Effect of maternal food restriction on fetal rat lung lipid differentiation program.
Effect of maternal food restriction on fetal rat lung lipid differentiation program.
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DOI：
10.1002/ppul.21030
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发表时间：
2009-07
影响因子：
3.1
通讯作者：
Rehan, Virender K.
中科院分区：
文献类型：
--
作者：
Karadag, Ahmet;Sakurai, Reiko;Wang, Ying;Guo, Pinzheng;Desai, Mina;Ross, Michael G.;Torday, John S.;Rehan, Virender K.
关键词：
虽然“胎儿编程”已被广泛研究，在许多器官，只有有限的信息对肺的影响，在后代以下宫内生长受限（IUGR）。我们的目的是确定营养限制对肺结构和肺脂质分化程序在后代使用的动物模型母体食物限制（MFR）的影响。我们利用从妊娠第10天到足月的50%MFR的啮齿动物模型，然后使用肺形态学、Western印迹、真实的Time-RT-PCR和油红O染色，在出生后第1天（p）、第21天和第9个月（9个月）检查后代的肺结构和发育。在出生后第1天，MFR幼崽的体重显著低于对照幼崽，但在p21和9 M时，它们的体重显著增加。然而，在检查的所有时间点，两组之间的肺重量（表示为体重的百分比）均无差异。MFR组在p1和9 M时肺泡数量显著减少，间隔厚度显著增加，表明MFR后代的肺结构显著改变。此外，虽然在p1时，与对照组相比，MFR组的肺脂质蓄积显著减少，但在9 M时，肺脂质蓄积显著增加。甲状旁腺激素相关蛋白/过氧化物酶体增殖物激活受体γ信号通路和表面活性剂合成存在显着的时间变化。我们的结论是，MFR通过影响特定的上皮-间充质信号通路改变胎肺脂质分化编程和肺形态，为克服这些影响的特定干预措施提供了可能性。
Although “fetal programming” has been extensively studied in many organs, there is only limited information on pulmonary effects in the offspring following intrauterine growth restriction (IUGR). We aimed to determine the effects of nutrient restriction on the lung structure and lung lipid differentiation programs in offspring using an animal mode of maternal food restriction (MFR). We utilized a rodent model of 50% MFR from day 10 of gestation to term and then using lung morphology, Western blotting, Real Time- RT-PCR and oil red O staining, lung structure and development of the offspring were examined at postnatal days (p) 1, p21, and 9 months (9M). At postnatal day 1, MFR pups weighed significantly less compared to control pups, but at p21 and 9M, they weighed significantly more. However, lung weight, expressed as a percentage of body weight between the two groups was not different at all time-points examined. The MFR group had significantly decreased alveolar number and significantly increased septal thickness at p1 and 9M, indicating significantly altered lung structure in the MFR offspring. Furthermore, although at p1, compared to the control group, lung lipid accumulation was significantly decreased in the MFR group, at 9M, it was significantly increased. There were significant temporal changes in the Parathyroid Hormone-related Protein/Peroxisome Proliferator-Activated Receptor gamma signaling pathway and surfactant synthesis. We conclude that MFR alters fetal lung lipid differentiation programming and lung morphometry by affecting specific epithelial-mesenchymal signaling pathways, offering the possibility for specific interventions to overcome these effects.
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