Lysophosphatidylcholine triggers cell differentiation in the protozoan parasite Herpetomonas samuelpessoai through the CK2 pathway
- PMID: 31755068
- DOI: 10.2478/s11686-019-00135-8
Lysophosphatidylcholine triggers cell differentiation in the protozoan parasite Herpetomonas samuelpessoai through the CK2 pathway
Abstract
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 A2 (PLA2) 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, PLA2 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 PLA2 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, PLA2 phospholipase A2, PAFR putative PAF receptor in trypanosomatids [65], CK2 protein kinase CK2 [16].
Keywords: Herpetomonas samuelpessoai; Lysophosphatidylcholine; Phosphatidylcholine; Phospholipase A2; Platelet-activating factor; Protein kinase CK2.
References
-
- Imhof S, Roditi I (2015) The social life of African trypanosomes. Trends Parasitol 31:490–498 - PubMed
-
- Hoare CA, Wallace FG (1966) Developmental stages of trypanosomatid flagellates: a new terminology. Nature 212:1385–1386
-
- Wallace FG (1977) Development stages of trypanosomatids flagellates: a new terminology revisited. Protozoology 3:51–56
-
- Pacheco RS, Marzochi MC, Pires MQ, Brito CM, De Madeira M, Barbosa-Santos EG (1998) Parasite genotypically related to a monoxenous trypanosomatid of dog’s flea causing opportunistic infection in an HIV positive patient. Mem Inst Oswaldo Cruz 93:531–537 - PubMed
-
- Ranque PH, Nourrit J, Nicoli RM (1974) Systematic studies on Trypanosoma. The evolutionary stages of Trypanosoma. Bull Soc Pathol Éxot 67:377–387
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources