Loss of SIMPL compromises TNF-α-dependent survival of hematopoietic progenitors

Benson, Eric A.; Goebl, Mark G.; Yang, Feng Chun; Kapur, Reuben; McClintick, Jeanette N.; Sanghani, Sonal P.; Harrington, Maureen A.

doi:10.1016/j.exphem.2009.11.006

Cited by 4 publications

(4 citation statements)

References 48 publications

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“…This difference may result from the difference of cells to be used in the experiment. The loss of substrate that interacts with interleukin-1 receptor-associated kinase binding protein 1 (IRAKIBPI, also known as mouse pelle-like kinase (SIMPL) specifically inhibits the TNF-a-dependentTNFRl-dependent response in mouse embryo fibroblasts [31,36] and in mouse hematopoietic progenitors [37]. In this study, we showed thatthe downregulation of IRAKIBPI by siRNA transfection blocked NF-KB activation, proliferation and ERKl g/ activation which were induced by the addition of TNF-a in hBMSCs.…”

Section: Discussionmentioning

confidence: 99%

Role of IRAK1 on TNF-induced Proliferation and NF-?B Activation in Human Bone Marrow Mesenchymal Stem Cells

Kim

Cho

Lee

et al. 2012

Cell Physiol Biochem

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In this study, we determined the effect of TNF-α on hBMSCs proliferation as well as the role of IL-1 receptor-associated kinase 1 (IRAK1) on TNF-α signaling. Western blot analysis revealed that TNF-α treatment increased the phosphorylation of IRAK1 in hBMSCs. The downregulation of IRAK1 inhibited TNF-α-induced NF-ĸB activation and COX-2 expression. TNF-α treatment increased hBMSCs proliferation in a dose-dependent manner and increased ERK, JNK, and NF-ĸB activity. U0126, an ERK inhibitor, decreased hBMSCs proliferation and significantly blocked TNF-α -induced hBMSCs proliferation. In cells with IRAK1 or TRADD downregulation, the U0126 treatment inhibited hBMSCs proliferation and significantly suppressed TNF-α-induced hBMSCs proliferation. The downregulation of IRAK1 or TRADD inhibited TNF-α-induced ERK and JNK activation, and hBMSCs proliferation. Inhibition of NF-ĸB by decoy oligonucleotides reduced the TNF-α-induced hBMSCs proliferation. Immunoprecipitation analysis showed that IRAK1 does not physically interact with TNF receptor 1 (TNFR1) even in the presence of TNF-α. Suppression of IRAK1 binding protein (IRAK1BP1) inhibited TNF-α-induced increase of the proliferation and ERK1 phosphorylation of hBMSCs in the presence of TNF-α. Our data indicate that TNF-α modulates hBMSCs proliferation through ERK signaling pathways, and that IRAK1 plays an important role in TNF-α-induced NF-ĸB activation in hBMSCs.

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Section: Discussionmentioning

confidence: 99%

Role of IRAK1 on TNF-induced Proliferation and NF-?B Activation in Human Bone Marrow Mesenchymal Stem Cells

Kim

Cho

Lee

et al. 2012

Cell Physiol Biochem

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“…Refer to Benson et al (2010) report and our previous report (Zou, Chan, Shelley, & Yoder, 2006;Zou, Hu, & Wu, 2007). In summary, for primitive erythroid progenitor (BFU-E and CFU-E) assays, mouse BMMNCs were cultured in 0.9% methylcellulose, 15% FCS with SCF (100 ng/ml), IL-3 (1 ng/ml), and Epo (5 U/ml).…”

Section: Assays For Hematopoietic Progenitorsmentioning

confidence: 99%

Hematopoietic stem/progenitor cell differentiation towards myeloid lineage is modulated by LIGHT/LIGHT receptor signaling

Chen

Liu

et al. 2017

Journal Cellular Physiology

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The cytokine LT-related inducible ligand that competes for glycoprotein D binding to herpesvirus entry mediator on T cells (LIGHT) is a member of the tumor necrosis factor (TNF) superfamily. It is expressed primarily on activated T lymphocytes, and detectable on monocytes, granulocytes, and immune dendritic cells. It mainly plays a role in immune regulation including T cell activation and dendritic cell maturation. We recently reported its role as an inducer in embryonic stem cell differentiation, but its role in regulation of adult stem cell has not been defined. In the present study, we examined the expression of LIGHT receptor in Lin c-kit Sca-1 hematopoietic stem/progenitor cells (HSC/HPCs). We found that HSC express HVEM, a LIGHT receptor, on its surface. We further identified the role of LIGHT in promoting myeloid differentiation of HSCs driven by granulocyte-monocyte colony stimulating factor (GM-CSF). Further studies showed that LIGHT enhances both GM-CSF and GM-CSF receptor (GM-CSFR) expression in HSCs. LIGHT stimulation increases PU.1 expression in HSC/HPCs. In vivo administration of LIGHT increases the colony-forming unit-granulocyte/monocyte (CFU-GM) colony formation and plasma GM-CSF level. Altogether, the data suggest LIGHT promote myeloid differentiation of HSC/HPCs.

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“…In the serum of mice with hematopoietic dysfunction, PH ameliorated increases in the levels of TNF-α and MIP-1α. TNF-α is a negative regulator of hematopoiesis and can inhibit the proliferation of HPCs [46] and reduce the proliferation and differentiation of HSCs [47]. MIP-1α, derived from monocytes, neutrophils, and lymphocytes, can inhibit HSPCs proliferation [48].…”

Section: Discussionmentioning

confidence: 99%

The Involvement of Macrophage Colony Stimulating Factor on Protein Hydrolysate Injection Mediated Hematopoietic Function Improvement

Wang

Zhang

Meng

et al. 2021

Cells

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Protein hydrolysate injection (PH) is a sterile solution of hydrolyzed protein and sorbitol that contains 17 amino acids and has a molecular mass of 185.0–622.0 g/mol. This study investigated the effect of PH on hematopoietic function in K562 cells and mice with cyclophosphamide (CTX)-induced hematopoietic dysfunction. In these myelosuppressed mice, PH increased the number of hematopoietic cells in the bone marrow (BM) and regulated the concentration of several factors related to hematopoietic function. PH restored peripheral blood cell concentrations and increased the numbers of hematopoietic stem cells and progenitor cells (HSPCs), B lymphocytes, macrophages, and granulocytes in the BM of CTX-treated mice. Moreover, PH regulated the concentrations of macrophage colony stimulating factor (M-CSF), interleukin (IL)-2, and other hematopoiesis-related cytokines in the serum, spleen, femoral condyle, and sternum. In K562 cells, the PH-induced upregulation of hematopoiesis-related proteins was inhibited by transfection with M-CSF siRNA. Therefore, PH might benefit the BM hematopoietic system via the regulation of M-CSF expression, suggesting a potential role for PH in the treatment of hematopoietic dysfunction caused by cancer therapy.

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Loss of SIMPL compromises TNF-α-dependent survival of hematopoietic progenitors

Cited by 4 publications

References 48 publications

Role of IRAK1 on TNF-induced Proliferation and NF-?B Activation in Human Bone Marrow Mesenchymal Stem Cells

Role of IRAK1 on TNF-induced Proliferation and NF-?B Activation in Human Bone Marrow Mesenchymal Stem Cells

Hematopoietic stem/progenitor cell differentiation towards myeloid lineage is modulated by LIGHT/LIGHT receptor signaling

The Involvement of Macrophage Colony Stimulating Factor on Protein Hydrolysate Injection Mediated Hematopoietic Function Improvement

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