溶血磷脂酰胆碱通过CK2途径触发原生动物寄生虫塞缪尔佩索阿赫氏鞭毛虫的细胞分化。
Lysophosphatidylcholine triggers cell differentiation in the protozoan parasite Herpetomonas samuelpessoai through the CK2 pathway.
作者信息
Dutra Fernando L, Vieira Danielle P, Coelho Felipe S, Adade Camila M, Atella Geórgia C, Silva Neto Mário A C, Lopes Angela H
机构信息
Instituto de Microbiologia Paulo de Góes, Universidade Federal do Rio de Janeiro, Cidade Universitária, Ilha do Fundão, Rio de Janeiro, RJ, 21941-590, Brazil.
Polo Avançado da Universidade Federal do Rio de Janeiro, Macaé, Rio de Janeiro, 27930-560, Brazil.
出版信息
Acta Parasitol. 2020 Mar;65(1):108-117. doi: 10.2478/s11686-019-00135-8. Epub 2019 Oct 22.
BACKGROUND
Protozoa are distantly related to vertebrates but present some features of higher eukaryotes, making them good model systems for studying the evolution of basic processes such as the cell cycle. Herpetomonas samuelpessoai is a trypanosomatid parasite isolated from the hemipteran insect Zelus leucogrammus. Lysophosphatidylcholine (LPC) is implicated in the transmission and establishment of Chagas disease, whose etiological agent is Trypanosoma cruzi. LPC is synthesized by T. cruzi and its vectors, the hemipteran Rhodnius prolixus and Triatoma infestans. Platelet-activating factor (PAF), a phospholipid with potent and diverse physiological and pathophysiological actions, is a powerful inducer of cell differentiation in Herpetomonas muscarum muscarum and T. cruzi. The enzyme phospholipase A (PLA) catalyzes the hydrolysis of the 2-ester bond of 3-sn-phosphoglyceride, transforming phosphatidylcholine (PC) into LPC.
METHODS
In this study, we evaluated cellular differentiation, PLA activity and protein kinase CK2 activity of H. samuelpessoai in the absence and in the presence of LPC and PAF.
RESULTS
We demonstrate that both PC and LPC promoted a twofold increase in the cellular differentiation of H. samuelpessoai, through CK2, with a concomitant inhibition of its cell growth. Intrinsic PLA most likely directs this process by converting PC into LPC.
CONCLUSIONS
Our results suggest that the actions of LPC on H. samuelpessoai occur upon binding to a putative PAF receptor and that the protein kinase CK2 plays a major role in this process. Cartoon depicting a model for the synthesis and functions of LPC in Herpetomonas samuelpessoai, based upon our results regarding the role of LPC on the cell biology of Trypanosoma cruzi [28-32]. N nucleus, k kinetoplast, PC phosphatidylcholine, LPC lysophosphatidylcholine, PLA phospholipase A, PAFR putative PAF receptor in trypanosomatids [65], CK2 protein kinase CK2 [16].
背景
原生动物与脊椎动物的亲缘关系较远，但具有一些高等真核生物的特征，这使它们成为研究细胞周期等基本过程进化的良好模型系统。塞缪尔佩索阿赫氏鞭毛虫是一种从半翅目昆虫白带猎蝽中分离出的锥虫类寄生虫。溶血磷脂酰胆碱（LPC）与恰加斯病的传播和发病有关，恰加斯病的病原体是克氏锥虫。LPC由克氏锥虫及其传播媒介半翅目昆虫长红猎蝽和大锥蝽合成。血小板活化因子（PAF）是一种具有强大且多样生理和病理生理作用的磷脂，是家蝇赫氏鞭毛虫和克氏锥虫细胞分化的有力诱导剂。磷脂酶A（PLA）催化3 - sn - 磷脂酰甘油2 - 酯键的水解，将磷脂酰胆碱（PC）转化为LPC。
方法
在本研究中，我们评估了在不存在和存在LPC及PAF的情况下，塞缪尔佩索阿赫氏鞭毛虫的细胞分化、PLA活性和蛋白激酶CK2活性。
结果
我们证明，PC和LPC均通过CK2使塞缪尔佩索阿赫氏鞭毛虫的细胞分化增加了两倍，同时抑制其细胞生长。内在PLA很可能通过将PC转化为LPC来指导这一过程。
结论
我们的结果表明，LPC对塞缪尔佩索阿赫氏鞭毛虫的作用是在与假定的PAF受体结合后发生的，并且蛋白激酶CK2在这一过程中起主要作用。基于我们关于LPC对克氏锥虫细胞生物学作用的结果，描绘塞缪尔佩索阿赫氏鞭毛虫中LPC合成和功能模型的示意图。N细胞核，k动基体，PC磷脂酰胆碱，LPC溶血磷脂酰胆碱，PLA磷脂酶A，PAFR锥虫类中假定的PAF受体[65]，CK2蛋白激酶CK2[16]。
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