Mechanisms and Regulation of Surfactant Lipid Synthesis

2015 ◽  
pp. 121-132 ◽  
Author(s):  
Joseph J. Batenburg ◽  
Lambert M. G. Van Golde ◽  
Martin Post ◽  
Alfons C. J. de Vries
Keyword(s):  
Lipid Synthesis ◽  
Surfactant Lipid

IL-4 increases surfactant and regulates metabolism in vivo

2000 ◽  
Vol 278 (1) ◽  
pp. L75-L80 ◽  
Author(s):  
Machiko Ikegami ◽  
Jeffrey A. Whitsett ◽  
Zissis C. Chroneos ◽  
Gary F. Ross ◽  
Jacquelyn A. Reed ◽  
...  
Keyword(s):  
Lipid Synthesis ◽  
Fold Increase ◽  
Surfactant Protein ◽  
Clara Cells ◽  
Wild Type ◽  
Surfactant Lipid ◽  
Alveolar Proteinosis ◽  
Selective Increase

Mice that express interleukin (IL)-4 in Clara cells (CCSP-IL-4) develop chronic airway inflammation and an alveolar proteinosis-like syndrome. To identify the role of IL-4 in surfactant homeostasis, we measured lipid and protein metabolism in the lungs of CCSP-IL-4 mice in vivo. Alveolar saturated phosphatidylcholine (Sat PC) pools were increased 6.5-fold and lung tissue Sat PC pools were increased 4.8-fold in the IL-4 transgenic mice. Whereas surfactant protein (SP) A was increased proportionately to Sat PC, SP-D was increased approximately 90-fold in the IL-4 mice compared with wild-type mice and was associated with 2.8-fold increase in SP-D mRNA. The incorporation of palmitate and choline into Sat PC was increased about twofold in CCSP-IL-4 mice. Although trace doses of radiolabeled Sat PC were cleared from the air spaces and lungs of CCSP-IL-4 mice more slowly than in wild-type mice, net clearance of Sat PC from the lungs of CCSP-IL-4 mice was sixfold higher in the IL-4 mice than in wild-type mice because of the larger Sat PC pool sizes. Expression of IL-4 in Clara cells increased surfactant lipid synthesis and clearance, establishing a new equilibrium with increased surfactant pools and an alveolar proteinosis associated with a selective increase in SP-D protein, demonstrating a previously unexpected effect of IL-4 in pulmonary surfactant homeostasis.

scholarly journals Apolipoprotein A-I, A-II, C-II, and H expression in the developing lung and sex difference in surfactant lipids

2008 ◽  
Vol 200 (3) ◽  
pp. 321-330 ◽  
Author(s):  
Pierre R Provost ◽  
Eric Boucher ◽  
Yves Tremblay
Keyword(s):  
Sex Difference ◽  
Expression Profiles ◽  
Secretory Granules ◽  
Lipid Synthesis ◽  
Fetal Lung ◽  
Basal Membrane ◽  
Mrna Accumulation ◽  
Apolipoprotein A ◽  
Surfactant Lipid

A sex difference in surfactant lipids is associated with a higher incidence of respiratory distress syndrome for males in cases of preterm birth. In animal models, the sex difference in surfactant lipids was shown to be androgen receptor-dependent. This report examines expression of apolipoprotein (apo)A-I, apoA-II, apoC-II, apoE, apoH, and lipoprotein lipase (LPL) by quantitative real-time PCR in pools of male and female fetal lung tissues from various mouse litters from gestation day (GD) 15.5 to 18.5, and in various adult tissues. Although the expression profiles of ApoA-I, ApoA-II, ApoC-II, and ApoH are complex, these genes are co-regulated and they all present a sex difference (P=0.0896, 0.0896, 0.0195, and 0.0607 respectively) with higher expression for females for several litters. Pulmonary expression of apoA-I, apoA-II, and apoH were specific to the developing lung. ApoE and LPL mRNAs showed a significant increase from GD 17.5 to 18.5. An increase in apoA-I-, apoA-II-, apoC-II-, and apoH-mRNA accumulation was observed from GD 16.5 to 17.5 in correlation with the emergence of mature type II pneumonocytes. These four apolipoprotein genes are co-regulated with type 2 and 5 17β-hydroxysteroid dehydrogenases, which are respectively involved in inactivation and synthesis of androgens. Finally, apoC-II was detected by immunohistochemistry in epithelial cells of the distal epithelium. Positive signals looking like secretory granules were located near the basal membrane. Our results are compatible with a role for apolipoproteins in lipid metabolism and transport in the developing lung in association with the sex difference in surfactant lipid synthesis.

scholarly journals Effects of intratracheal instillation of TNF-α on surfactant metabolism

2000 ◽  
Vol 88 (1) ◽  
pp. 10-16 ◽  
Author(s):  
Ronald G. Salome ◽  
Diann M. McCoy ◽  
Alan J. Ryan ◽  
Rama K. Mallampalli
Keyword(s):  
Active Material ◽  
Lipid Synthesis ◽  
Intratracheal Instillation ◽  
Alveolar Type ◽  
Choline Transport ◽  
Tnf Α ◽  
Key Enzyme ◽  
Surfactant Lipid ◽  
Surface Active Material

Tumor necrosis factor-α (TNF-α) has been shown to play an integral role in the pathogenesis of the acute respiratory distress syndrome. This disorder is characterized by a deficiency of alveolar surfactant, a surface-active material that is composed of key hydrophobic proteins and the major lipid disaturated phosphatidylcholine (DSPC). We investigated how TNF-α might alter DSPC content in rat lungs by instilling the cytokine (2.5 μg) intratracheally for 10 min and then assaying parameters of DSPC synthesis and degradation in alveolar type II epithelial cells, which produce surfactant. Cells isolated from rats given TNF-α had 26% lower levels of phosphatidylcholine compared with control. TNF-α treatment also decreased the ability of these cells to incorporate [3H]choline into DSPC by 45% compared with control isolates. There were no significant differences in the levels of choline substrate or choline transport between the groups. However, TNF-α produced a 64% decrease in the activity of cytidylyltransferase, the rate-regulatory enzyme required for DSPC synthesis. TNF-α administration in vivo also tended to stimulate phospholipase A2 activity, but it did not alter other parameters for DSPC degradation such as activities for phosphatidylcholine-specific phospholipase C or phospholipase D. These observations indicate that TNF-α decreases the levels of surfactant lipid by decreasing the activity of a key enzyme involved in surfactant lipid synthesis. The results do not exclude stimulatory effects of the cytokine on phosphatidylcholine breakdown.

scholarly journals Very low density lipoproteins stimulate surfactant lipid synthesis in vitro.

1997 ◽  
Vol 99 (8) ◽  
pp. 2020-2029 ◽  
Author(s):  
R K Mallampalli ◽  
R G Salome ◽  
S L Bowen ◽  
D A Chappell
Keyword(s):  
Lipid Synthesis ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Very Low Density Lipoproteins ◽  
Surfactant Lipid

scholarly journals Apolipoprotein C-II and lipoprotein lipase show a temporal and geographic correlation with surfactant lipid synthesis in preparation for birth

2010 ◽  
Vol 10 (1) ◽  
pp. 111 ◽  
Author(s):  
Mélissa Côté ◽  
Pierre R Provost ◽  
Marie-Christine Gérard-Hudon ◽  
Yves Tremblay
Keyword(s):  
Lipoprotein Lipase ◽  
Lipid Synthesis ◽  
Apolipoprotein C ◽  
Surfactant Lipid

Fine Structural Localization of Acyltransferases Involved in Lipid Synthesis in Intestinal Mucosa.

1970 ◽  
Vol 28 ◽  
pp. 54-55
Author(s):  
R. J. Barrnett ◽  
J. A. Higgins
Keyword(s):  
Smooth Endoplasmic Reticulum ◽  
Lipid Synthesis ◽  
Mucosal Cell ◽  
Structural Localization ◽  
Morphological Studies ◽  
Mucosal Cells ◽  
Initial Appearance ◽  
Sh Group ◽  
Hydrolysis Of ◽  
Intestinal Mucosal Cells

The main products of intestinal hydrolysis of dietary triglycerides are free fatty acids and monoglycerides. These form micelles from which the lipids are absorbed across the mucosal cell brush border. Biochemical studies have indicated that intestinal mucosal cells possess a triglyceride synthesising system, which uses monoglyceride directly as an acylacceptor as well as the system found in other tissues in which alphaglycerophosphate is the acylacceptor. The former pathway is used preferentially for the resynthesis of triglyceride from absorbed lipid, while the latter is used mainly for phospholipid synthesis. Both lipids are incorporated into chylomicrons. Morphological studies have shown that during fat absorption there is an initial appearance of fat droplets within the cisternae of the smooth endoplasmic reticulum and that these subsequently accumulate in the golgi elements from which they are released at the lateral borders of the cell as chylomicrons.We have recently developed several methods for the fine structural localization of acyltransferases dependent on the precipitation, in an electron dense form, of CoA released during the transfer of the acyl group to an acceptor, and have now applied these methods to a study of the fine structural localization of the enzymes involved in chylomicron lipid biosynthesis. These methods are based on the reduction of ferricyanide ions by the free SH group of CoA.

In Vitro Incorporation of Sodium Acetate-l-C14 into Leukocyte Lipids of Normal and Leukaemic Subjects as a Function of Incubation Time

1962 ◽  
Vol 02 (02) ◽  
pp. 165-172
Author(s):  
C Miras ◽  
G Lewis ◽  
J Mantzos
Keyword(s):  
Sodium Acetate ◽  
Linear Part ◽  
Lipid Synthesis ◽  
Normal Subjects ◽  
Cytostatic Agents ◽  
Time Intervals ◽  
Total Blood ◽  
Effect Of Treatment ◽  
Product Relation

Summary1. Separated leukocytes or total blood from normal subjects, untreated leukaemic patients and from leukaemic patients treated with cytostatic agents were incubated with CH3COONa-l-C14. Radioactivity of mixed lipids was measured at standard time intervals.2. The time incorporation curve observed with leukocytes from treated leukaemic patients showed after an initial linear part, a more rapid levelling off than the curves observed with leukocytes from untreated and normal subjects.3. Therefore, an indirect effect of treatment on leukocyte lipid synthesis seems to be present.4. Phospholipid and neutral lipid synthesis by leukaemic leukocytes was also studied. The results give no evidence that these fractions as a whole have any precursor-product relation.

Sign in / Sign up

Export Citation Format

Share Document