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http://dx.doi.org/10.3347/kjp.2011.49.2.177

Calpains are Involved in Entamoeba histolytica-Induced Death of HT-29 Colonic Epithelial Cells  

Jang, Yun-Soo (Department of Environmental Medical Biology, Yonsei University College of Medicine)
Song, Kyoung-Ju (Department of Environmental Medical Biology, Yonsei University College of Medicine)
Kim, Ju-Young (Department of Environmental Medical Biology, Yonsei University College of Medicine)
Lee, Young-Ah (Department of Environmental Medical Biology, Yonsei University College of Medicine)
Kim, Kyeong-Ah (Department of Environmental Medical Biology, Yonsei University College of Medicine)
Lee, Sang-Kyou (Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University)
Shin, Myeong-Heon (Department of Environmental Medical Biology, Yonsei University College of Medicine)
Publication Information
Parasites, Hosts and Diseases / v.49, no.2, 2011 , pp. 177-180 More about this Journal
Abstract
Entamoeba histolytica is an enteric tissue-invading protozoan parasite that can cause amebic colitis and liver abscess in humans. E. histolytica has the capability to kill colon epithelial cells in vitro; however, information regarding the role of calpain in colon cell death induced by ameba is limited. In this study, we investigated whether calpains are involved in the E. histolytica-induced cell death of HT-29 colonic epithelial cells. When HT-29 cells were co-incubated with E. histolytica, the propidium iodide stained dead cells markedly increased compared to that in HT-29 cells incubated with medium alone. This pro-death effect induced by ameba was effectively blocked by pretreatment of HT-29 cells with the calpain inhibitor, calpeptin. Moreover, knockdown of m- and ${\mu}$-calpain by siRNA significantly reduced E. histolytica-induced HT-29 cell death. These results suggest that m- and ${\mu}$-calpain may be involved in colon epithelial cell death induced by E. histolytica.
Keywords
Entamoeba histolytica; host cell death; calpain; HT-29 colon epithelial cells;
Citations & Related Records

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