Original Research ARTICLE
A calpain-like protein is involved in the execution phase of programmed cell death of Entamoeba histolytica
- 1Infectómica y Patogénesis Molecular, Centro de Investigación y de Estudios Avanzados (CINVESTAV), Mexico
- 2Biomedicina Molecular 1, ENMyH, Instituto Politécnico Nacional, Mexico
Oxygen or nitrogen oxidative species and chemical stress induce the programmed cell death (PCD) of Entamoeba histolytica trophozoites. PCD caused by the aminoglycoside G418 is reduced by incubation with the cysteine protease inhibitor E-64; however, no typical caspases or metacaspases have been detected in this parasite. Calpain, a cysteine protease activated by calcium, has been suggested to be part of a specific PCD pathway in this parasite because the specific calpain inhibitor Z-Leu-Leu-Leu-al diminishes the PCD of trophozoites. Here, we predicted the hypothetical 3D structure of a calpain-like protein of E. histolytica and produced specific antibodies against it. We detected the protein in the cytoplasm and near the nucleus. Its expression gradually increased during incubation with G418, with the highest level after 9 h of treatment. In addition, a specific calpain-like siRNA sequence reduced the cell death rate by 65%. All these results support the hypothesis that the calpain-like protein is one of the proteases involved in the execution phase of PCD in E. histolytica. The hypothetical interactome of the calpain-like protein suggests that it may activate or regulate other proteins that probably participate in PCD, including those with EF-hand domains or other calcium-binding sites.
Keywords: Entamoeba histolytica, Cysteine Proteases, programmed cell death, protein overexpression, Calcium binding sites, Calpain
Received: 24 May 2018;
Accepted: 06 Sep 2018.
Edited by:Brice ROTUREAU, Institut Pasteur, France
Reviewed by:Friedrich Frischknecht, Universität Heidelberg, Germany
Michael Duchene, Medizinische Universität Wien, Austria
Marcos L. Gazarini, Federal University of São Paulo, Brazil
Copyright: © 2018 Domínguez-Fernández, Rodriguez, Sánchez Monroy, Gomez, Medel Flores and PEREZ ISHIWARA. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Dr. GUILLERMO PEREZ ISHIWARA, Instituto Politécnico Nacional, Biomedicina Molecular 1, ENMyH, Mexico City, Mexico, email@example.com