scholarly journals Alterations in the self-renewal and differentiation ability of bone marrow mesenchymal stem cells in a mouse model of rheumatoid arthritis

2010 ◽  
Vol 12 (4) ◽  
pp. R149 ◽  
Author(s):  
Sindhu T Mohanty ◽  
Lucksy Kottam ◽  
Alessandra Gambardella ◽  
Martin J Nicklin ◽  
Les Coulton ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Mouse Model ◽  
The Self ◽  
Self Renewal ◽  
Marrow Mesenchymal Stem Cells

scholarly journals Bone marrow mesenchymal stem cells in rheumatoid arthritis, spondyloarthritis, and ankylosing spondylitis: problems rather than solutions?

2019 ◽  
Vol 21 (1) ◽  
Author(s):  
Jean-Marie Berthelot ◽  
Benoit Le Goff ◽  
Yves Maugars
Keyword(s):  
Rheumatoid Arthritis ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Ankylosing Spondylitis ◽  
Animal Models ◽  
Subchondral Bone ◽  
Frequent Relapses ◽  
Marrow Mesenchymal Stem Cells ◽  
Bone Cortex

Abstract Background Bone marrow mesenchymal stem cells (BM-MSCs) can dampen inflammation in animal models of inflammatory rheumatisms and human osteoarthritis. They are expected to be a solution for numerous human conditions. However, in rheumatoid arthritis (RA) and spondyloarthritis (SpA), subsets of subchondral BM-MSCs might conversely fuel synovitis and enthesitis. Main text Abnormal behaviour of BM-MSCs and/or their progeny has been found in RA and SpA. BM-MSCs also contribute to the ossifying processes observed in ankylosing spondylitis. Some synovial fibroblastic stem cells probably derive from BM-MSCs, but some stem cells can also migrate through the bare zone area of joints, not covered by cartilage, into the synovium. BM-MSCs can also migrate in the synovium over tendons. Sub-populations of bone marrow stem cells also invade the soft tissue side of enthesis via small holes in the bone cortex. The present review aims (1) to make a focus on these two aspects and (2) to put forward the hypothesis that lasting epigenetic changes of some BM-MSCs, induced by transient infections of the bone marrow close to the synovium and/or entheses (i.e. trained immunity of BM-MSCs and/or their progeny), contribute to the pathogenesis of inflammatory rheumatisms. Such hypothesis would fit with (1) the uneven distribution and/or flares of arthritis and enthesitis observed at the individual level in RA and SpA (reminiscent of what is observed following reactive arthritis and/or in Whipple’s disease); (2) the subchondral bone marrow oedema and erosions occurring in many RA patients, in the bare zone area; and (3) the frequent relapses of RA and SpA despite bone marrow transplantation, whereas most BM-MSCs resist graft preconditioning. Conclusion Some BM-MSCs might be more the problem than the solution in inflammatory rheumatisms. Subchondral bone marrow BM-MSCs and their progeny trafficking through the bare zone area of joints or holes in the bone cortex of entheses should be thoroughly studied in RA and SpA respectively. This may be done first in animal models. Mini-arthroscopy of joints could also be used in humans to specifically sample tissues close to the bare zone and/or enthesis areas.

scholarly journals Heparan Sulfate Enhances the Self-Renewal and Therapeutic Potential of Mesenchymal Stem Cells from Human Adult Bone Marrow

2012 ◽  
Vol 21 (11) ◽  
pp. 1897-1910 ◽  
Author(s):  
Torben Helledie ◽  
Christian Dombrowski ◽  
Bina Rai ◽  
Zophia X.H. Lim ◽  
Ian Lee Hock Hin ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Heparan Sulfate ◽  
Therapeutic Potential ◽  
The Self ◽  
Self Renewal ◽  
Adult Bone Marrow ◽  
Human Adult ◽  
Adult Bone

scholarly journals Bone Marrow Mesenchymal Stem Cells Regulate IL-4 and INF-γ Expression in AR Mouse Model

2020 ◽  
Author(s):  
Chuanliang Zhao ◽  
Jingwen Sun ◽  
Xiaojing Cai ◽  
Wentao Zou ◽  
Jiaxiong Zhang
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Flow Cytometry ◽  
Mesenchymal Stem Cells ◽  
Mouse Model ◽  
Th1 Cell ◽  
Differentiation Potential ◽  
Th2 Cell ◽  
Marrow Mesenchymal Stem Cells

Abstract Background: Bone marrow mesenchymal stem cells can promote the recovery of immune balance and regulate the balance of Th1/2 cells. Allergic rhinitis is a disease with Th1/2 imbalance mediated by IgE. It’s unclear whether BMSCs could regulate AR disease. In this study, the possible role of BMSCs was explored. Methods : AR mouse model was established by ovalbumin (OVA). 18 models were randomly divided into three groups: AR-sensitized, Stem-cell-returned, Medium-returned; six unsensitized mouses named normal-control. IgE, IL-4 and INF-γ levels were measured by Elisa. Observing migration of BMSCs by immunofluorescence. Flow cytometry used to detect changes of Th1/2. STAT 4/6 protein level was detected by Western-blot. Results : After OVA-sensitization, IgE, IL-4 and STAT6 levels were higher, INF-γ and STAT4 level was lower. Flow cytometry revealed a decrease in Th1 cell and an increase in Th2 cell in AR group. After BMSCs treatment, t IgE, IL-4 and STAT6 levels in SCRg and MRg were lower than that in AR group, and tINF-γ and STAT4 level were higher than hat inAR group. Flow cytometry showed that the content of Th1 cell increased while Th2 cell decreased. Conclusions: BMSCs return treatment could decrease the expression of IL-4, promote the expression of INF-γ and regulate the balance of Th cell, and the mechanism was closely related to STAT4/6 signaling pathway. However there was no statistical difference between SCRg and MRg, so the role of BMSCs maybe achieved through paracrine function rather than multi-directional differentiation potential.

CKIP-1 contributes to osteogenic differentiation of mouse bone marrow mesenchymal stem cells

2021 ◽  
Vol 16 (9) ◽  
pp. 847-859
Author(s):  
Qiannan Niu ◽  
Shuning Shen ◽  
Jiaojiao He ◽  
Lei Wang
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Mouse Model ◽  
Signaling Pathway ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Negative Regulator ◽  
Mouse Bone Marrow ◽  
Marrow Mesenchymal Stem Cells

Background: Osteogenesis greatly depends on the differentiation of bone marrow mesenchymal stem cells (BMSCs). CKIP-1 is considered to be a negative regulator of BMSCs. Methods: We established a  CKIP-1 knockout mouse model, then isolated and cultured BMSCs from wild-type and knockout groups. Results: Our data demonstrated that CKIP-1 knockout significantly increased bone structure in the experimental mouse model and enhanced BMSC proliferation. CKIP-1 knockout contributed to osteoblastic and adipogenic differentiation. Furthermore, CKIP-1 regulated osteogenesis in BMSCs via the MAPK signaling pathway, and BMSCs from the  CKIP-1 knockout mice were effective in repairing the skull defect null mice. Conclusion: Our results concluded that silencing of CKIP-1 promoted osteogenesis in experimental mice and increased BMSCs differentiation via upregulation of the MAPK signaling pathway.

scholarly journals A Member of the Nuclear Receptor Superfamily, Designated as NR2F2, Supports the Self-Renewal Capacity and Pluripotency of Human Bone Marrow-Derived Mesenchymal Stem Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Ni Zhu ◽  
Huafang Wang ◽  
Binsheng Wang ◽  
Jieping Wei ◽  
Wei Shan ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Nuclear Receptor ◽  
Adipogenic Differentiation ◽  
The Self ◽  
Human Bone ◽  
Self Renewal ◽  
Nuclear Receptor Superfamily ◽  
Colony Forming Capacity

Mesenchymal stem cells are characterized with self-renewal capacity and pluripotency. NR2F2 is a nuclear receptor that has been detected in the mesenchymal compartment of developing organs. However, whether NR2F2 plays a role in the stemness maintenance of mesenchymal stem cells has not been explored yet. In this study, we investigated the function of NR2F2 in bone marrow-derived mesenchymal stem cells via shRNA-mediated knock-down of NR2F2. The suppression of NR2F2 impaired the colony-forming efficacy of mesenchymal stem cells. The inhibition of colony-forming capacity may be attributed to the acceleration of senescence through upregulation of P21 and P16. The downregulation of NR2F2 also suppressed both osteogenic and adipogenic differentiation processes. In conclusion, NR2F2 plays an important role in the stemness maintenance of bone marrow-derived mesenchymal stem cells.

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