Heparin and PGE2 inhibit DNA synthesis in human airway smooth muscle cells in culture

Johnson, Patricia A.; Armour, C. L.; Carey, David; Black, Judith L.

doi:10.1152/ajplung.1995.269.4.l514

Cited by 73 publications

(84 citation statements)

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“…However, it may also activate other pathways, which could inhibit another cytokine. PGE 2 decreases FBS-induced proliferation of ASM and fibroblasts (9,28). Interestingly, we found that the prostaglandins did not have any pro-or antiproliferative effects on quiesced mesenchymal cells, suggesting that the effects on ECM proteins and cytokine were independent of an effect on cell number.…”

Section: L247mentioning

confidence: 61%

Prostaglandins but not leukotrienes alter extracellular matrix protein deposition and cytokine release in primary human airway smooth muscle cells and fibroblasts

Burgess

Brock

et al. 2012

American Journal of Physiology-Lung Cellular and Molecular Phys

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Prostaglandins but not leukotrienes alter extracellular matrix protein deposition and cytokine release in primary human airway smooth muscle cells and fibroblasts. Am J Physiol Lung Cell Mol Physiol 303: L239-L250, 2012. First published May 25, 2012 doi:10.1152/ajplung.00097.2012.-Eicosanoids are lipid-signaling mediators released by many cells in response to various stimuli. Increasing evidence suggests that eicosanoids such as leukotrienes and prostaglandins (PGs) may directly mediate remodeling. In this study, we assessed whether these substances could alter extracellular matrix (ECM) proteins and the inflammatory profiles of primary human airway smooth muscle cells (ASM) and fibroblasts. PGE 2 decreased both fibronectin and tenascin C in fibroblasts but only fibronectin in ASM. PGD 2 decreased both fibronectin and tenascin C in both ASM and fibroblasts, whereas PGF 2␣ had no effect on ECM deposition. The selective PGI2 analog, MRE-269, decreased fibronectin but not tenascin C in both cell types. All the PGs increased IL-6 and IL-8 release in a dose-dependent manner in ASM and fibroblasts. Changes in ECM deposition and cytokine release induced by prostaglandins in both ASM and fibroblasts were independent of an effect on cell number. Neither the acute nor repeated stimulation with leukotrienes had an effect on the deposition of ECM proteins or cytokine release from ASM or fibroblasts. We concluded that, collectively, these results provide evidence that PGs may contribute to ECM remodeling to a greater extent than leukotrienes in airway cells.

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Section: L247mentioning

confidence: 61%

Prostaglandins but not leukotrienes alter extracellular matrix protein deposition and cytokine release in primary human airway smooth muscle cells and fibroblasts

Burgess

Brock

et al. 2012

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Kaneko et al demonstrated that, although PGE 1 inhibited the growth of human dermal keratinocytes, PGI 1 analogs and PGE 1 enhanced the proliferation of dermal fibroblasts [31]. Moreover, it has been demonstrated that PGE 2 had a biphasic effect on airway smooth muscle cells, with 10 Ϫ6 M causing inhibition and 10 Ϫ7 M causing an increase in DNA synthesis [32]. Although PGE production has been shown to be a self-regulated response that serves to limit the unopposed humoral stimulation of myelopoiesis [24], our data clearly demonstrate that PGE 2 could be a growth-regulatory effector molecule downstream of NO.…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide enhances the growth of U937 human leukemic cells through a cyclooxygenase-mediated pathway

Jea

Liu

Wang

et al. 1998

Journal of Leukocyte Biology

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The mechanisms of exogenous nitric oxide (NO)-enhanced growth of the U937 human myeloid leukemic cells were examined using sodium nitroprusside (SNP) as a NO donor. Treatment with 0.1 mM SNP for 72 h caused a 45 ؎ 2% increase in U937 cell growth with significantly increased S/G 2 ؉M-phase and decreased G 0 /G 1 -phase of the cell cycle. The growth-enhancing effect of SNP was blocked by indomethacin, a cyclooxygenase inhibitor, but not by H7, a broad spectrum kinase inhibitor, or PD98059, a mitogenactivated protein kinase inhibitor. SNP treatment resulted in a dose-dependent increase in prostaglandin E 2 (PGE 2 ) production. Furthermore, the addition of exogenous PGE 2 not only enhanced U937 cell growth but restored the indomethacin-inhibited mitogenic effect of SNP. We suggest that NO can enhance cell growth through activating the cyclooxygenase pathway and that PGE 2 may be an effector molecule for NO-regulated cell proliferation. Our data provide a mechanistic insight into the regulatory role of NO in myelopoiesis. J. Leukoc. Biol. 64: 451-458; 1998.

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“…Human ASM cells were obtained from subjects without and with asthma by methods adapted from those previously described (26,29), in accordance with procedures approved by the Sydney South West Area Health Service Ethics Committee and the Human Ethics Committee of the University of Sydney. A minimum of three different primary cell lines was used for each experiment.…”

Section: Methodsmentioning

confidence: 99%

Effect of IL-6 trans-signaling on the pro-remodeling phenotype of airway smooth muscle

Ammit¹,

Moir²,

Oliver³

et al. 2007

American Journal of Physiology-Lung Cellular and Molecular Phys

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Heparin and PGE2 inhibit DNA synthesis in human airway smooth muscle cells in culture

Cited by 73 publications

References 0 publications

Prostaglandins but not leukotrienes alter extracellular matrix protein deposition and cytokine release in primary human airway smooth muscle cells and fibroblasts

Prostaglandins but not leukotrienes alter extracellular matrix protein deposition and cytokine release in primary human airway smooth muscle cells and fibroblasts

Nitric oxide enhances the growth of U937 human leukemic cells through a cyclooxygenase-mediated pathway

Effect of IL-6 trans-signaling on the pro-remodeling phenotype of airway smooth muscle

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