Department of Neonatology, First Huai'an Hospital Affiliated to Nanjing Medical University/Pediatric Diagnosis and Treatment Respiratory Key Laboratory of Huai'an, Huai'an, Jiangsu 223300, China.
Zhongguo Dang Dai Er Ke Za Zhi. 2021 Dec 15;23(12):1289-1294. doi: 10.7499/j.issn.1008-8830.2108125.
To study the role of the low-density lipoprotein receptor-related protein 1 (LRP1)-proline-rich tyrosine kinase 2 phosphorylation (pPyk2)-matrix metalloproteinases 9 (MMP9) pathway in hyperoxia-induced lung injury in neonatal rats.
A total of 16 neonatal rats were randomly placed in chambers containing room air (air group) or 95% medical oxygen (hyperoxia group) immediately after birth, with 8 rats in each group. All of the rats were sacrificed on day 8 of life. Hematoxylin and eosin staining was used to observe the pathological changes of lung tissue. ELISA was used to measure the levels of soluble LRP1 (sLRP1) and MMP9 in serum and bronchoalveolar lavage fluid (BALF). Western blot was used to measure the protein expression levels of LRP1, MMP9, Pyk2, and pPyk2 in lung tissue. RT-PCR was used to measure the mRNA expression levels of LRP1 and MMP9 in lung tissue.
The hyperoxia group had significantly higher levels of sLRP1 and MMP9 in serum and BALF than the air group (<0.05). Compared with the air group, the hyperoxia group had significant increases in the protein expression levels of LRP1, MMP9, and pPyk2 in lung tissue (<0.05). The hyperoxia group had significantly higher relative mRNA expression levels of LRP1 and MMP9 in lung tissue than the air group (<0.05).
The activation of the LRP1-pPyk2-MMP9 pathway is enhanced in hyperoxia-induced lung injury in neonatal rats, which may be involved in the pathogenesis of bronchopulmonary dysplasia.
研究低密度脂蛋白受体相关蛋白 1（LRP1）-脯氨酸丰富的酪氨酸激酶 2 磷酸化（pPyk2）-基质金属蛋白酶 9（MMP9）通路在新生大鼠高氧诱导肺损伤中的作用。
共 16 只新生大鼠出生后立即随机放入含有室内空气（空气组）或 95%医用氧气（高氧组）的室中，每组 8 只。所有大鼠均在生后第 8 天处死。苏木精-伊红染色观察肺组织的病理变化。ELISA 法检测血清和支气管肺泡灌洗液（BALF）中可溶性 LRP1（sLRP1）和 MMP9 的水平。Western blot 法检测肺组织中 LRP1、MMP9、Pyk2 和 pPyk2 的蛋白表达水平。RT-PCR 法检测肺组织中 LRP1 和 MMP9 的 mRNA 表达水平。
高氧组血清和 BALF 中的 sLRP1 和 MMP9 水平明显高于空气组（<0.05）。与空气组相比，高氧组肺组织中 LRP1、MMP9 和 pPyk2 的蛋白表达水平明显升高（<0.05）。高氧组肺组织中 LRP1 和 MMP9 的相对 mRNA 表达水平明显高于空气组（<0.05）。
LRP1-pPyk2-MMP9 通路在新生大鼠高氧诱导的肺损伤中被激活，可能参与了支气管肺发育不良的发病机制。
