Uptake of [<sup>14</sup>C] choline and incorporation into lung phospholipid by the isolated perfused rat lung

Johnson, Rodger G.; Lugg, Moira A.; Nicholas, Terence E.

doi:10.1007/bf02533531

Cited by 12 publications

(3 citation statements)

References 16 publications

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“…(CDP-choline) pathway, which requires the circulating chohne to be transported into the lung by the alveolar epithelium. It has been suggested that this trans-c~llular t~sport process may be rate-limiting for the biosynthesis of pulmonary PC (70,71). In addition, alveolar type II epithelial cells have developed two types of "active" chol~ne transport mechanisms to regulate the pulmonary chohne content (68): The first is a high-affinity, Na+-depend~nt system (K m of 1.5 JlM: Kj of 1.7 JlM for HC-3)…”

Section: Systems For Choline Transportmentioning

confidence: 99%

Choline Transport for Phospholipid Synthesis

Michel

Yuan

Ramsubir

et al. 2006

Exp Biol Med (Maywood)

277

267

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Choline is an essential nutrient for all cells because it plays a role in the synthesis of the membrane phospholipid components of the cell membranes, as a methyl-group donor in methionine metabolism as well as in the synthesis of the neurotransmitter acetylcholine. Choline deficiency affects the expression of genes involved in cell proliferation, differentiation, and apoptosis, and it has been associated with liver dysfunction and cancer. Abnormal choline transport and metabolism have been implicated in a number of neurodegenerative disorders such as Alzheimer's and Parkinson's disease. Therefore, the study of choline transport and the characteristics of choline transporters are of central importance to understanding the mechanisms that underlie membrane integrity and cell signaling in such disorders. Kinetic studies with radiolabeled choline and inhibitors distinguish three systems for choline transport: (i) low-affinity facilitated diffusion, (ii) high-affinity, Na+-dependent transport, and (iii) intermediate-affinity, Na+-independent transport. It is only recently, however, that the proteins having transport characteristics of at least one of these systems have been identified. They include (i) polyspecific organic cation transporters (OCTs) with low affinity for choline, (ii) high-affinity choline transporters (CHT1s), and (iii) intermediate-affinity choline transporter-like (CTL1) proteins. CHT1 and CTL1 but not OCT transporters are selectively inhibited with hemicholinium-3 and essentially display characteristics of specialized transporters for targeted choline metabolism. CHT1 is abundant in neurons and almost exclusively supplies choline for acetyl-choline synthesis. The focus here is more on newly-discovered CTL1 choline transporters. They are expressed in different organisms and cell types, apparently not for the biosynthesis of acetylcholine but for the production of the most abundant metabolite of choline, the membrane lipid phosphatidylcholine.

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Section: Systems For Choline Transportmentioning

confidence: 99%

Choline Transport for Phospholipid Synthesis

Michel

Yuan

Ramsubir

et al. 2006

Exp Biol Med (Maywood)

277

267

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“…Indeed, previous studies have suggested that choline transport into ATII cells could be the rate-limiting step in pulmonary PC biosynthesis. 8,9) Moreover, we demonstrated that choline transporter-like protein 1 (CTL1) plays a role in supplying choline to ATII cells for PC biosynthesis. 10) Although little is known about other mechanisms, CTL1-mediated choline transport is considered to be the first step of CDP-choline pathway.…”

mentioning

confidence: 99%

Involvement of Choline Transporter-Like Proteins, CTL1 and CTL2, in Glucocorticoid-Induced Acceleration of Phosphatidylcholine Synthesis via Increased Choline Uptake

Nakamura

Fujiwara

Ishiguro

et al. 2010

Biological & Pharmaceutical Bulletin

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Phosphatidylcholine (PC) production is accelerated by glucocorticoid, such as dexamethasone (DEX), which enhances fetal lung maturation, promotes differentiation of alveolar type II (ATII) cells, and increases production of both lipid and protein components of lung surfactant. We previously demonstrated that inhibition of choline uptake by ATII cells leads to a decrease of PC synthesis. Since choline uptake may play a critical role in PC production and lung surfactant homeostasis for normal breathing, it is of interest to characterize transporters controlling the disposition of choline in ATII cells. Therefore, we studied the gene regulation and activity of choline transporters in A549 cells, a human ATII cell line. A549 cells were exposed to DEX for 24 h, and mRNA expression levels of choline transporters-like protein 1, (CTL1) and CTL2, were measured using realtime reverse transcription polymerase chain reaction. CTL1 and CTL2 mRNAs were strongly induced by DEX treatment of A549 cells, and the DEX-treated cells showed a significant increase in initial uptake rate of

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“…In the present experiments we used [3H]-choline as the phospholipid precursor, as we had found that about 90% of the label subsequently detected in the lung was as phosphatidylcholine (Johnson et al, 1979), the principal phospholipid in surfactant. We chose to lavage the lungs 5 h after the infusion of choline, for at this time PLalvsp.act is about 60% of maximal labelling which occurs at between 8 and 12 h (Power et al, 1986).…”

Section: Validation Of Methodsmentioning

confidence: 99%

Control of alveolar surfactant in rats at rest and during prolonged hyperpnoea: pharmacological evidence for two tissue pools of surfactant

Barr

Nicholas

Power

1988

British J Pharmacology

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Propranolol, atropine and indomethacin (i.p.) affect neither the amount (PLalv), nor the specific activity (PLalvsp.act.) of alveolar surfactant‐type phospholipids lavaged from the lungs of unanaesthetized rats, either at rest or made hyperpnoeic for 24 h with 5%CO2/13%O2/82%N2. Whereas salbutamol (280 μg kg−1 body weight, i.p.) consistently increased PLalv and PLalvsp.act., pilocarpine (1.5, 3, 10 and 50 mg kg−1, i.p.) and labetalol (1 and 5 mg kg−1, i.p.) had no effect. The dose of pilocarpine reported by others to release surfactant (150 mg kg−1) induced marked salivation, diarrhoea, chromodacryorrhoea and a three‐fold increase in tidal volume. In the isolated perfused lung of the rat, salbutamol (1.5 μm) consistently increased PLalvsp.act, whereas pilocarpine (0.1 and 1 μM) had no effect on these variables. In the isolated perfused lung, the maximum amount of surfactant that could be released by salbutamol (0.5 mM) was smaller than that which could be released in response to an increase in tidal volume (peak inflation pressure 28 cmH2O). When the concentration of salbutamol in the isolated perfused lung was adjusted to produce the same increase in PLalv as did a single simulated deep breath, the PLalvsp.act was significantly increased by salbutamol, but not by the simulated deep breath. We conclude, that neither the autonomic nervous system nor the prostaglandin system is essential for the release of surfactant at rest or during hyperpnoea. Furthermore, we suggest that two pools of surfactant, with different release mechanisms, exist in lung tissue.

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Uptake of [¹⁴C] choline and incorporation into lung phospholipid by the isolated perfused rat lung

Cited by 12 publications

References 16 publications

Choline Transport for Phospholipid Synthesis

Choline Transport for Phospholipid Synthesis

Involvement of Choline Transporter-Like Proteins, CTL1 and CTL2, in Glucocorticoid-Induced Acceleration of Phosphatidylcholine Synthesis via Increased Choline Uptake

Control of alveolar surfactant in rats at rest and during prolonged hyperpnoea: pharmacological evidence for two tissue pools of surfactant

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Uptake of [14C] choline and incorporation into lung phospholipid by the isolated perfused rat lung

Cited by 12 publications

References 16 publications

Choline Transport for Phospholipid Synthesis

Choline Transport for Phospholipid Synthesis

Involvement of Choline Transporter-Like Proteins, CTL1 and CTL2, in Glucocorticoid-Induced Acceleration of Phosphatidylcholine Synthesis via Increased Choline Uptake

Control of alveolar surfactant in rats at rest and during prolonged hyperpnoea: pharmacological evidence for two tissue pools of surfactant

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Uptake of [¹⁴C] choline and incorporation into lung phospholipid by the isolated perfused rat lung