The Sca-1+ mesenchymal stromal cells modulate macrophage commitment and function

Chen, Yaozhen; Chen, Yan; Yin, Dandan; Wang, Shaobin; Liu, Zheng; Fan, Wen; Li, Na; Xin, Jiajia; Hu, Xingbin; Zhang, Huijie; Yin, Wen

doi:10.3906/biy-1507-113

Cited by 4 publications

(6 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…On the basis of these criteria, some MSCs subpopulations are well‐characterized such as nestin + MSCs (Méndez‐Ferrer et al, ), leptin + MSCs (Ding et al, ), Mx1 + MSCs (Park et al, ), and CXCL12‐abundant reticular (CAR) cells (Sugiyama et al, ). We have previously showed bone associated CD45 − Ter119 − CD31 − CD146 − CD166 − Sca‐1 + cells (short for Sca‐1 + MSCs) were one subpopulation of MSCs in adult mice, which were participated in the self‐renew and differentiation of HSC in adult mice, and we found Sca‐1 + MSCs were negative for the surface markers of hematopoietic cells, such as CD11c/Ter119/CD11b/Gr1/B220 (Chen et al, ). Rosado et al () reported that the inhibition of B‐cell proliferation by MSCs was mediated by T cells.…”

Section: Introductionmentioning

confidence: 61%

Sca‐1⁺mesenchymal stromal cells inhibit splenic marginal zone B lymphocytes commitment through Caspase‐3

Chen

Yang

Zhang

et al. 2016

Cell Biology International

Self Cite

View full text Add to dashboard Cite

Mesenchymal stromal cells (MSCs) have been characterized as an important component of hematopoietic niche, which are capable of modulating the immune system through interaction with a wide range of immune cells. Marginal zone B cells, one main type of mature B lymphocytes, play a central role in eliciting antibody response against pathogens. However, how MSCs and its subpopulations regulate marginal zone B cells commitment is unknown yet. In this study, we assessed the contribution of Sca-1(+) MSCs on marginal zone B cells commitment. Our results showed that Sca-1(+) MSCs inhibit the commitment of marginal zone B lymphocytes. The inhibition was exerted through lowered Caspase-3 expression. Furthermore, we found marginal zone B lymphocytes in spleen of Caspase-3 knockout mice decreased and Caspase-3 knockout Sca-1(+) MSCs accounted for the MZB lymphocytes decrease. In conclusion, our investigation provided clues about Sca-1(+) MSCs regulation on the commitment of marginal zone B cells through Caspase-3 gene.

show abstract

Section: Introductionmentioning

confidence: 61%

Sca‐1⁺mesenchymal stromal cells inhibit splenic marginal zone B lymphocytes commitment through Caspase‐3

Chen

Yang

Zhang

et al. 2016

Cell Biology International

Self Cite

View full text Add to dashboard Cite

show abstract

“…At P < 0.05, the difference was considered statistically significant. (Wen et al, 2015;Chen et al, 2016aChen et al, , 2016b + cells using the transwell system ( Figures 1D-1F). Taken together, these data suggest that Sca1 + MSCs promoted DC commitment and that cell-to-cell contact was needed for the promotion.…”

Section: Statistical Analysesmentioning

confidence: 99%

“…CD11c + , CD146 + , and CD166 + cells were less than 0.5%. The proportion of TER119 + and CD3 + cells was no more than 0.8% (Wen et al, 2015;Chen et al, 2016aChen et al, , 2016b. Undoubtedly, niche components are instrumental to HSC self-renewal and differentiation, but in terms of lineage commitment, there are limited data available.…”

mentioning

confidence: 99%

“…+ MSCs A bone-related MSC mixture and Sca1 + MSCs were isolated using a previously described method (Wen et al, 2015;Chen et al, 2016aChen et al, , 2016b. Tibias and femurs were excised from mice of 8-12 weeks old.…”

Section: Preparation Of Mscs and Sca1mentioning

confidence: 99%

“…Sca1 is one of the MSC markers (Morikawa et al, 2009). Many markers were used to identify in situ and/ or to isolate MSCs in mice, such as CD29, CD51, CD73, CD90, CD105, CD106, CD135, C-KIT, nestin, PDGFRα, and Sca1, but the lack of specific markers impedes identification of MSC functions (Galderisi and Giordano, 2014 (Wen et al, 2015;Chen et al, 2016aChen et al, , 2016b. Undoubtedly, niche components are instrumental to HSC self-renewal and differentiation, but in terms of lineage commitment, there are limited data available.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

The Sca1+ mesenchymal stromal subpopulation promotesdendritic cell commitment in the niche

Li¹,

Yin²,

Zhang³

et al. 2017

Turk J Biol

Self Cite

View full text Add to dashboard Cite

IntroductionDendritic cells (DCs) are essential mediators in innate and adaptive immune responses. Except for Langerhans cells, DCs are derived from hematopoietic stem cells (HSCs) (Belz and Nutt, 2012;Satpathy et al., 2012;Seillet and Belz, 2013). Evidence has shown that self-renewing or the differentiation of HSCs, including DC commitment, mainly occurs in the bone marrow, with a high probability of being regulated by the hematopoietic microenvironment (niche) (Schraml et al., 2013). However, little is known about how the endosteal niche regulates the development of DC progenitors in bone marrow. Mesenchymal stromal cells (MSCs) are the most important components in the niche (Frenette et al., 2013). Recently, Jiang et al. (2005) reported that MSCs inhibited DC differentiation and maturation (Spaggiari et al., 2009;Zhang et al., 2009;Lai et al., 2010), as well as DC effector properties, including antigen processing and presentation to T cells (Chiesa et al., 2011).MSCs are actually heterogenic mixtures. A recent study reported that different subpopulations of MSCs served as unclassical niche components in bone marrow, such as CXCL12-abundant reticular (CAR) cells (Sugiyama et al., 2006;Ding and Morrison, 2013), nestin + cells (Mendez-Ferrer et al., 2010), Mx-cre + cells (Park et al., 2012), leptin + receptor-expressing mesenchymal cells (Ding et al., 2012), adipocytes (Naveiras et al., 2009), CD146 + cells, CD166 + cells (Hudson et al., 2011), and CD271 + cells (Mabuchi et al., 2013). Sca1 is one of the MSC markers (Morikawa et al., 2009). Many markers were used to identify in situ and/ or to isolate MSCs in mice, such as CD29, CD51, CD73, CD90, CD105, CD106, CD135, C-KIT, nestin, PDGFRα, and Sca1, but the lack of specific markers impedes identification of MSC functions (Galderisi and Giordano, 2014). Previously we enzymatically dissociated bone and separated the Sca1 + MSCs from the MSC mixture. Previously we also checked the purity of Sca1 + MSCs after isolation. Sca1 + MSCs were more than 80%, while CD45 + ,

show abstract

Melanoma-Induced Anemia Could be Rescued by Sca-1⁺Mesenchymal Stromal Cells in Mice

Chen

Yin

Zhang

et al. 2017

Stem Cells and Development

View full text Add to dashboard Cite

The intrinsic basis of cancer-related anemia (CRA) is erythropoiesis disorder, which is a common complication of cancer and exerts a negative influence on the life quality of cancer patients. Cell therapy using mesenchymal stromal cells (MSCs) is considered as a promising method in cancer treatment. Furthermore, MSCs have been used to cure few type of anemia and be considered as a potential strategy to recover anemia radically. However, none reports its application in CRA treatment. In CRA model mice, we found that the number of linc-kitSca-1 and Sca-1 MSCs was decreased. And CRA resulted in an increased number of proerythroblasts and basophilic erythroblasts and decreased number of orthochromatic erythroblasts. Furthermore, in CRA model mice transplanted with Sca-1 MSCs and MSCs, the levels of red blood cell count and Hb in peripheral blood were obviously increased. And the accumulation of proerythroblasts and basophilic erythroblasts was inhibited. In addition, the expression patterns of GATA-1 and GATA-2, which is pivotal to anemia, were remarkably recovered. Our results demonstrated that either MSCs or its subpopulation could effectively recover CRA erythropoiesis through GATA-1/GATA-2 signaling, which outstrips the traditional symptomatic therapy.

show abstract

The Sca-1+ mesenchymal stromal cells modulate macrophage commitment and function

Cited by 4 publications

References 36 publications

Sca‐1⁺mesenchymal stromal cells inhibit splenic marginal zone B lymphocytes commitment through Caspase‐3

Sca‐1⁺mesenchymal stromal cells inhibit splenic marginal zone B lymphocytes commitment through Caspase‐3

The Sca1+ mesenchymal stromal subpopulation promotesdendritic cell commitment in the niche

Melanoma-Induced Anemia Could be Rescued by Sca-1⁺Mesenchymal Stromal Cells in Mice

Contact Info

Product

Resources

About

The Sca-1+ mesenchymal stromal cells modulate macrophage commitment and function

Cited by 4 publications

References 36 publications

Sca‐1+mesenchymal stromal cells inhibit splenic marginal zone B lymphocytes commitment through Caspase‐3

Sca‐1+mesenchymal stromal cells inhibit splenic marginal zone B lymphocytes commitment through Caspase‐3

The Sca1+ mesenchymal stromal subpopulation promotesdendritic cell commitment in the niche

Melanoma-Induced Anemia Could be Rescued by Sca-1+Mesenchymal Stromal Cells in Mice

Contact Info

Product

Resources

About

Sca‐1⁺mesenchymal stromal cells inhibit splenic marginal zone B lymphocytes commitment through Caspase‐3

Sca‐1⁺mesenchymal stromal cells inhibit splenic marginal zone B lymphocytes commitment through Caspase‐3

Melanoma-Induced Anemia Could be Rescued by Sca-1⁺Mesenchymal Stromal Cells in Mice