Two kinds of ferritin protect ixodid ticks from iron overload and consequent oxidative stress.

Two kinds of ferritin protect ixodid ticks from iron overload and consequent oxidative stress.
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DOI:
10.1371/journal.pone.0090661
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发表时间:
2014
期刊:
影响因子:
3.7
通讯作者:
Tanaka T
Tanaka T
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Galay RL;Umemiya-Shirafuji R;Bacolod ET;Maeda H;Kusakisako K;Koyama J;Tsuji N;Mochizuki M;Fujisaki K;Tanaka T

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蜱是专性吸血寄生虫,已成功开发出对抗宿主免疫和止血机制的对抗手段,但它们科普血液中潜在有毒分子的能力仍不清楚。铁在各种生理过程中很重要,但过量时对活细胞有毒性。我们以前报道,硬蜱长角血蜱有一个细胞内(HIFER 1)和分泌(HIFER 2)铁蛋白,这两个是至关重要的成功的血液喂养和繁殖。铁蛋白基因的RNA干扰沉默导致摄食能力下降,体重下降,血餐后死亡率高,繁殖力下降,中肠细胞形态异常。在另一种硬蜱--蓖麻硬蜱中,铁蛋白基因沉默后,以前也有类似的发现。在这里,我们证明了铁蛋白在保护硬蜱免受氧化应激中的作用。通过检测Hlfer沉默蜱在吸血和注射柠檬酸铁铵(FAC)后的脂质过氧化产物丙二醛(MDA)和蛋白质氧化产物羰基化水平,评价Hlfer沉默蜱的氧化应激。在Hlfer沉默的蜱中注射FAC导致高死亡率。与注射荧光素酶(对照)的蜱相比,在Hlfer沉默的蜱中检测到更高水平的MDA和蛋白质羰基,这两种蜱在血液喂养和FAC注射后。通过在天然HIFER上增加的染色证明的三价铁积累在全蜱和中肠两者中从铁注射后72小时起观察到。此外,在Hlfer敲低后观察到弱铁染色。综上所述,这些结果表明,蜱铁蛋白是重要的抗氧化分子,保护硬蜱在血液喂养期间免受铁介导的氧化应激。
Ticks are obligate hematophagous parasites that have successfully developed counteractive means against their hosts' immune and hemostatic mechanisms, but their ability to cope with potentially toxic molecules in the blood remains unclear. Iron is important in various physiological processes but can be toxic to living cells when in excess. We previously reported that the hard tick Haemaphysalis longicornis has an intracellular (HlFER1) and a secretory (HlFER2) ferritin, and both are crucial in successful blood feeding and reproduction. Ferritin gene silencing by RNA interference caused reduced feeding capacity, low body weight and high mortality after blood meal, decreased fecundity and morphological abnormalities in the midgut cells. Similar findings were also previously reported after silencing of ferritin genes in another hard tick, Ixodes ricinus. Here we demonstrated the role of ferritin in protecting the hard ticks from oxidative stress. Evaluation of oxidative stress in Hlfer-silenced ticks was performed after blood feeding or injection of ferric ammonium citrate (FAC) through detection of the lipid peroxidation product, malondialdehyde (MDA) and protein oxidation product, protein carbonyl. FAC injection in Hlfer-silenced ticks resulted in high mortality. Higher levels of MDA and protein carbonyl were detected in Hlfer-silenced ticks compared to Luciferase-injected (control) ticks both after blood feeding and FAC injection. Ferric iron accumulation demonstrated by increased staining on native HlFER was observed from 72 h after iron injection in both the whole tick and the midgut. Furthermore, weak iron staining was observed after Hlfer knockdown. Taken together, these results show that tick ferritins are crucial antioxidant molecules that protect the hard tick from iron-mediated oxidative stress during blood feeding.
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