAAT增强子结合蛋白β（C/EBPβ）、Runt相关转录因子2（RUNX2）和基质金属蛋白酶13（MMP13）的表达水平也随着变性的加重而升高（Western blot检测为4.89、5.77和6.3倍） ). 在体外，白细胞介素 (IL)-1β 刺激手术期间从 LFJ 刮下的软骨细胞，以建立损伤模型。分析了 C/EBPβ 和 RUNX2 与软骨细胞上活性 caspase-3 的关联。C/EBPβ、RUNX2和MMP13的高表达水平与caspase-3的表达水平一致，在刺激36小时后达到峰值。免疫荧光表明 C/EBPβ、RUNX2 和 MMP13 与活性 caspase-3 共标记。此外，免疫沉淀数据提示 C/EBPβ 能够与 RUNX2 相互作用。C/EBPβ 的敲低显着降低了 MMP13 和活性 caspase-3 的表达水平（Western blot 分析检测到的 2.48 和 2.89 倍）并抑制了软骨细胞凋亡，流式细胞术进一步证明了这一点。综上所述，本研究的结果表明，C/EBPβ 可与 RUNX2 相互作用，通过调节 MMP13 的表达来诱导人 LFJ 变性中的软骨细胞凋亡。