Very low density lipoproteins stimulate surfactant lipid synthesis in vitro.

Mallampalli, Rama K.; Salome, Ronald G.; Bowen, Susan L.; Chappell, David

doi:10.1172/jci119370

Cited by 26 publications

(22 citation statements)

References 54 publications

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“…Thus, although the retroorbital route bypasses intestinal absorption, Intralipid pharmacokinetics resembles that of chylomicrons in fatty meal and should not have a major adverse impact on our results. TG-rich lipoproteins can be used for surfactant biosynthesis in the lungs ( 69,70 ), but impact of CIH on surfactant biosynthesis has not been studied. CD146+ CD11b Ϫ cells were responsible for the vast majority of TG uptake in the lung.…”

Section: Role Of the Lungs In Tg Clearance During Cihmentioning

confidence: 99%

Effect of chronic intermittent hypoxia on triglyceride uptake in different tissues

Yao

Shin

Jun

et al. 2013

Journal of Lipid Research

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This article is available online at http://www.jlr.org signifi cant cardiovascular morbidity and mortality (2)(3)(4). Several lines of evidence demonstrated that OSA is associated with dyslipidemia and accelerated atherosclerosis ( 5-12 ). A randomized, placebo-controlled clinical trial of continuous positive airway pressure (CPAP) has shown that OSA treatment with CPAP markedly reduces postprandial hyperlipidemia ( 13 ). Postprandial hypertriglyceridemia may confer risk for myocardial infarction, isch emic heart disease, stroke, and death (14)(15)(16)(17)(18)(19)(20). Therefore, it is conceivable that postprandial hyperlipidemia contributes to the cardiovascular risk of OSA. The pathogenesis of postprandial hyperlipidemia in OSA is unknown.We developed a mouse model of CIH, which mimics oxyhemoglobin desaturations in patients with OSA ( 21-23 ). Using this model, we have recently shown that CIH impairs chylomicron clearance in mice and inhibits a key enzyme of triglyceride-rich lipoprotein clearance, lipoprotein lipase (LPL), in adipose tissue ( 24 ). CIH also upregulated a potent LPL inhibitor, adipose angiopoietin-like protein 4 (Angptl4) ( 24 ). However, the effect of CIH on triglyceride (TG) uptake by adipose tissue has not been explored; contribution of other organs and tissues to lipoprotein clearance during CIH is unknown. Finally, the role of Angptl4 in CIH-induced metabolic dysfunction has not been determined.We hypothesized that CIH impairs TG uptake by adipose tissue depots and other organs and tissues via Angptl4. We exposed C57BL/6J mice to CIH for four weeks while treating them with Angptl4-neutralizing antibodies (Ab) or placebo (vehicle solution) and examined plasma clearance and tissue uptake of [H 3 ]triolein-Intralipid. Abstract Chronic intermittent hypoxia (CIH) inhibits plasma lipoprotein clearance and adipose lipoprotein lipase (LPL)activity in association with upregulation of an LPL inhibitor angiopoietin-like protein 4 (Angptl4). We hypothesize that CIH inhibits triglyceride (TG) uptake via Angptl4 and that an anti-Angptl4-neutralizing antibody would abolish the effects of CIH. Male C57BL/6J mice were exposed to four weeks of CIH or intermittent air (IA) while treated with Ab (30 mg/kg ip once a week). TG clearance was assessed by [H 3 ]triolein administration retroorbitally. CIH delayed TG clearance and suppressed TG uptake and LPL activity in all white adipose tissue depots, brown adipose tissue, and lungs, whereas heart, liver, and spleen were not affected. CD146+ CD11b ؊ pulmonary microvascular endothelial cells were responsible for TG uptake in the lungs and its inhibition by CIH. Antibody to Angptl4 decreased plasma TG levels and increased TG clearance and uptake into adipose tissue and lungs in both control and CIH mice to a similar extent, but did not reverse the effects of CIH. The antibody reversed the effects of CIH on LPL in adipose tissue and lungs. In conclusion, CIH inactivates LPL by upregulating Angptl4, but inhibition of TG uptake occurs predominantly via an A...

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Section: Role Of the Lungs In Tg Clearance During Cihmentioning

confidence: 99%

Effect of chronic intermittent hypoxia on triglyceride uptake in different tissues

Yao

Shin

Jun

et al. 2013

Journal of Lipid Research

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“…The MLE-12 and CHO cell lines were purchased from American Type Culture Collection (Manassas, VA). Radiolabeled lipoproteins were prepared as described (15). Lactacystin, A23187, N-acetyl-Leu-Leu-Nle-CHO (ALLN), recombinant rat calpain II, and calpastatin were purchased from Calbiochem (La Jolla, CA).…”

Section: Methodsmentioning

confidence: 99%

“…Lipoproteins-Cellular catabolism of lipoproteins was determined as described (15). Surface binding and internalization were defined as radioactivity that was released or remained cell-associated, respectively, following incubation of cells at 4°C in buffer containing 10 mg/ml tripolyphosphate.…”

Section: Cell Surface Binding Internalization and Degradation Of Oxmentioning

confidence: 99%

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Oxidized Lipoproteins Inhibit Surfactant Phosphatidylcholine Synthesis via Calpain-mediated Cleavage of CTP:Phosphocholine Cytidylyltransferase

Zhou

Ryan

Medh

et al. 2003

Journal of Biological Chemistry

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“…HDL and low density lipoprotein (LDL) can stimulate primary cultures of type II cells to secrete PC (11). Very low density lipoproteins (VLDL) stimulate surfactant lipid synthesis in immortalized or primary rat alveolar pre-type II epithelial cells (12). Because PLTP is highly expressed in the lung, and regulates lipoprotein metabolism, it is conceivable that this protein might play a role in surfactant metabolism.…”

mentioning

confidence: 99%

Expression of Plasma Phospholipid Transfer Protein mRNA in Normal and Emphysematous Lungs and Regulation by Hypoxia

Jiang¹,

DʼArmiento²,

Mallampalli³

et al. 1998

Journal of Biological Chemistry

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The lung is the major site expressing plasma phospholipid transfer protein (PLTP) mRNA in humans and mice, suggesting that this protein might have an important role in maintaining normal function of this organ. In the lung of human collagenase transgenic mice, an emphysematous animal model, PLTP mRNA was 3-fold higher than in control mice. However, the mRNA in other tissues was not changed. To further assess the expression and function of PLTP, we measured PLTP mRNA level in lung tissue of two emphysematous patients and found that the mRNA was 4-fold higher than in control subjects. In situ hybridization on mouse lung suggested positive staining in alveolar type II epithelial cells. In addition, immortalized rat alveolar pre-type II epithelial cells and freshly isolated mature rat alveolar type II epithelial cells both highly expressed PLTP mRNA, and the former cells actively secreted PLTP activity into the medium. To examine the possible mechanisms leading to high levels of PLTP expression in vivo, we exposed the pre-type II cells to hypoxia and demonstrated induction of PLTP mRNA and a coordinate increase in secreted PLTP activity. Thus, the PLTP gene is highly expressed in alveolar type II epithelial cells and is induced during hypoxia and in emphysema. These observations suggest that a hypoxic stimulus occurring in emphysema may be a novel mechanism that contributes to enhanced expression of PLTP.

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Very low density lipoproteins stimulate surfactant lipid synthesis in vitro.

Cited by 26 publications

References 54 publications

Effect of chronic intermittent hypoxia on triglyceride uptake in different tissues

Effect of chronic intermittent hypoxia on triglyceride uptake in different tissues

Oxidized Lipoproteins Inhibit Surfactant Phosphatidylcholine Synthesis via Calpain-mediated Cleavage of CTP:Phosphocholine Cytidylyltransferase

Expression of Plasma Phospholipid Transfer Protein mRNA in Normal and Emphysematous Lungs and Regulation by Hypoxia

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