The transcriptome of the human mast cell leukemia cells HMC-1.2: an approach to identify specific changes in the gene expression profile in KitD816V systemic mastocytosis

Haenisch, Britta; Herms, Stefan; Molderings, Gerhard J.

doi:10.1007/s12026-013-8391-1

Cited by 6 publications

(3 citation statements)

References 16 publications

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“…This database was last accessed in March 2023. These data were supplemented with data on the expression of proteins in human MCs which had been investigated by, and were published in, Liang et al ( 2018 ), Motakis et al ( 2014 ), Haenisch et al ( 2013 ), Okayama ( 2005 ), Halloran et al ( 2019 ), and Babina et al ( 2004 ). In addition, the PubMed database was searched with the phrase human “mast cell*” mediator* .…”

Section: Methodsmentioning

confidence: 99%

A survey of the currently known mast cell mediators with potential relevance for therapy of mast cell-induced symptoms

Molderings

Afrin

2023

Naunyn-Schmiedeberg's Arch Pharmacol

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Mast cells (MCs) occupy a central role in immunological as well as non-immunological processes as reflected in the variety of the mediators by which MCs influence other cells. Published lists of MC mediators have all shown only subsets—usually quite small—of the full repertoire. The full repertoire of MC mediators released by exocytosis is comprehensively compiled here for the first time. The compilation of the data is essentially based on the largely cytokine-focused database COPE®, supplemented with data on the expression of substances in human MCs published in several articles, plus extensive research in the PubMed database. Three hundred and ninety substances could be identified as mediators of human MCs which can be secreted into the extracellular space by activation of the MC. This number might still be an underestimate of the actual number of MC mediators since, in principle, all substances produced by MCs can become mediators because of the possibility of their release by diffusion into the extracellular space, mast cell extracellular traps, and intercellular exchange via nanotubules. When human MCs release mediators in inappropriate manners, this may lead to symptoms in any or all organs/tissues. Thus, such MC activation disorders may clinically present with a myriad of potential combinations of symptoms ranging from trivial to disabling or even life-threatening. The present compilation can be consulted by physicians when trying to gain clarity about MC mediators which may be involved in patients with MC disease symptoms refractory to most therapies.

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Section: Methodsmentioning

confidence: 99%

A survey of the currently known mast cell mediators with potential relevance for therapy of mast cell-induced symptoms

Molderings

Afrin

2023

Naunyn-Schmiedeberg's Arch Pharmacol

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“…Immortalized leukemic cell lines, like the HMC-1 line usually contain oncogenic mutations, e.g. in the KIT gene (18), which influences studies on MC biology. Furthermore, the HMC-1 cell line does not express a functional FcεR1 on the cell surface impeding studies on IgE receptor signaling.…”

Section: Introductionmentioning

confidence: 99%

Transformation of primary murine peritoneal mast cells by constitutive KIT activation as a result of lostCdkn2a/Arfexpression

Capellmann

Sonntag

Schueler

et al. 2023

Preprint

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Mast cells (MCs) are immune cells of the myeloid lineage distributed in tissues throughout the body. Phenotypically, they are a heterogeneous group characterized by different protease repertoires stored in secretory granules and differential presence of receptors. To adequately address aspects of MC biology either primary MCs isolated from human or mouse tissue or different human MC lines, like HMC-1.1 and -1.2, or rodent MC lines like L138.8A or RBL-2H3 are frequently used. Nevertheless, cellular systems to study MC functions are very limited. We have generated a murine connective tissue-like MC line, termed PMC-306, derived from primary peritoneal MCs (PMCs), which spontaneously transformed. We analyzed PMC-306 cells regarding MC surface receptor expression, effector functions and respective signaling pathways, and found that the cells reacted very similar to primary wildtype (WT) PMCs. In this regard, stimulation with MAS-related G-protein-coupled receptor member B2 (MRGPRB2) ligands induced respective signaling and effector functions. Furthermore, PMC-306 cells revealed significantly accelerated cell cycle progression, which however was still dependent on IL-3 and stem cell factor (SCF). Phenotypically, PMC-306 cells adopted an immature connective tissue-like MCs appearance. The reason for immortalization most likely is the loss of the two critical cell cycle regulators Cdkn2a/INK4A and Arf/p19, respectively. The loss of Cdkn2a and Arf expression could be mimicked in primary bone marrow-derived mast cells (BMMCs) by SCF supplementation strongly arguing for an involvement of KIT activation in the transformation process. Hence, this new cell line might be a useful tool to study further aspects of PMC function and to address tumorigenic processes associated with MC leukemia.

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“…Immortalized leukemic cell lines, like the HMC-1 lines usually contain oncogenic mutations, e.g. in the KIT gene ( 18 ), which influences studies on MC biology. Furthermore, the HMC-1 cell lines do not express a functional FcεR1 on the cell surface impeding studies on IgE receptor signaling.…”

Section: Introductionmentioning

confidence: 99%

Transformation of primary murine peritoneal mast cells by constitutive KIT activation is accompanied by loss of Cdkn2a/Arf expression

et al. 2023

View full text Add to dashboard Cite

Mast cells (MCs) are immune cells of the myeloid lineage distributed in tissues throughout the body. Phenotypically, they are a heterogeneous group characterized by different protease repertoires stored in secretory granules and differential presence of receptors. To adequately address aspects of MC biology either primary MCs isolated from human or mouse tissue or different human MC lines, like HMC-1.1 and -1.2, or rodent MC lines like L138.8A or RBL-2H3 are frequently used. Nevertheless, cellular systems to study MC functions are very limited. We have generated a murine connective tissue-like MC line, termed PMC-306, derived from primary peritoneal MCs (PMCs), which spontaneously transformed. We analyzed PMC-306 cells regarding MC surface receptor expression, effector functions and respective signaling pathways, and found that the cells reacted very similar to primary wildtype (WT) PMCs. In this regard, stimulation with MAS-related G-protein-coupled receptor member B2 (MRGPRB2) ligands induced respective signaling and effector functions. Furthermore, PMC-306 cells revealed significantly accelerated cell cycle progression, which however was still dependent on interleukine 3 (IL-3) and stem cell factor (SCF). Phenotypically, PMC-306 cells adopted an immature connective tissue-like MCs appearance. The observation of cellular transformation was accompanied by the loss of Cdkn2a and Arf expression, which are both described as critical cell cycle regulators. The loss of Cdkn2a and Arf expression could be mimicked in primary bone marrow-derived mast cells (BMMCs) by sustained SCF supplementation strongly arguing for an involvement of KIT activation in the regulation of Cdkn2a/Arf expression. Hence, this new cell line might be a useful tool to study further aspects of PMC function and to address tumorigenic processes associated with MC leukemia.

show abstract

The transcriptome of the human mast cell leukemia cells HMC-1.2: an approach to identify specific changes in the gene expression profile in KitD816V systemic mastocytosis

Cited by 6 publications

References 16 publications

A survey of the currently known mast cell mediators with potential relevance for therapy of mast cell-induced symptoms

A survey of the currently known mast cell mediators with potential relevance for therapy of mast cell-induced symptoms

Transformation of primary murine peritoneal mast cells by constitutive KIT activation as a result of lostCdkn2a/Arfexpression

Transformation of primary murine peritoneal mast cells by constitutive KIT activation is accompanied by loss of Cdkn2a/Arf expression

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