Histamine stimulation of MMP-1(collagenase-1) secretion and gene expression in gastric epithelial cells: Role of EGFR transactivation and the MAP kinase pathway

Ancha, Hanumantha R.; Kurella, Ravi; Stewart, Charles A.; Damera, Gautam; Ceresa, Brian P.; Harty, Richard F.

doi:10.1016/j.biocel.2007.06.003

Cited by 21 publications

(15 citation statements)

References 27 publications

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“…The precise mechanisms regulating how the stimulation of H1 receptors induces the activation of JAK2 in keratinocytes should be investigated in the future. It is reported that the stimulation of certain G-protein-coupled receptors including histamine receptors transactivates epidermal growth factor receptor (EGFR) or generates reactive oxygen species (ROS) [40,41], and that both signals can activate JAK2 [33,40,42]. However, neither the EGFR tyrosine kinase inhibitor AG1478 nor the antioxidant diphenyleneiodonium suppressed the JAK2 autophosphorylation induced by histamine in human keratinocytes (data not shown).…”

Section: Discussionmentioning

confidence: 81%

Histamine induces human β-defensin-3 production in human keratinocytes

Ishikawa

Kanda

Hau

et al. 2009

Journal of Dermatological Science

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Section: Discussionmentioning

confidence: 81%

Histamine induces human β-defensin-3 production in human keratinocytes

Ishikawa

Kanda

Hau

et al. 2009

Journal of Dermatological Science

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“…This ligand-dependent mechanism involves several MMPs, including MMP-1 MMP-2, MMP-7, MMP-9 and MMP-14 and has been shown to be involved in GPCR mediated transactivation of multiple PTKRs such as EGFR, vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR) (Overland and Insel 2015;Ancha et al 2007;Carbajal et al 2011;Hao et al 2004). In rat mesenteric arteries, phenylephrine stimulated EGFR transactivation was dependent on MMP-7 as the response was blocked by the MMP inhibitor GM6001 as well as MMP-7 specific antibodies.…”

Section: Gpcr Transactivation Of Protein Tyrosine Kinase Receptorsmentioning

confidence: 99%

Insights into cellular signalling by G protein coupled receptor transactivation of cell surface protein kinase receptors

Chaplin

Thach

Hollenberg

et al. 2017

J. Cell Commun. Signal.

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G protein coupled receptor (GPCR) signalling is mediated by transactivation independent and transactivation dependent pathways. GPCRs transactivate protein tyrosine kinase receptors (PTKRs) and protein serine/threonine kinase receptors (PS/TKR). Since the initial observations of transactivation dependent signalling, there has been an effort to understand the mechanisms behind this phenomena. GPCR signalling has evolved to include biased signalling. Biased signalling, whereby selected ligands can activate the same GPCR that can generate multiple signals, but drive only a unique response. To date, there has been no focus on the ability of biased agonists to activate the PTKR and PS/TKR transactivation pathways differentially. As such, this represents a novel direction for future research. This review will discuss the main mechanisms of GPCR mediated receptor transactivation and the pathways involved in intracellular responses.

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“…These biochemical events may result through the activation of G protein–coupled receptors (GPCRs) or calcium-dependent signaling pathways. A study by Ancha et al showed the role of H2 receptor, a GPCR, in the regulation of MMP-1 expression and secretion in cultured gastric cells [17]. Savina et al demonstrated that increased intracellular calcium concentrations in K562 leukemia cells trigger Rab11-mediated fusion of MVBs with the plasma membrane and release exosomes [18].…”

Section: Introductionmentioning

confidence: 99%

Extracellular Membrane Vesicles Derived from 143B Osteosarcoma Cells Contain Pro-Osteoclastogenic Cargo: A Novel Communication Mechanism in Osteosarcoma Bone Microenvironment

Garimella

Washington

Isaacson

et al. 2014

Translational Oncology

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The bone microenvironment (BME) is the main hub of all skeletal related pathological events in osteosarcoma leading to tumor induced bone destruction, and decreasing overall bone quality and bone strength. The role of extra-cellular membrane vesicles (EMVs) as mediators of intercellular communication in modulating osteosarcoma-BME is unknown, and needs to be investigated. It is our hypothesis that osteosarcoma-EMVs contain pro-osteoclastogenic cargo which increases osteoclastic activity, and dysregulated bone remodeling in the osteosarcoma-BME. In this study, EMVs were isolated from the conditioned media of 143B and HOS human osteosarcoma cell cultures using differential ultracentrifugation. Nano-particle tracking analysis determined EMVs in the size range of 50-200 nm in diameter. The EMV yield from 143B cells was relatively higher compared to HOS cells. Transmission electron microscopy confirmed the ultrastructure of 143B-EMVs and detected multivesicular bodies. Biochemical characterization of 143B-EMVs detected the expression of bioactive pro-osteoclastic cargo including matrix metalloproteinases-1 and -13 (MMP-1, -13), transforming growth factor-β (TGF-β), CD-9, and receptor activator of nuclear factor kappa-β ligand (RANKL). Detection of a protein signature that is uniquely pro-osteoclastic in 143B-EMVs is a novel finding, and is significant as EMVs represent an interesting mechanism for potentially mediating bone destruction in the osteosarcoma-BME. This study further demonstrates that 143B cells actively mobilize calcium in the presence of ionomycin, and forskolin, and induce cytoskeleton rearrangements leading to vesicular biogenesis. In conclusion, this study demonstrates that 143B osteosarcoma cells generate EMVs mainly by mechanisms involving increased intracellular calcium or cAMP levels, and contain pro-osteoclastic cargo.

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Histamine stimulation of MMP-1(collagenase-1) secretion and gene expression in gastric epithelial cells: Role of EGFR transactivation and the MAP kinase pathway

Cited by 21 publications

References 27 publications

Histamine induces human β-defensin-3 production in human keratinocytes

Histamine induces human β-defensin-3 production in human keratinocytes

Insights into cellular signalling by G protein coupled receptor transactivation of cell surface protein kinase receptors

Extracellular Membrane Vesicles Derived from 143B Osteosarcoma Cells Contain Pro-Osteoclastogenic Cargo: A Novel Communication Mechanism in Osteosarcoma Bone Microenvironment

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