Interleukin 4 increases type 5 acid phosphatase mrna expression in murine bone marrow macrophages

1994 ◽  
Vol 54 (3) ◽  
pp. 365-371 ◽  
Author(s):  
D. L. Lacey ◽  
J. M. Erdmann ◽  
H.-L. Tan
2020 ◽  
Vol 88 (11) ◽  
Author(s):  
Mohamed Mohamed Elashiry ◽  
Mahmoud Elashiry ◽  
Rana Zeitoun ◽  
Ranya Elsayed ◽  
Fucong Tian ◽  
...  

ABSTRACT Enterococcus faecalis, long implicated in serious systemic infections and failure of root canal treatment, is a persistent inhabitant of oral periapical lesions. Dendritic cells (DCs) and other innate immune cells patrol the oral mucosa for infecting microbes. Dendritic cells are efficient at capturing microbes when immature, whereupon they can transform into potent antigen-presenting cells upon full maturation. Autophagy, a sophisticated intracellular process first described for elimination of damaged organelles, regulates DC maturation and other important immune functions of DCs. The present study examined how E. faecalis influences the differentiation of murine bone marrow-derived stem cells (BMSCs) into functional DCs in the presence of the cytokines granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4). Although the viability and differentiation of DCs were not affected by E. faecalis, expression of the autophagy-related proteins ATG7, Beclin1, and LC3bI/II were significantly suppressed in an mTOR-dependent manner. Ultrastructurally, E. faecalis was identified in single-membrane vacuoles, some of which were in the process of binary fission. Bacterium-containing autophagosomes were absent within the cytoplasm. Accessory molecules (major histocompatibility complex class II [MHC-II], CD80, and CD86) and anti-inflammatory cytokine (transforming growth factor β1 [TGF-β1]) were suppressed in E. faecalis-induced DCs, while IL-1β, tumor necrosis factor alpha (TNF-α), and IL-12 levels were upregulated. When pulsed with ovalbumin (OVA), the E. faecalis-induced DCs showed reduction in CD4+ OVA-specific OT-II T cell proliferation. It is concluded that E. faecalis promotes the differentiation of bone marrow stem cells into CD11c-positive DCs with aberrant immune functions while retaining the capability of proinflammatory cytokine induction.


2018 ◽  
Vol 4 (1) ◽  
pp. 94-98
Author(s):  
Yumiko Kawata ◽  
Eiji Ikami ◽  
Junya Nojima ◽  
Shoichiro Kokabu ◽  
Tetsuya Yoda ◽  
...  

Adipose-derived Mesenchymal stem cells have emerged as an attractive alternative source of cell therapy. While radiation therapy is an important application for head and neck cancer, the effect of adipose-derived mesenchymal stem cells on irradiated bone marrow-derived Mesenchymal stem cells is still unclear. Herein, we explored how clinical total radiation dose affect gene expression related with differentiation on murine bone marrow-derived mesenchymal stem cells and how murine adipose-derived mesenchymal stem cells affect irradiated murine bone marrow-derived mesenchymal stem cells. The clinical total radiation dose upregulates osterix mRNA expression. Moreover, adiposederived mesenchymal stem cells dramatically promoted the upregulation of osterix mRNA expression whereas inhibited NFATc1 mRNA expression. Taken as a whole, irradiated bone marrow-derived mesenchymal stem cells co-cultured with adipose-derived mesenchymal stem cells may exhibit osteogenic property.


Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3805-3805
Author(s):  
Archibald S. Perkins ◽  
Jacob J. del Campo ◽  
Ying-Yi Xiao ◽  
Yi Zhang ◽  
Sharon J. Lin ◽  
...  

Abstract Retroviral insertion at the Evi1 locus causes high level of expression of the gene in myeloid neoplasms in mice and in nonmalignant expansions of myeloid cells in humans and monkeys. In these settings, it is suggested that EVI1 confers a survival advantage on myeloid cells. Here, we investigate the survival phenotype in DA-1 cells, a leukemic cell line with provirally activated Evi1. We report that short hairpin-mediated suppression of Evi1 in DA-1 cells induces apoptosis via the intrinsic/mitochondrial pathway: DNA fragmentation and histone release are both induced, as is reduction in mitochondrial membrane potential. In addition, procasapses 3 and 9, but not caspase 8 or Bid, are cleaved following Evi1 knockdown; phosphoAKT remains unchanged. Furthermore, mRNA expression profiling following Evi1 suppression show transcriptional changes in several apoptotic regulators, including a 3.5-fold decrease in Bcl2a1 (bfl/A1), a prosurvival member of the Bcl-2 family. To assess whether EVI1 regulates Bcl2a1 expression in a cell type other than DA-1 cells, we transduced primary murine Lin-/Sca-1+/c-Kit+ cells with EVI1 via retroviral vector, and then assessed the expression of Bcl2a1. This revealed that EVI1 induced a more than five-fold increase in Bcl2a1 mRNA expression, as measured by quantitative PCR. Furthermore, transduction of primary murine bone marrow cells with retroviruses bearing either Bcl2a1 or Evi1 resulted in a significant decrease in spontaneous apoptosis, as assessed by the activity of caspases 3 and 7. To further test if Bcl2a1 is necessary for leukemic transformation by Evi1, we assessed the ability of Evi1 to confer serial replating ability on primary bone marrow cells from Bcl2a1−/− mice. Bone marrow was harvested from Bcl2a1−/− and C57BL6 mice and transduced with retrovirus containing either no gene or Evi1. While in C57BL6 mice, Evi1 induced a significant increase in colonies, bone marrow from Bcl2a1−/− mice were resistant to transformation by Evi1. To show that this was due to the lack of Bcl2a1, the gene was added back via retrovirus. While Bcl2a1 by itself did not induce significant number of colonies over vector, when introduced into Bcl2a1−/− cells together with Evi1, there was a significant increase in colony formation. These data indicate that transformation of bone marrow cells by Evi1 depends on the presence of the Bcl2a1 gene. We further show EVI1 can transcriptionally upregulate a BCL2A1::luc reporter that harbors 1.37 kb of the human BCL2A1 upstream sequence. Our analysis of the Bcl2a1 promoter indicates that the effect of EVI1 is likely indirect. Based on our findings, we propose that EVI1 acts to block apoptosis in DA-1 cells by transcriptionally activating Bcl2a1.


Endocrinology ◽  
1995 ◽  
Vol 136 (6) ◽  
pp. 2367-2376 ◽  
Author(s):  
D L Lacey ◽  
J M Erdmann ◽  
S L Teitelbaum ◽  
H L Tan ◽  
J Ohara ◽  
...  

Author(s):  
Marieke Goedhart ◽  
Stephanie Gessel ◽  
Robbert van der Voort ◽  
Edith Slot ◽  
Beth Lucas ◽  
...  

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