Interleukin-1 beta enhances human multipotent mesenchymal stromal cell proliferative potential and their ability to maintain hematopoietic precursor cells

Bigildeev, Alexey; Zezina, Ekaterina; Shipounova, Irina N.; Ni, Drize

doi:10.1016/j.cyto.2014.10.018

Cited by 23 publications

(14 citation statements)

References 60 publications

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“…23–27 In our earlier studies, we found that acidic bile salts stimulated human esophageal squamous epithelial cells in culture to secrete potent pro-inflammatory cytokines [interleukin (IL)-8 and IL-1β], and that conditioned media from those cells increased migration of inflammatory cells in a transwell assay system. 7,8 Cytokines like IL-8 and IL-1β also have pro-proliferative effects, 28,29 which might have contributed to esophageal basal cell and papillary hyperplasia observed in the absence of surface erosions. In esophageal epithelial cells in culture, moreover, PPIs inhibit secretion of IL-8 through acid-independent mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Association of Acute Gastroesophageal Reflux Disease With Esophageal Histologic Changes

Dunbar

Agoston

Odze

et al. 2016

JAMA

195

149

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Section: Discussionmentioning

confidence: 99%

Association of Acute Gastroesophageal Reflux Disease With Esophageal Histologic Changes

Dunbar

Agoston

Odze

et al. 2016

JAMA

195

149

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“…This leads to the dimerization of intracellular TIR complexes, which then engages the MYD88-IRAK4 complex, thereby activating multiple downstream pathways, including NF-κB and p38 MAPK, in multiple organ systems (see Figure 1 ) ( 82 ). IL-1β is an important stromal growth factor in the maintenance of multipotent mesenchymal stromal cells and enhances the ability of stromal cells to maintain HSCs, as shown in both in vitro mouse studies and long term culture-initiating cell assays on human cells ( 83 , 84 ). A study by Pietras et al elucidated the function of IL-1β in normal HSC in vivo .…”

Section: Il-1βmentioning

confidence: 97%

Inflammatory Signaling Pathways in Preleukemic and Leukemic Stem Cells

2017

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Hematopoietic stem cells (HSCs) are a rare subset of bone marrow cells that usually exist in a quiescent state, only entering the cell cycle to replenish the blood compartment, thereby limiting the potential for errors in replication. Inflammatory signals that are released in response to environmental stressors, such as infection, trigger active cycling of HSCs. These inflammatory signals can also directly induce HSCs to release cytokines into the bone marrow environment, promoting myeloid differentiation. After stress myelopoiesis is triggered, HSCs require intracellular signaling programs to deactivate this response and return to steady state. Prolonged or excessive exposure to inflammatory cytokines, such as in prolonged infection or in chronic rheumatologic conditions, can lead to continued HSC cycling and eventual HSC loss. This promotes bone marrow failure, and can precipitate preleukemic states or leukemia through the acquisition of genetic and epigenetic changes in HSCs. This can occur through the initiation of clonal hematopoiesis, followed by the emergence preleukemic stem cells (pre-LSCs). In this review, we describe the roles of multiple inflammatory signaling pathways in the generation of pre-LSCs and in progression to myelodysplastic syndrome (MDS), myeloproliferative neoplasms, and acute myeloid leukemia (AML). In AML, activation of some inflammatory signaling pathways can promote the cycling and differentiation of LSCs, and this can be exploited therapeutically. We also discuss the therapeutic potential of modulating inflammatory signaling for the treatment of myeloid malignancies.

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“…It is also important to take into account IL-1b-mediated regulation of the fibroblast cell proliferation rate as reported previously. 48,49 For this reason, the cell number was measured after stimulation and used to normalize secreted protein levels. Consistent with previous reports, we detected increased proliferation after IL-1b stimulation of conjunctival fibroblasts in serum-free conditions (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Inflammatory Cytokine-Mediated Regulation of Thrombospondin-1 and CD36 in Conjunctival Cells

Soriano-Romaní

Contreras-Ruiz

García-Posadas

et al. 2015

Journal of Ocular Pharmacology and Therapeutics

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Purpose: Increased expression of transforming growth factor-b2 (TGF-b2) is reported in the conjunctiva of dry eye patients with no increase of anti-inflammatory activity of TGF-b2. Our aim was to compare the expression of molecules involved in TGF-b2 activation, thrombospondin-1 (TSP-1) and CD36, during murine and human conjunctival inflammation. Methods: Human conjunctival tissue from cadaveric donors, human conjunctival epithelial primary cells and fibroblasts, and murine conjunctivas were immunostained for TSP-1, CD36, or TGF-b2. Inflamed conjunctival tissues were obtained from C57BL/6 wild-type (WT) mice induced to develop experimental dry eye (EDE) with 10 days of desiccating conditions and scopolamine injections and TSP-1-deficient (TSP1 -/ -) mice, which spontaneously develop Sjögren's syndrome-associated conjunctival inflammation with age. Immunostaining intensities were compared using ImageJ software. Cultures of human conjunctival fibroblasts were stimulated with IL-1b and both secreted protein and message levels of TSP-1, CD36, and TGF-b2 were analyzed. Results: TSP-1 and CD36 were detectable in human and murine conjunctival tissues as well as primary conjunctival epithelial cells and fibroblasts. Increased conjunctival immunostaining of TGF-b2 and reduced CD36 were detected in EDE mice compared with WT mice. Interestingly, increased TGF-b2 and CD36 conjunctival immunostaining was detected in TSP1-/ -mice. The expression of TSP-1 and CD36 was downregulated in IL-1b-stimulated conjunctival fibroblasts at both the protein and message level, while active TGFb2 was undetected. Conclusions: The absence or reduced expression of either of the molecules involved in TGF-b2 activation supports proinflammatory conditions in the conjunctiva. Changes in TSP-1 and CD36 may serve as potential biomarkers of conjunctival inflammation.

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Interleukin-1 beta enhances human multipotent mesenchymal stromal cell proliferative potential and their ability to maintain hematopoietic precursor cells

Cited by 23 publications

References 60 publications

Association of Acute Gastroesophageal Reflux Disease With Esophageal Histologic Changes

Association of Acute Gastroesophageal Reflux Disease With Esophageal Histologic Changes

Inflammatory Signaling Pathways in Preleukemic and Leukemic Stem Cells

Inflammatory Cytokine-Mediated Regulation of Thrombospondin-1 and CD36 in Conjunctival Cells

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