Marconi Guya Diletta, Zara Susi, De Colli Marianna, Di Valerio Valentina, Rapino Monica, Zaramella Patrizia, Dedja Arben, Macchi Veronica, De Caro Raffaele, Porzionato Andrea
Department of Pharmacy, University "G. d'Annunzio" Chieti-Pescara, Chieti, Italy.
Department of Medicine and Ageing Sciences, University "G. d'Annunzio" Chieti-Pescara, Chieti, Italy.
PLoS One. 2014 Aug 12;9(8):e105005. doi: 10.1371/journal.pone.0105005. eCollection 2014.
Premature newborns are frequently exposed to hyperoxic conditions and experimental data indicate modulation of liver metabolism by hyperoxia in the first postnatal period. Conversely, nothing is known about possible modulation of growth factors and signaling molecules involved in other hyperoxic responses and no data are available about the effects of hyperoxia in postnatal liver haematopoiesis. The aim of the study was to analyse the effects of hyperoxia in the liver tissue (hepatocytes and haemopoietic cells) and to investigate possible changes in the expression of Vascular Endothelial Growth Factor (VEGF), Matrix Metalloproteinase 9 (MMP-9), Hypoxia-Inducible Factor-1α (HIF-1α), endothelial Nitric Oxide Synthase (eNOS), and Nuclear Factor-kB (NF-kB). Experimental design of the study involved exposure of newborn rats to room air (controls), 60% O2 (moderate hyperoxia), or 95% O2 (severe hyperoxia) for the first two postnatal weeks. Immunohistochemical and Western blot analyses were performed. Severe hyperoxia increased hepatocyte apoptosis and MMP-9 expression and decreased VEGF expression. Reduced content in reticular fibers was found in moderate and severe hyperoxia. Some other changes were specifically produced in hepatocytes by moderate hyperoxia, i.e., upregulation of HIF-1α and downregulation of eNOS and NF-kB. Postnatal severe hyperoxia exposure increased liver haemopoiesis and upregulated the expression of VEGF (both moderate and severe hyperoxia) and eNOS (severe hyperoxia) in haemopoietic cells. In conclusion, our study showed different effects of hyperoxia on hepatocytes and haemopoietic cells and differential involvement of the above factors. The involvement of VEGF and eNOS in the liver haemopoietic response to hyperoxia may be hypothesized.
早产新生儿经常暴露于高氧环境中,实验数据表明出生后第一阶段高氧会调节肝脏代谢。相反,对于参与其他高氧反应的生长因子和信号分子的可能调节情况一无所知,也没有关于高氧对出生后肝脏造血作用影响的数据。本研究的目的是分析高氧对肝脏组织(肝细胞和造血细胞)的影响,并研究血管内皮生长因子(VEGF)、基质金属蛋白酶9(MMP - 9)、缺氧诱导因子 - 1α(HIF - 1α)、内皮型一氧化氮合酶(eNOS)和核因子 - kB(NF - kB)表达的可能变化。该研究的实验设计包括在出生后的前两周将新生大鼠暴露于室内空气(对照组)、60%氧气(中度高氧)或95%氧气(重度高氧)环境中。进行了免疫组织化学和蛋白质印迹分析。重度高氧增加了肝细胞凋亡和MMP - 9表达,并降低了VEGF表达。在中度和重度高氧环境中发现网状纤维含量减少。中度高氧在肝细胞中产生了一些其他特定变化,即HIF - 1α上调以及eNOS和NF - kB下调。出生后暴露于重度高氧会增加肝脏造血,并上调造血细胞中VEGF(中度和重度高氧)和eNOS(重度高氧)的表达。总之,我们的研究表明高氧对肝细胞和造血细胞有不同影响,且上述因子的参与情况也有所不同。可以推测VEGF和eNOS参与了肝脏对高氧的造血反应。