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首页> 外文期刊>American Journal of Physiology >Amino-terminal and midmolecule parathyroid hormone-related protein, phosphatidylcholine, and type II cell proliferation in silica-injured lung.
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Amino-terminal and midmolecule parathyroid hormone-related protein, phosphatidylcholine, and type II cell proliferation in silica-injured lung.

机译：二氧化硅损伤的肺中氨基末端和分子中的甲状旁腺激素相关蛋白，磷脂酰胆碱和II型细胞增殖。

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摘要

Acute silica lung injury is marked by alveolar phospholipidosis and type II cell proliferation. Parathyroid hormone-related protein (PTHrP) 1-34 could have a regulatory role in this process because it stimulates phosphatidylcholine secretion and inhibits type II cell growth. Other regions of the PTHrP molecule may have biological activity and can also exert pulmonary effects. This study examined the temporal pattern for expression of several regions of PTHrP after silica lung injury and evaluated the effects of changes in expression on cell proliferation and lung phospholipids. Expression of all PTHrP regions fell at 4 days after injury. Reversing the decline in PTHrP 1-34 or PTHrP 67-86 with one intratracheal dose and four daily subcutaneous doses of PTHrP 1-34 or PTHrP 67-86 stimulated bronchoalveolar lavage disaturated phosphatidylcholine (DSPC) levels. Cell culture studies indicate that the peptides exerted direct effects on DSPC secretion by type II cells. Neither peptide affected type II cell proliferation with this dosing regimen, but addition of an additional intratracheal dose resulted in significant inhibition of growth, consistent with previous effects of PTHrP 1-34 in hyperoxic lung injury. These studies establish a regulatory role for PTHrP 1-34 and PTHrP 67-86 in DSPC metabolism and type II cell proliferation in silica injury. Growth inhibitory effects of PTHrP could interact with phospholipid stimulation by affecting type II cell numbers. Further studies are needed to explore the complex interactions of PTHrP-derived peptides and the type II cell response at various stages of silica lung injury.
机译：急性矽肺损伤以肺泡磷脂变性和II型细胞增殖为特征。甲状旁腺激素相关蛋白（PTHrP）1-34在此过程中可能起调节作用，因为它刺激磷脂酰胆碱分泌并抑制II型细胞生长。 PTHrP分子的其他区域可能具有生物学活性，也可能发挥肺部作用。这项研究检查了二氧化硅肺损伤后PTHrP多个区域表达的时间模式，并评估了表达变化对细胞增殖和肺磷脂的影响。损伤后第4天，所有PTHrP区域的表达均下降。用一气管内剂量和每日四次皮下剂量的PTHrP 1-34或PTHrP 67-86刺激支气管肺泡灌洗去饱和磷脂酰胆碱（DSPC）水平来逆转PTHrP 1-34或PTHrP 67-86的下降。细胞培养研究表明，该肽对II型细胞的DSPC分泌具有直接作用。两种肽均不影响这种给药方案的II型细胞增殖，但是添加额外的气管内剂量不会显着抑制生长，这与先前PTHrP 1-34在高氧性肺损伤中的作用一致。这些研究确立了PTHrP 1-34和PTHrP 67-86在二氧化硅损伤中DSPC代谢和II型细胞增殖中的调节作用。 PTHrP的生长抑制作用可能通过影响II型细胞数量而与磷脂刺激相互作用。需要进一步的研究，以探索PTHrP衍生肽与二氧化硅肺损伤不同阶段的复杂相互作用和II型细胞应答。

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