From growth factor dependence to growth factor responsiveness: The genesis of an alveolar macrophage cell line

Helmke, Ronald J.; Boyd, R L; German, Victor F.; Mangos, J. A.

doi:10.1007/bf02620974

Cited by 106 publications

(68 citation statements)

References 21 publications

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“…The results were obtained in rat alveolar macrophages as these cell lines are a reliable source of iNOS [22,23]. Differences in the NOS systems have been found between cell types of animals of different species and humans [9].…”

Section: Discussionmentioning

confidence: 88%

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Inhibition of nitric oxide synthase by nasal decongestants

Westerveld¹,

Voss²,

Hee³

et al. 2000

Eur Respir J

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The nasal decongestants oxymetazoline and xylometazoline are frequently used in the topical treatment of rhinitis and sinusitis. As nitric oxide (NO) is thought to play a role in inflammation of the upper respiratory tract, the aim of this study was to examine the in vitro effects of these compounds on the activity and the expression of NO producing enzymes, including the inducible form of NO synthase (iNOS) and the constitutive isoform of NO synthase (cNOS).Experiments concerning the effects of both compounds on enzymatic activity and enzyme induction of iNOS were performed in a lipopolysaccharide (LPS) induced rat alveolar macrophage cell line (NR8383) using the Griess assay and the 3 H-citrulline assay respectively. The effects on cNOS were examined in fresh rat synaptosomes using the 3 H-citrulline assay. The direct scavenging properties of both compounds were investigated using a amperometric NO sensor.Oxymetazoline and xylometazoline were shown to have a dose dependent inhibitory effect on total iNOS activity indicated by nitrite/nitrate formation in the Griess assay. This effect was found to be due to an inhibition of induction of the enzyme rather than inhibition of the enzyme activity, as was investigated in two separate experiments using the 3 H-citrulline assay. Inhibition of cNOS was moderate and in the same order of magnitude as the inhibition of enzymatic iNOS activity. Direct scavenging of NO could not be detected.As constitutive nitric oxide synthase activity is thought to serve beneficial physiological functions, and exaggerated inducible nitric oxide synthase activity may cause exacerbation of the inflammatory process, pharmacological treatment influencing the nitric oxide generating system should focus on inhibition of inducible nitric oxide synthase alone. The specific characteristics of these decongestants in vitro suggests suitability for this application and may indicate an additional beneficial effect in the treatment of upper respiratory tract inflammation. Eur Respir J 2000; 16: 437±444.

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Section: Discussionmentioning

confidence: 88%

“…A rat pulmonary alveolar macrophage cell line, NR8383, was used as the source of iNOS [22,23]. Cells were maintained in culture at a floating cell concentration of 10 5 cells .…”

Section: Cell Culture and Induction Of Nitric Oxide Synthasementioning

confidence: 99%

Inhibition of nitric oxide synthase by nasal decongestants

Westerveld¹,

Voss²,

Hee³

et al. 2000

Eur Respir J

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“…NR8383 is a well-characterized, semi-adherent macrophage cell line that is derived from normal Sprague-Dawley rat lung (15). The NR8383 cell line was purchased from American Type Culture Collection (Manassas, VA) and was maintained in DMEM/Ham's F-12 (DMEM-F12; Life Technologies BRL, Gaithersburg, MD) with 100 U/ml penicillin and 10% fetal calf serum (FCS; Trace Biosciences, Melbourne, Victoria, Australia).…”

Section: Macrophage Culturementioning

confidence: 99%

Interferon-γ Augments Acute Macrophage-Mediated Renal Injury Via a Glucocorticoid-Sensitive Mechanism

Ikezumi¹,

Atkins²,

Nikolic-Paterson³

2003

Journal of the American Society of Nephrology

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Abstract. Macrophages have been implicated in causing renal injury in both human and experimental kidney disease. The aim of the current study was to determine whether modulating the state of macrophage activation directly affects the capacity of these cells to cause renal injury. This was investigated using an adoptive transfer model in which macrophage activation can be manipulated in vitro, using interferon-␥ (IFN-␥) or dexamethasone (Dex), and then macrophage-mediated renal injury determined in vivo. In this model, rats were made leukopenic by administration of cyclophosphamide (CyPh). Two days later (day 0), animals were injected with sheep anti-GBM serum followed by a single injection of rat NR8383 macrophages on day 1 and then killed 3 or 24 h after cell transfer. NR8383 macrophages were incubated IFN-␥ and/or Dex before adoptive transfer into animals. Induction of proteinuria and glomerular cell proliferation (PCNAϩ cells) in this model was dependent on transfer of NR8383 macrophages. Exposure of macrophages to IFN-␥ for 18 h (but not 3 h) before transfer caused a twofold increase in the degree of proteinuria and glomerular cell proliferation compared with unstimulated cells

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“…This cell line was initiated from a normal adult male Sprague-Dawley rat and NR8383 cells exhibit the phenotype of mature macrophages, including phagocytic capabilities, nonspecific esterase activity, Fc receptor expression, oxidative burst potential, capacity to secrete interleukin-1 (IL-1), TNF-␣, and IL-6, and a replicative response to exogenous growth factors [40][41][42]. NR8383 cells were passaged in vitro in F12 Nutrient Mixture (GIBCO-BRL, Grand Island, NY) supplemented with 15% heat-inactivated fetal calf serum (Summit, Ft. Collins, CO), 100 units/mL penicillin, 100 µg/mL streptomycin, and 0.25 µg/mL Fungizone at 37°C in a humidified incubator with 5% (v/v) CO 2 .…”

Section: Cellsmentioning

confidence: 99%