Contact-dependent abrogation of bone marrow-derived plasmacytoid dendritic cell differentiation by murine mesenchymal stem cells

Hackstein, Holger; Tschipakow, Inna; Bein, Gregor; Nold, Philipp; Brendel, Cornelia; Baal, Nelli

doi:10.1016/j.bbrc.2016.05.108

Cited by 9 publications

(11 citation statements)

References 41 publications

(38 reference statements)

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“…in the present study, the effects of BMScs on nPc migration were investigated via a Transwell cell migration assay. The results of the present study revealed that pre-culturing BMScs for 24 h and co-culturing BMSCs and NPCs for 24 h may significantly improve nPc migration compared with pre-culturing BMScs for 48 h. These findings suggested that 24 h may be an optimal duration for nPc migration; the BMScs exhibited a stronger ability to promote nPc migration with in relatively a shorter duration of pre-culture of 24 h than 48 h. These observations may be associated with the decreased cell growth and proliferation due to contact-dependent inhibition when BMScs are pre-cultured for 48 h (42)(43)(44).…”

Section: Discussionmentioning

confidence: 92%

miR‑210 enhances mesenchymal stem cell‑modulated neural precursor cell migration

et al. 2020

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The migration of endogenous neural stem cells and neural precursor cells (nPcs) to sites of injury is essential for neuroregeneration following hypoxic-ischemic events. Bone marrow-derived mesenchymal stem cells (BMScs) are a potential therapeutic source of cells following central nervous system damage; however, few studies have investigated the effects of BMScs on cell migration. Thus, in the present study, the effects of BMScs on nPc migration were investigated. in the present study, BMScs and nPcs were isolated and cultured from mice. The effects of BMScs on the migration of nPcs were analyzed using a Transwell cell migration assay. BMScs were transfected with microrna-210 (mir-210) mimics and inhibitors to examine the effects of the respective upregulation and downregulation of mir-210 in BMScs on the migration of nPcs. Then, mir-210 expression in BMScs were quantified and the expression levels of vascular endothelial growth factor-c (VeGF-c), brain derived neurotrophic factor (BdnF) and chemokine c-c motif ligand 3 (ccl3) in the supernatant under hypoxic conditions were investigated via reverse transcription-quantitative polymerase chain reaction (rT-qPcr) and eliSa. Subsequently, the expression of VeGF-c, BdnF and ccl3 in BMScs overexpressing mir-210 or BMScs suppressing mir-210 was examined by rT-qPcr and western blot analyses. BMScs promoted the migration of nPc, particularly when pre-cultured with BMScs for 24 h and co-cultured with nPcs for 24 h; the mir-210 expression levels increased under hypoxic conditions. additionally, the migration of nPcs was also increased when the BMScs overexpressed mir-210 compared with the BMScs transfected with a negative control mir and BMScs with downregulated mir-210 levels. The expression levels of VeGF-c increased in the BMScs that overexpressed mir-210 and were decreased in BMScs transfected with a mir-210 inhibitor. The results of the present study indicated that BMScs promote the migration of nPcs. overexpression of mir-210 in BMScs enhanced nPc migration and may be associated with increases in VeGF-c expression levels.

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Section: Discussionmentioning

confidence: 92%

miR‑210 enhances mesenchymal stem cell‑modulated neural precursor cell migration

et al. 2020

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“…MSCs can also induce the production of regulatory DCs and evade apoptosis, further enhancing phagocytosis and inhibiting T cell activation and proliferation ( 97 , 98 ). Bone marrow MSCs derived from C57BL/6 mice abolished the generation of functional IFN-α-producing pDCs, while they interfered with the maturation of mDCs ( 99 ). Significantly increased CD1c+ DCs and decreased proteinuria levels in SLE patients after human umbilical cord MSCT demonstrated that proliferation of tolerogenic CD1c+ DCs and inhibition of their apoptosis were promoted through IFNγ-FLT3L-FLT3 interactions ( 93 ).…”

Section: Immunomodulatory Activity Of Mscs On Dcsmentioning

confidence: 99%

Immunomodulatory Activity of Mesenchymal Stem Cells in Lupus Nephritis: Advances and Applications

Luo

et al. 2022

Front. Immunol.

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Lupus nephritis (LN) is a significant cause of various acute and chronic renal diseases, which can eventually lead to end-stage renal disease. The pathogenic mechanisms of LN are characterized by abnormal activation of the immune responses, increased cytokine production, and dysregulation of inflammatory signaling pathways. LN treatment is an important issue in the prevention and treatment of systemic lupus erythematosus. Mesenchymal stem cells (MSCs) have the advantages of immunomodulation, anti-inflammation, and anti-proliferation. These unique properties make MSCs a strong candidate for cell therapy of autoimmune diseases. MSCs can suppress the proliferation of innate and adaptive immune cells, such as natural killer cells (NKs), dendritic cells (DCs), T cells, and B cells. Furthermore, MSCs suppress the functions of various immune cells, such as the cytotoxicity of T cells and NKs, maturation and antibody secretion of B cells, maturation and antigen presentation of DCs, and inhibition of cytokine secretion, such as interleukins (ILs), tumor necrosis factor (TNF), and interferons (IFNs) by a variety of immune cells. MSCs can exert immunomodulatory effects in LN through these immune functions to suppress autoimmunity, improve renal pathology, and restore kidney function in lupus mice and LN patients. Herein, we review the role of immune cells and cytokines in the pathogenesis of LN and the mechanisms involved, as well as the progress of research on the immunomodulatory role of MSCs in LN.

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“…Apart from pDCs, T cells, B cells and NK cells are also involved in IFN production in SLE ( 97 ). However, MSCs can inhibit the generation and function of pDCs ( 98 ). Accordingly, MSCs are ideal therapeutic way for SLE patients due to their inhibitory effects on pDCs and type I IFN.…”

Section: Regulatory Effects Of Mscs and Msc-evs On Dendritic Cellsmentioning

confidence: 99%

Immunomodulatory Effect of MSCs and MSCs-Derived Extracellular Vesicles in Systemic Lupus Erythematosus

Yang

Sun²,

Yi-peng

et al. 2021

Front. Immunol.

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Systemic lupus erythematosus (SLE) is a common autoimmune connective tissue disease with unclear etiology and pathogenesis. Mesenchymal stem cell (MSC) and MSC derived extracellular vesicles (EVs) play important roles in regulating innate and adaptive immunity, which are involved in many physiological and pathological processes and contribute to the immune homeostasis in SLE. The effects of MSCs and EVs on SLE have been drawing more and more attention during the past few years. This article reviews the immunomodulatory effects and underlying mechanisms of MSC/MSC-EVs in SLE, which provides novel insight into understanding SLE pathogenesis and guiding the biological therapy.

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Contact-dependent abrogation of bone marrow-derived plasmacytoid dendritic cell differentiation by murine mesenchymal stem cells

Cited by 9 publications

References 41 publications

miR‑210 enhances mesenchymal stem cell‑modulated neural precursor cell migration

miR‑210 enhances mesenchymal stem cell‑modulated neural precursor cell migration

Immunomodulatory Activity of Mesenchymal Stem Cells in Lupus Nephritis: Advances and Applications

Immunomodulatory Effect of MSCs and MSCs-Derived Extracellular Vesicles in Systemic Lupus Erythematosus

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