Autor: |
Muneaki Hashimoto, Motomichi Doi, Nagomi Kurebayashi, Koji Furukawa, Hiroko Hirawake‐Mogi, Yoshihiro Ohmiya, Takashi Sakurai, Toshihiro Mita, Katsuhiko Mikoshiba, Takeshi Nara |
Jazyk: |
angličtina |
Rok vydání: |
2016 |
Předmět: |
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Zdroj: |
FEBS Open Bio, Vol 6, Iss 12, Pp 1178-1185 (2016) |
Druh dokumentu: |
article |
ISSN: |
2211-5463 |
DOI: |
10.1002/2211-5463.12126 |
Popis: |
Regulation of intracellular Ca2+ concentration ([Ca2+]i) is vital for eukaryotic organisms. Recently, we identified a Ca2+ channel (TcIP3R) associated with intracellular Ca2+ stores in Trypanosoma cruzi, the parasitic protist that causes Chagas disease. In this study, we measured [Ca2+]i during the parasite life cycle and determined whether TcIP3R is involved in the observed variations. Parasites expressing R‐GECO1, a red fluorescent, genetically encoded Ca2+ indicator for optical imaging that fluoresces when bound to Ca2+, were produced. Using these R‐GECO1‐expressing parasites to measure [Ca2+]i, we found that the [Ca2+]i in epimastigotes was significantly higher than that in trypomastigotes and lower than that in amastigotes, and we observed a positive correlation between TcIP3R mRNA expression and [Ca2+]i during the parasite life cycle both in vitro and in vivo. We also generated R‐GECO1‐expressing parasites with TcIP3R expression levels that were approximately 65% of wild‐type (wt) levels (SKO parasites), and [Ca2+]i in the wt and SKO parasites was compared. The [Ca2+]i in SKO parasites was reduced to approximately 50–65% of that in wt parasites. These results show that TcIP3R is the determinant of [Ca2+]i in T. cruzi. Since Ca2+ signaling is vital for these parasites, TcIP3R is a promising drug target for Chagas disease. |
Databáze: |
Directory of Open Access Journals |
Externí odkaz: |
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