ArticleParasites & vectors2022
Cryptosporidium parvum regulates HCT-8 cell autophagy to facilitate survival via inhibiting miR-26a and promoting miR-30a expression.
Article in Parasites & vectors, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Azithromycin Mitigates Experimental Cryptosporidiosis-Driven Ileocecal Adenocarcinoma by Modulating Autophagy, Apoptosis, and PI3K/AKT Signaling.Biomedicines · 2026Article
- The role of autophagy in protozoan infections.Frontiers in cellular and infection microbiology · 2026Review
- MiR-125b-5p targets Bak1 to regulate HCT-8 cell apoptosis in response to Cryptosporidium parvum infection via mitochondrial pathway.Parasites & vectors · 2025Article
- STAT1-IFITM3 promotes autophagy in epithelial cells to controlLife science alliance · 2025Article
- miRNA, New Perspective to World of Intestinal Protozoa and Toxoplasma.Acta parasitologica · 2024Review
- MiR-199a-3p regulates HCT-8 cell autophagy and apoptosis in response to Cryptosporidium parvum infection by targeting MTOR.Communications biology · 2024Article
- Preparation, Characterization, and Oral Bioavailability of Solid Dispersions ofInternational journal of molecular sciences · 2024Article
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Authors and funding
9 authors at 2 institutions in 1 country.
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Abstract
backgroundCryptosporidium parvum is an important zoonotic parasite, which not only causes economic losses in animal husbandry but also harms human health. Due to the lack of effective measures for prevention and treatment, it is important to understand the pathogenesis and survival mechanism of C. parvum. Autophagy is an important mechanism of host cells against parasite infection through key regulatory factors such as microRNAs and MAPK pathways. However, the regulatory effect of C. parvum on autophagy has not been reported. Here, we demonstrated that C. parvum manipulated autophagy through host cellular miR-26a, miR-30a, ERK signaling and P38 signaling for parasite survival.
methodsThe expression of Beclin1, p62, LC3, ERK and P38 was detected using western blotting in HCT-8 cells infected with C. parvum as well as treated with miR-26a-mimic, miR-30a-mimic, miR-26a-mimic or miR-30a-inhibitor post C. parvum infection. The qPCR was used to detect the expression of miR-26a and miR-30a and the number of C. parvum in HCT-8 cells. Besides, the accumulation of autophagosomes was examined using immunofluorescence.
resultsThe expression of Beclin1 and p62 was increased, whereas LC3 expression was increased initially at 0-8 h but decreased at 12 h and then increased again in C. parvum-infected cells. C. parvum inhibited miR-26a-mimic-induced miR-26a but promoted miR-30a-mimic-induced miR-30a expression. Suppressing miR-30a resulted in increased expression of LC3 and Beclin1. However, upregulation of miR-26a reduced ERK/P38 phosphorylation, and inhibiting ERK/P38 signaling promoted Beclin1 and LC3 while reducing p62 expression. Treatment with miR-26a-mimic, autophagy inducer or ERK/P38 signaling inhibitors reduced but treatment with autophagy inhibitor or miR-30a-mimic increased parasite number.
conclusionsThe study found that C. parvum could regulate autophagy by inhibiting miR-26a and promoting miR-30a expression to facilitate the proliferation of parasites. These results revealed a new mechanism for the interaction of C. parvum with host cells.
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