Cellular Phosphatidylcholine level

Within the enterocyte, retinol is bound to cellular retinol binding protein (CRBP 11) and is esterified by lecithin retinol acyltransferase (LRAT), which uses phosphatidylcholine as the fatty acid donor, mainly yielding retinyl palmitate, although small amounts of stearate and oleate are also formed. At unphysiologically high levels of retinol, when CRBP 11 is saturated, acyl coenzyme A (CoA) retinol acyltransferase (ARAT) esterifies the free retinol that accumulates in intracellular membranes. Then the retinyl esters enter the lymphatic circulation and then the bloodstream (in chylomicrons), together with dietary lipid and carotenoids (Norum et al., 1986 Olson, 1986 Blomhoff et al., 1991 Green et al., 1993 Harrison and Hussain, 2001). 

Volinsky, R. and Kinnunen, P.K. 2013. Oxidized phosphatidylcholines in membrane-level cellular signaling From biophysics to physiology and molecular pathology. FEES I, 280, 2806-2816. 

Miles et al. 1998). Using antibodies against two known types of cNOS, i.e., eNOS and bNOS, and an antibody against iNOS, positive results were obtained with the anti-eNOs antibody only. The amount of NO formed was much less than that produced by eNOS in other cells, i.e., alveolar type 11 cells and endothelial cells. Some properties of the alveolar macrophage eNOS are similar to and some are different from the eNOS in these other cell types. Alveolar macrophage NO levels do not seem to be related to cellular metaboUsm. NO production was increased approximately threefold in the presence of dipalmitoyl phosphatidylcholine vesicles or pulmonary surfactant. 

Cellular levels of phosphatidylcholine (PC) have been known to be influenced by plant hormones [1] as well as by environmental stimuli such as low temperature [2]. However, little is known about the mechanism of regulation, and biological meanings are open to conjecture. For better understanding of the phenomena, it is essential to clone the gene of interest. 

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