دورية أكاديمية

Nucleus Pulposus Cells Induce M2 Polarization of RAW264.7 via CX3CL1/CX3CR1 Pathway and M2 Macrophages Promote Proliferation and Anabolism of Nucleus Pulposus Cells

التفاصيل البيبلوغرافية
العنوان: Nucleus Pulposus Cells Induce M2 Polarization of RAW264.7 via CX3CL1/CX3CR1 Pathway and M2 Macrophages Promote Proliferation and Anabolism of Nucleus Pulposus Cells
المؤلفون: Xiao-Tao Wu, Bo-Wen Wan, Xin-Min Feng, Yu-Ping Tao, Yong-Xiang Wang, Hui-Hui Sun
المصدر: Stem Cells International, Vol 2023 (2023)
بيانات النشر: Hindawi Limited, 2023.
سنة النشر: 2023
المجموعة: LCC:Internal medicine
مصطلحات موضوعية: Internal medicine, RC31-1245
الوصف: Background. The mechanisms underlying M2 macrophage polarization induced by nucleus pulposus (NP) cells are unclear. The effects that M2-polarized macrophages have on NP cells are also controversial. Methods. Transcriptome sequencing was performed to detect the gene change profiles between NP cells from ruptured intervertebral disc (IVD) and normal IVD. The main difference on biological activities between the two cell groups were analyzed by GO analysis and KEGG analysis. Virus transduction, flow cytometry, immunofluorescence, RT-PCR, western blot, CCK-8, TUNEL staining, and AO/EB staining were performed to explore the interactions between NP cells and RAW264.7 macrophages. Statistics were performed using SPSS26. Results. 801 upregulated and 276 downregulated genes were identified in NP cells from ruptured IVD in mouse models. According to GO and KEGG analysis, we found that the differentially expressed genes (DEG) were dominantly enriched in inflammatory response, extracellular matrix degradation, blood vessel morphogenesis, immune effector process, ossification, chemokine signaling pathway, macrophage activation, etc. CX3CL1 was one of the top 20% DEG, and we confirmed that both NP tissue and cells expressed remarkably higher level of CX3CL1 in mouse models (p
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1687-9678
Relation: https://doaj.org/toc/1687-9678
DOI: 10.1155/2023/6400162
URL الوصول: https://doaj.org/article/abced1719aaa43b2a3117b551e0102a2
رقم الأكسشن: edsdoj.bced1719aaa43b2a3117b551e0102a2
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:16879678
DOI:10.1155/2023/6400162