Interleukin-6 Knockout Inhibits Senescence of Bone Mesenchymal Stem Cells in High-Fat Diet-Induced Bone Loss
Obesity, a chronic low-grade inflammatory state, not only promotes bone loss, but also accelerates cell senescence. However, little is known about the mechanisms that link obesity, bone loss, and cell senescence. Interleukin-6 (IL-6), a pivotal inflammatory mediator increased during obesity, is a ca...
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| Published in: | Frontiers in endocrinology (Lausanne) Vol. 11; p. 622950 |
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| Abstract | Obesity, a chronic low-grade inflammatory state, not only promotes bone loss, but also accelerates cell senescence. However, little is known about the mechanisms that link obesity, bone loss, and cell senescence. Interleukin-6 (IL-6), a pivotal inflammatory mediator increased during obesity, is a candidate for promoting cell senescence and an important part of senescence-associated secretory phenotype (SASP). Here, wild type (WT) and (IL-6 KO) mice were fed with high-fat diet (HFD) for 12 weeks. The results showed IL-6 KO mice gain less weight on HFD than WT mice. HFD induced trabecular bone loss, enhanced expansion of bone marrow adipose tissue (BMAT), increased adipogenesis in bone marrow (BM), and reduced the bone formation in WT mice, but it failed to do so in IL-6 KO mice. Furthermore, IL-6 KO inhibited HFD-induced clone formation of bone marrow cells (BMCs), and expression of senescence markers (p53 and p21). IL-6 antibody inhibited the activation of STAT3 and the senescence of bone mesenchymal stem cells (BMSCs) from WT mice
, while rescued IL-6 induced senescence of BMSCs from IL-6 KO mice through the STAT3/p53/p21 pathway. In summary, our data demonstrated that IL-6 KO may maintain the balance between osteogenesis and adipogenesis in BM, and restrain senescence of BMSCs in HFD-induced bone loss. |
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| AbstractList | Obesity, a chronic low-grade inflammatory state, not only promotes bone loss, but also accelerates cell senescence. However, little is known about the mechanisms that link obesity, bone loss, and cell senescence. Interleukin-6 (IL-6), a pivotal inflammatory mediator increased during obesity, is a candidate for promoting cell senescence and an important part of senescence-associated secretory phenotype (SASP). Here, wild type (WT) and (IL-6 KO) mice were fed with high-fat diet (HFD) for 12 weeks. The results showed IL-6 KO mice gain less weight on HFD than WT mice. HFD induced trabecular bone loss, enhanced expansion of bone marrow adipose tissue (BMAT), increased adipogenesis in bone marrow (BM), and reduced the bone formation in WT mice, but it failed to do so in IL-6 KO mice. Furthermore, IL-6 KO inhibited HFD-induced clone formation of bone marrow cells (BMCs), and expression of senescence markers (p53 and p21). IL-6 antibody inhibited the activation of STAT3 and the senescence of bone mesenchymal stem cells (BMSCs) from WT mice
in vitro
, while rescued IL-6 induced senescence of BMSCs from IL-6 KO mice through the STAT3/p53/p21 pathway. In summary, our data demonstrated that IL-6 KO may maintain the balance between osteogenesis and adipogenesis in BM, and restrain senescence of BMSCs in HFD-induced bone loss. Obesity, a chronic low-grade inflammatory state, not only promotes bone loss, but also accelerates cell senescence. However, little is known about the mechanisms that link obesity, bone loss, and cell senescence. Interleukin-6 (IL-6), a pivotal inflammatory mediator increased during obesity, is a candidate for promoting cell senescence and an important part of senescence-associated secretory phenotype (SASP). Here, wild type (WT) and (IL-6 KO) mice were fed with high-fat diet (HFD) for 12 weeks. The results showed IL-6 KO mice gain less weight on HFD than WT mice. HFD induced trabecular bone loss, enhanced expansion of bone marrow adipose tissue (BMAT), increased adipogenesis in bone marrow (BM), and reduced the bone formation in WT mice, but it failed to do so in IL-6 KO mice. Furthermore, IL-6 KO inhibited HFD-induced clone formation of bone marrow cells (BMCs), and expression of senescence markers (p53 and p21). IL-6 antibody inhibited the activation of STAT3 and the senescence of bone mesenchymal stem cells (BMSCs) from WT mice in vitro, while rescued IL-6 induced senescence of BMSCs from IL-6 KO mice through the STAT3/p53/p21 pathway. In summary, our data demonstrated that IL-6 KO may maintain the balance between osteogenesis and adipogenesis in BM, and restrain senescence of BMSCs in HFD-induced bone loss. Obesity, a chronic low-grade inflammatory state, not only promotes bone loss, but also accelerates cell senescence. However, little is known about the mechanisms that link obesity, bone loss, and cell senescence. Interleukin-6 (IL-6), a pivotal inflammatory mediator increased during obesity, is a candidate for promoting cell senescence and an important part of senescence-associated secretory phenotype (SASP). Here, wild type (WT) and (IL-6 KO) mice were fed with high-fat diet (HFD) for 12 weeks. The results showed IL-6 KO mice gain less weight on HFD than WT mice. HFD induced trabecular bone loss, enhanced expansion of bone marrow adipose tissue (BMAT), increased adipogenesis in bone marrow (BM), and reduced the bone formation in WT mice, but it failed to do so in IL-6 KO mice. Furthermore, IL-6 KO inhibited HFD-induced clone formation of bone marrow cells (BMCs), and expression of senescence markers (p53 and p21). IL-6 antibody inhibited the activation of STAT3 and the senescence of bone mesenchymal stem cells (BMSCs) from WT mice , while rescued IL-6 induced senescence of BMSCs from IL-6 KO mice through the STAT3/p53/p21 pathway. In summary, our data demonstrated that IL-6 KO may maintain the balance between osteogenesis and adipogenesis in BM, and restrain senescence of BMSCs in HFD-induced bone loss. |
| Author | Li, Huifang Liu, Yi Xie, Ying Liang, Yan Tian, Li Li, Yujue Zhang, Jie Lu, Lingyun Chen, Xiang Yu, Xijie |
| AuthorAffiliation | 5 Department of Rheumatology and Immunology, Rare Disease Center, West China Hospital, Sichuan University , Chengdu , China 3 Department of Integrated Traditional Chinese and Western Medicine, West China Hospital, Sichuan University , Chengdu , China 1 Department of Endocrinology and Metabolism, Laboratory of Endocrinology and Metabolism, Rare Disease Center, West China Hospital, Sichuan University , Chengdu , China 2 Department of General Practice, West China Hospital, Sichuan University , Chengdu , China 4 Research Core Facility, West China Hospital, Sichuan University , Chengdu , China |
| AuthorAffiliation_xml | – name: 5 Department of Rheumatology and Immunology, Rare Disease Center, West China Hospital, Sichuan University , Chengdu , China – name: 1 Department of Endocrinology and Metabolism, Laboratory of Endocrinology and Metabolism, Rare Disease Center, West China Hospital, Sichuan University , Chengdu , China – name: 3 Department of Integrated Traditional Chinese and Western Medicine, West China Hospital, Sichuan University , Chengdu , China – name: 2 Department of General Practice, West China Hospital, Sichuan University , Chengdu , China – name: 4 Research Core Facility, West China Hospital, Sichuan University , Chengdu , China |
| Author_xml | – sequence: 1 givenname: Yujue surname: Li fullname: Li, Yujue organization: Department of General Practice, West China Hospital, Sichuan University, Chengdu, China – sequence: 2 givenname: Lingyun surname: Lu fullname: Lu, Lingyun organization: Department of Integrated Traditional Chinese and Western Medicine, West China Hospital, Sichuan University, Chengdu, China – sequence: 3 givenname: Ying surname: Xie fullname: Xie, Ying organization: Department of Endocrinology and Metabolism, Laboratory of Endocrinology and Metabolism, Rare Disease Center, West China Hospital, Sichuan University, Chengdu, China – sequence: 4 givenname: Xiang surname: Chen fullname: Chen, Xiang organization: Department of Endocrinology and Metabolism, Laboratory of Endocrinology and Metabolism, Rare Disease Center, West China Hospital, Sichuan University, Chengdu, China – sequence: 5 givenname: Li surname: Tian fullname: Tian, Li organization: Department of Endocrinology and Metabolism, Laboratory of Endocrinology and Metabolism, Rare Disease Center, West China Hospital, Sichuan University, Chengdu, China – sequence: 6 givenname: Yan surname: Liang fullname: Liang, Yan organization: Research Core Facility, West China Hospital, Sichuan University, Chengdu, China – sequence: 7 givenname: Huifang surname: Li fullname: Li, Huifang organization: Research Core Facility, West China Hospital, Sichuan University, Chengdu, China – sequence: 8 givenname: Jie surname: Zhang fullname: Zhang, Jie organization: Research Core Facility, West China Hospital, Sichuan University, Chengdu, China – sequence: 9 givenname: Yi surname: Liu fullname: Liu, Yi organization: Department of Rheumatology and Immunology, Rare Disease Center, West China Hospital, Sichuan University, Chengdu, China – sequence: 10 givenname: Xijie surname: Yu fullname: Yu, Xijie organization: Department of Endocrinology and Metabolism, Laboratory of Endocrinology and Metabolism, Rare Disease Center, West China Hospital, Sichuan University, Chengdu, China |
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| Copyright | Copyright © 2021 Li, Lu, Xie, Chen, Tian, Liang, Li, Zhang, Liu and Yu. Copyright © 2021 Li, Lu, Xie, Chen, Tian, Liang, Li, Zhang, Liu and Yu 2021 Li, Lu, Xie, Chen, Tian, Liang, Li, Zhang, Liu and Yu |
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| Keywords | senecence osteoporosis IL-6 obesity bone mesenchymal stem cells |
| Language | English |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Reviewed by: Sadiq Umar, University of Illinois at Chicago, United States; Yong-Can Huang, Peking University Shenzhen Hospital, China This article was submitted to Bone Research, a section of the journal Frontiers in Endocrinology Edited by: Deborah Veis, Washington University School of Medicine in St. Louis, United States |
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| Title | Interleukin-6 Knockout Inhibits Senescence of Bone Mesenchymal Stem Cells in High-Fat Diet-Induced Bone Loss |
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