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Expression of iron regulatory proteins in full-term swine placenta.
Reproduction in Domestic Animals ( IF 1.6 ) Pub Date : 2020-05-25 , DOI: 10.1111/rda.13730
Kandasamy Rajamanickam 1 , Venkatasubramanian Leela 1 , Gopalakrishnan Suganya 1 , Sabiha Hayath Basha 2 , Manoharan Parthiban 3 , Natesan Pazhanivel 4 , Angappan Mangala Gowri 2
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In swine, even though the pregnant sows were with iron abundance, the inborn iron reserve of piglets was compromised. This indicates the insufficiency of molecular machinery involved in local placental iron flux. Here, we investigated the expression of iron regulatory proteins like hepcidin and ferroportin and also their association with iron reserve, inflammation and oxidative stress in placenta of full‐term pregnant sows (n = 6). Amplification and sequencing of placental DNA confirmed the presence of hepcidin (MN579557) and ferroportin (MN565887) sequences and their 100% identity with existing GenBank data. Real‐time amplification of placental mRNA revealed significant higher expression of hepcidin (p < .05) than ferroportin. Western blot analysis of placental tissues revealed specific bands for both hepcidin (~8 kDa) and ferroportin (~62 kDa) molecules. Immunohistochemistry revealed the immunoreactivity for both proteins in the cytoplasm and membrane of trophoblastic cells of the placenta. Hepcidin and ferroportin expressions were positively associated with placental non‐haem iron reserve (p < .0001; p = .033), lipid peroxidation (p = .0060; p < .0001) and reactive oxygen species level (p = .0092; p = .0292). Hepcidin expression was positively associated with interleukin – 6 (p = .0002) and interferon gamma (p < .0001) expressions but ferroportin expression was negatively associated with interleukin‐6 (p = .0005), interleukin‐1β (p = .0226) and interferon gamma (p = .0059) expressions. This indicates hepcidin and ferroportin may have a role in controlling the local placental iron flux by acting as a molecular bridge between iron trafficking and inflammation.

中文翻译:

铁调节蛋白在足月猪胎盘中的表达。

在猪中,即使妊娠母猪的铁含量很高,仔猪的先天铁储备也会受到损害。这表明参与局部胎盘铁通量的分子机制不足。这里,我们调查铁调节蛋白等铁调素和膜铁转运蛋白以及它们与铁储备,炎症和氧化应激在足月妊娠母猪(胎盘关联的表达Ñ  = 6)。胎盘DNA的扩增和测序证实了hepcidin(MN579557)和ferroportin(MN565887)序列的存在以及它们与现有GenBank数据的100%一致性。胎盘mRNA的实时扩增显示hepcidin(p <.05)。胎盘组织的蛋白质印迹分析揭示了铁调素(〜8 kDa)和铁转运蛋白(〜62 kDa)分子的特异性条带。免疫组织化学揭示了胎盘滋养细胞细胞质和膜中两种蛋白质的免疫反应性。Hepcidin和ferroportin的表达与胎盘非血红素铁储备(p  <.0001; p  = .033),脂质过氧化(p  = .0060; p  <.0001)和活性氧水平(p  = .0092; p  = .0292)。Hepcidin表达与白介素– 6(p  = .0002)和γ干扰素(p <.0001)表达,但铁转运蛋白表达与白介素-6(p  = .0005),白介素-1β(p  = .0226)和γ干扰素(p  = .0059)呈负相关。这表明铁调素和铁转运蛋白可能通过充当铁运输和炎症之间的分子桥而在控制局部胎盘铁通量中起作用。
更新日期:2020-05-25
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