Key result
Nitric oxide exposure in mouse macrophages up-regulated 81 genes related to signaling, apoptosis, and inflammation, including Gucy1a3, Pkcα, and Lck.
This study identifies 81 NO-dependent genes in murine macrophages, highlighting specific pathways in signaling, apoptosis, and inflammation.
These murine macrophage findings warrant clinical caution; hypothesis-generating for NO pathways in human cardiovascular inflammation.
Nitric oxide (NO) has been known to play important roles in numerous physiologic processes including neurotransmission, vasorelaxation, and cellular apoptosis. Using a mouse cDNA gene chip, we examined expression patterns and time course of NO‐dependent genes in mouse macrophage RAW264.7 cells. Genes shown to be up‐regulated more than two fold or at least at two serial time points were further selected and validated by RT‐PCR. Finally, 81 selected genes were classified by function as signaling, apoptosis, inflammation, transcription, translation, ionic homeostasis and metabolism. Among those, genes related with signaling, apoptosis and inflammation, such as guanylate cyclase 1, soluble, alpha3 (Gucy1a3); protein kinase C, alpha (Pkcα); lymphocyte protein tyrosine kinase (Lck); BCL2/adenovirus E1B 19 kDa‐interacting protein (Bnip3); apoptotic protease activating factor 1 (Apaf1); X‐linked inhibitor of apoptosis (Xiap); cyclin G1 (Ccng1); chemokine (C‐C motif) ligand 4 (Ccl4); B cell translocation gene 2, anti‐proliferative (Btg2); lysozyme 2 (Lyz2); secreted phosphoprotein 1 (Spp1); heme oxygenase (decycling) 1 (Hmox1); CD14 antigen (Cd14); and granulin (Grn) may play important roles in NO‐dependent responses in murine macrophages.
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Nan et al. (2008) studied this question. Nitric oxide (NO) was evaluated on Gene expression patterns and time course of NO-dependent genes. Nitric oxide exposure in mouse macrophages up-regulated 81 genes related to signaling, apoptosis, and inflammation, including Gucy1a3, Pkcα, and Lck.
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