Effects of LTB4 and Ca++ ionophore A23187 on the release by human alveolar macrophages of factors controlling fibroblast functions

Polla, B. S.; Rochemonteix, B de; Junod, A F; Dayer, J.-M.

doi:10.1016/0006-291x(85)90188-3

Cited by 4 publications

(1 citation statement)

References 16 publications

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“…It has been reported that LTB4 stimulated the cell proliferation in many cancers through binding with their corresponding receptors [ 22 , 23 ] and was also involved in tumor angiogenesis [ 24 ]. In lung cancer, the expression of LTB4 was found to increase with progression of tumor [ 25 ] and modulated lung fibroblast functions [ 26 ]. Interestingly, PTGR1 was a key enzyme in the regulation of inflammatory mediator LTB4 [ 27 , 28 ], but the biological function of PTGR1 remains largely unknown.…”

Section: Discussionmentioning

confidence: 99%

High Expression of PTGR1 Promotes NSCLC Cell Growth via Positive Regulation of Cyclin-Dependent Protein Kinase Complex

Huang

Zhou

Zhang

et al. 2016

BioMed Research International

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Lung cancer has been the most common cancer and the main cause of cancer-related deaths worldwide for several decades. PTGR1 (prostaglandin reductase 1), as a bifunctional enzyme, has been involved in the occurrence and progression of cancer. However, its impact on human lung cancer is rarely reported. In this study, we found that PTGR1 was overexpressed in lung cancer based on the analyses of Oncomine. Moreover, lentivirus-mediated shRNA knockdown of PTGR1 reduced cell viability in human lung carcinoma cells 95D and A549 by MTT and colony formation assay. PTGR1 depletion led to G2/M phase cell cycle arrest and increased the proportion of apoptotic cells in 95D cells by flow cytometry. Furthermore, silencing PTGR1 in 95D cells resulted in decreased levels of cyclin-dependent protein kinase complex (CDK1, CDK2, cyclin A2, and cyclin B1) by western blotting and then PTGR1 is positively correlated with cyclin-dependent protein by using the data mining of the Oncomine database. Therefore, our findings suggest that PTGR1 may play a role in lung carcinogenesis through regulating cell proliferation and is a potential new therapeutic strategy for lung cancer.

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Section: Discussionmentioning

confidence: 99%

High Expression of PTGR1 Promotes NSCLC Cell Growth via Positive Regulation of Cyclin-Dependent Protein Kinase Complex

Huang

Zhou

Zhang

et al. 2016

BioMed Research International

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Regulation of Macrophage-Derived Fibroblast Growth Factor Release by Arachidonate Metabolites

Phan¹,

McGarry²,

Loeffler³

et al. 1987

Journal of Leukocyte Biology

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The macrophage is a source of many mediators with direct and indirect fibrogenic potential. In this study, release of macrophage-derived fibroblast growth factor (MDGF) activity by murine peritoneal macrophages is examined with regard to its regulation by arachidonate metabolites. Upon stimulation with 10 micrograms/ml lipopolysaccharide (LPS), resident peritoneal macrophages from CBA/J mice released MDGF activity into media rapidly, reaching maximal levels in approximately 1 h. Lysates of these stimulated cells also revealed significantly increased cell-associated MDGF activity, composing 45% of the total assayable activity. This activity, as assayed by radioactive thymidine incorporation by primary cultures of rat lung fibroblasts, was separable from interleukin-1 (IL-1) activity by reverse phase high performance liquid chromatography (HPLC). Furthermore, purified murine IL-1 had no MDGF activity in this assay system. This stimulated MDGF release was enhanced by the cyclooxygenase inhibitors indomethacin, ibuprofen, and aspirin at micromolar concentrations, but inhibited in a dose-dependent manner by prostaglandin E2 (PGE2). On the other hand, nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor was inhibitory at 0.1 and 0.4 microM but not at 2.5 microM. Zymosan-stimulated macrophages also markedly increased MDGF release, albeit with a different time course which was characterized by a delay of approximately 7 h before peak levels were attained. Such stimulation, which is known to cause increased lipoxygenase activity, was also inhibited by 0.5 microM NDGA. In contrast, the lipoxygenase pathway products leukotrienes B4 (LTB4) and C4 (LTC4) stimulated MDGF release in a dose-dependent (10(-10)-10(-8) M) manner, with LTC4 being more potent on a per unit dose basis. Stimulation by LTC4 was inhibited by the putative leukotriene receptor antagonist, FPL55712, while LTD4 and LTE4 did not stimulate MDGF release, thus suggesting the mediation of this effect by specific LTC4 receptors. These data suggest also that products of the cyclooxygenase and lipoxygenase pathways are potentially important both as exogenous (ie, derived from cells other than the macrophage itself) and auto- or self-regulators of macrophage MDGF release. This, in turn, implies that cyclooxygenase products are antifibrogenic and important in maintaining or returning to the quiescent or normal state, whereas the lipoxygenase products are profibrogenic and important in induction of fibrosis or wound-healing and tissue repair. Any alteration in the balance between these two pathways may result in either a desirable or a harmful outcome.

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Cellular Calcium: Cell Growth and Differentiation

Fujita¹,

Nakao²

1988

Calcium in Human Biology

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Effects of LTB4 and Ca++ ionophore A23187 on the release by human alveolar macrophages of factors controlling fibroblast functions

Cited by 4 publications

References 16 publications

High Expression of PTGR1 Promotes NSCLC Cell Growth via Positive Regulation of Cyclin-Dependent Protein Kinase Complex

High Expression of PTGR1 Promotes NSCLC Cell Growth via Positive Regulation of Cyclin-Dependent Protein Kinase Complex

Regulation of Macrophage-Derived Fibroblast Growth Factor Release by Arachidonate Metabolites

Cellular Calcium: Cell Growth and Differentiation

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