Inflammatory Microenvironment Accelerates Bone Marrow Mesenchymal Stem Cell Aging
MSC senescence is considered a contributing factor in aging-related diseases. We investigated the influence of the inflammatory microenvironment on bone marrow mesenchymal stem cells (BMSCs) under aging conditions and the underlying mechanism to provide new ideas for stem cell therapy for age-relate...
| Main Authors: | , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Frontiers Media S.A.
2022-05-01
|
| Series: | Frontiers in Bioengineering and Biotechnology |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/articles/10.3389/fbioe.2022.870324/full |
| _version_ | 1828795519163432960 |
|---|---|
| author | Xin Peng Xin Peng Xin Peng Xin Zhou Xin Zhou Xin Zhou Ying Yin Beibei Luo Yang Liu Yang Liu Yang Liu Cheng Yang Cheng Yang Cheng Yang |
| author_facet | Xin Peng Xin Peng Xin Peng Xin Zhou Xin Zhou Xin Zhou Ying Yin Beibei Luo Yang Liu Yang Liu Yang Liu Cheng Yang Cheng Yang Cheng Yang |
| author_sort | Xin Peng |
| collection | DOAJ |
| description | MSC senescence is considered a contributing factor in aging-related diseases. We investigated the influence of the inflammatory microenvironment on bone marrow mesenchymal stem cells (BMSCs) under aging conditions and the underlying mechanism to provide new ideas for stem cell therapy for age-related osteoporosis. The BMSCs were cultured until passage 3 (P3) (young group) and passage 10 (P10) (aging group) in vitro. The supernatant was collected as the conditioned medium (CM). The young BMSCs were cultured in the CM of P3 or P10 cells. The effects of CM from different groups on the aging and stemness of the young BMSCs were examined. A Quantibody® mouse inflammation array on serum extracts from young (aged 8 weeks) and old (aged 78 weeks) mice was performed, and differentially expressed factors were screened out. We discovered that the CM from senescent MSCs changed the physiology of young BMSCs. Systemic inflammatory microenvironments changed with age in the mice. In particular, the pro-inflammatory cytokine IL-6 increased, and the anti-inflammatory cytokine IL-10 decreased. The underlying mechanism was investigated by GO and KEGG analyses, and there was a change in the JAK-STAT signaling pathway, which is closely related to IL-6 and IL-10. Collectively, our results demonstrated that the age-related inflammatory microenvironment has a significant effect on the biological functions of BMSCs. Targeted reversal of this inflammatory environment may provide a new strategy for stem cell therapy to treat aging-related skeletal diseases. |
| first_indexed | 2024-12-12T04:05:26Z |
| format | Article |
| id | doaj.art-e7464987949e43baa5588f7a4acc13bd |
| institution | Directory Open Access Journal |
| issn | 2296-4185 |
| language | English |
| last_indexed | 2024-12-12T04:05:26Z |
| publishDate | 2022-05-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Bioengineering and Biotechnology |
| spelling | doaj.art-e7464987949e43baa5588f7a4acc13bd2022-12-22T00:38:47ZengFrontiers Media S.A.Frontiers in Bioengineering and Biotechnology2296-41852022-05-011010.3389/fbioe.2022.870324870324Inflammatory Microenvironment Accelerates Bone Marrow Mesenchymal Stem Cell AgingXin Peng0Xin Peng1Xin Peng2Xin Zhou3Xin Zhou4Xin Zhou5Ying YinBeibei LuoYang Liu6Yang Liu7Yang Liu8Cheng Yang9Cheng Yang10Cheng Yang11Department of Stomatology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaSchool of Stomatology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaHubei Province Key Laboratory of Oral and Maxillofacial Development and Regeneration, Wuhan, ChinaDepartment of Stomatology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaSchool of Stomatology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaHubei Province Key Laboratory of Oral and Maxillofacial Development and Regeneration, Wuhan, ChinaDepartment of Stomatology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaSchool of Stomatology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaHubei Province Key Laboratory of Oral and Maxillofacial Development and Regeneration, Wuhan, ChinaDepartment of Stomatology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaSchool of Stomatology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaHubei Province Key Laboratory of Oral and Maxillofacial Development and Regeneration, Wuhan, ChinaMSC senescence is considered a contributing factor in aging-related diseases. We investigated the influence of the inflammatory microenvironment on bone marrow mesenchymal stem cells (BMSCs) under aging conditions and the underlying mechanism to provide new ideas for stem cell therapy for age-related osteoporosis. The BMSCs were cultured until passage 3 (P3) (young group) and passage 10 (P10) (aging group) in vitro. The supernatant was collected as the conditioned medium (CM). The young BMSCs were cultured in the CM of P3 or P10 cells. The effects of CM from different groups on the aging and stemness of the young BMSCs were examined. A Quantibody® mouse inflammation array on serum extracts from young (aged 8 weeks) and old (aged 78 weeks) mice was performed, and differentially expressed factors were screened out. We discovered that the CM from senescent MSCs changed the physiology of young BMSCs. Systemic inflammatory microenvironments changed with age in the mice. In particular, the pro-inflammatory cytokine IL-6 increased, and the anti-inflammatory cytokine IL-10 decreased. The underlying mechanism was investigated by GO and KEGG analyses, and there was a change in the JAK-STAT signaling pathway, which is closely related to IL-6 and IL-10. Collectively, our results demonstrated that the age-related inflammatory microenvironment has a significant effect on the biological functions of BMSCs. Targeted reversal of this inflammatory environment may provide a new strategy for stem cell therapy to treat aging-related skeletal diseases.https://www.frontiersin.org/articles/10.3389/fbioe.2022.870324/fullaging-related skeletal diseasesstem cell therapyinflammatory microenvironmentbone marrow mesenchymal stem cellaging |
| spellingShingle | Xin Peng Xin Peng Xin Peng Xin Zhou Xin Zhou Xin Zhou Ying Yin Beibei Luo Yang Liu Yang Liu Yang Liu Cheng Yang Cheng Yang Cheng Yang Inflammatory Microenvironment Accelerates Bone Marrow Mesenchymal Stem Cell Aging Frontiers in Bioengineering and Biotechnology aging-related skeletal diseases stem cell therapy inflammatory microenvironment bone marrow mesenchymal stem cell aging |
| title | Inflammatory Microenvironment Accelerates Bone Marrow Mesenchymal Stem Cell Aging |
| title_full | Inflammatory Microenvironment Accelerates Bone Marrow Mesenchymal Stem Cell Aging |
| title_fullStr | Inflammatory Microenvironment Accelerates Bone Marrow Mesenchymal Stem Cell Aging |
| title_full_unstemmed | Inflammatory Microenvironment Accelerates Bone Marrow Mesenchymal Stem Cell Aging |
| title_short | Inflammatory Microenvironment Accelerates Bone Marrow Mesenchymal Stem Cell Aging |
| title_sort | inflammatory microenvironment accelerates bone marrow mesenchymal stem cell aging |
| topic | aging-related skeletal diseases stem cell therapy inflammatory microenvironment bone marrow mesenchymal stem cell aging |
| url | https://www.frontiersin.org/articles/10.3389/fbioe.2022.870324/full |
| work_keys_str_mv | AT xinpeng inflammatorymicroenvironmentacceleratesbonemarrowmesenchymalstemcellaging AT xinpeng inflammatorymicroenvironmentacceleratesbonemarrowmesenchymalstemcellaging AT xinpeng inflammatorymicroenvironmentacceleratesbonemarrowmesenchymalstemcellaging AT xinzhou inflammatorymicroenvironmentacceleratesbonemarrowmesenchymalstemcellaging AT xinzhou inflammatorymicroenvironmentacceleratesbonemarrowmesenchymalstemcellaging AT xinzhou inflammatorymicroenvironmentacceleratesbonemarrowmesenchymalstemcellaging AT yingyin inflammatorymicroenvironmentacceleratesbonemarrowmesenchymalstemcellaging AT beibeiluo inflammatorymicroenvironmentacceleratesbonemarrowmesenchymalstemcellaging AT yangliu inflammatorymicroenvironmentacceleratesbonemarrowmesenchymalstemcellaging AT yangliu inflammatorymicroenvironmentacceleratesbonemarrowmesenchymalstemcellaging AT yangliu inflammatorymicroenvironmentacceleratesbonemarrowmesenchymalstemcellaging AT chengyang inflammatorymicroenvironmentacceleratesbonemarrowmesenchymalstemcellaging AT chengyang inflammatorymicroenvironmentacceleratesbonemarrowmesenchymalstemcellaging AT chengyang inflammatorymicroenvironmentacceleratesbonemarrowmesenchymalstemcellaging |