Parathyroid hormone-related protein response to hyperoxic lung injury.
Parathyroid hormone-related protein response to hyperoxic lung injury.
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甲状旁腺激素相关蛋白对高氧肺损伤的反应。
DOI：
10.1152/ajplung.00139.2001
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发表时间：
2002
期刊：
影响因子：
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通讯作者：
Deftos,LeonardJ
中科院分区：
文献类型：
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作者：
Hastings,RandolphH;Ryan,RitaM;D'Angio,CarlT;Holm,BruceA;Patel,Alka;Quintana,Rick;Biederman,Elana;Burton,DouglasW;Deftos,LeonardJ
甲状旁腺激素相关蛋白 (PTHrP) 是 II 型肺泡细胞的生长抑制剂。 85% 氧气造成肺损伤后 II 型细胞增殖在一定程度上是通过肺 PTHrP 下降来调节的。在这项研究中，我们研究了大鼠和兔子在 >95% 氧气诱导损伤后的肺 PTHrP。在成年大鼠中，高氧 48 小时后，肺 PTHrP 比对照组升高 10 倍，达到 6,356 ± 710 pg/ml（平均值 ± SE）。水平下降至 299 ± 78 pg/ml，PTHrP mRNA 染色在 60 小时时大大减少 (P< 0.05)，这是损伤最严重和肺细胞增殖最大的时刻。在成年兔中，肺 PTHrP 在高氧 64 小时后达到常氧恢复 24 小时后达到峰值 3,289 ± 230 pg/ml，然后在恢复 48 小时时降至 1,629 ± 153 pg/ml（P < 0.05）。 PTHrP 下降后不久，II 型细胞增殖达到顶峰。在新生兔中，在高氧的前 8 天，灌洗液 PTHrP 增加了 50%，而 II 型细胞生长则减少。 PTHrP 在 LD50 时下降，同时 II 型细胞分裂增加。总之，肺 PTHrP 在损伤后伴随 >95% 高氧最初升高，然后在损伤峰值附近下降。 PTHrP 的变化在时间上与 II 型细胞增殖相关，并可能调节肺损伤的修复。
Parathyroid hormone-related protein (PTHrP) is a growth inhibitor for alveolar type II cells. Type II cell proliferation after lung injury from 85% oxygen is regulated, in part, by a fall in lung PTHrP. In this study, we investigated lung PTHrP after injury induced by >95% oxygen in rats and rabbits. In adult rats, lung PTHrP rose 10-fold over controls to 6,356 ± 710 pg/ml (mean ± SE) at 48 h of hyperoxia. Levels fell to 299 ± 78 pg/ml, and staining for PTHrP mRNA was greatly reduced at 60 h (P< 0.05), the point of most severe injury and greatest pneumocyte proliferation. In adult rabbits, lung PTHrP peaked at 3,289 ± 230 pg/ml after 64 h of hyperoxia with 24 h of normoxic recovery and then dropped to 1,629 ± 153 pg/ml at 48 h of recovery (P< 0.05). Type II cell proliferation peaked shortly after the fall in PTHrP. In newborn rabbits, lavage PTHrP increased by 50% during the first 8 days of hyperoxia, whereas type II cell growth decreased. PTHrP declined at the LD50, concurrent with increased type II cell division. In summary, lung PTHrP initially rises after injury with >95% hyperoxia and then falls near the peak of injury. Changes in PTHrP are temporally related to type II cell proliferation and may regulate repair of lung injury.