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Effect of Nitric Oxide Donors on Human Lung Fibroblast Proliferation In Vitro*

Xiangder Liu, MD; Yunkui K. Zhu, MD; Hangjun Wang, MD; Tadashi Kohyama, MD; Fuqiang Wen, MD; Stephen I. Rennard, MD, FCCP
Author and Funding Information

*From the University of Nebraska Medical Center, Omaha, NE.

Correspondence to: Xiangder Liu, MD, Pulmonary and Critical Care Medicine Section, Department of Internal Medicine, University of Nebraska Medical Center, 600 South 42nd St, Omaha, NE 68198-5300



Chest. 2001;120(1_suppl):S13-S14. doi:10.1378/chest.120.1_suppl.S13
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Nitric oxide (NO) is an intracellular messenger molecule involved in modulating cell proliferation and apoptosis in a variety of cells. The present study was designed to determine if NO modulated the proliferation of human lung fibroblasts. Human fetal lung fibroblasts (HFL-1) were maintained in cell culture in Dulbecco’s Modified Eagle’s Medium in the presence of 4% fetal calf serum. Cell proliferation was determined by enumerating cells with a Coulter counter. Inhibition of endogenous NO production by N-nitro-L-arginine methylester had no effect on HFL-1 cell proliferation. Three different NO-generating compounds were evaluated. Sodium nitroprusside (SNP) and diethylenetetra-amine NONOate were both found to inhibit cell proliferation in a concentration dependent manner. In contrast, 5-amino-3-3(4-morpholiny)-1,2.3-oxadiazolium chloride (SIN-1) had no effect on HFL-1 cell proliferation (Table 1).

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