H3K14 hyperacetylation‑mediated c‑Myc binding to the miR‑30a‑5p gene promoter under hypoxia postconditioning protects senescent cardiomyocytes from hypoxia/reoxygenation injury

Xu, Lingbo; Zhang, Huiping; Wang, Yanhua; W, Guo; Gu, Lingyu; Ai, Yang; Ma, Shengchao; Yang, Yong; Wu, Kai; Jiang, Yideng

doi:10.3892/mmr.2021.12107

Cited by 2 publications

(2 citation statements)

References 35 publications

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“…However, MiR-30a mitigated autophagy in renal ischemia/reperfusion injury [43]. C-Myc promoted miR-30a-5p transcription to inhibit senescent cardiomyocyte autophagy [44]. In the present study, C. parvum-induced miR-30a also inhibited HCT-8 cell autophagy.…”

Section: Discussionsupporting

confidence: 47%

Cryptosporidium parvum regulates HCT-8 cell autophagy to facilitate survival via inhibiting miR-26a and promoting miR-30a expression

Jiang

Zhang

et al. 2022

Parasites Vectors

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Background Cryptosporidium 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. Methods The 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. Results The 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. Conclusions The 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. Graphical Abstract

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Section: Discussionsupporting

confidence: 47%

Cryptosporidium parvum regulates HCT-8 cell autophagy to facilitate survival via inhibiting miR-26a and promoting miR-30a expression

Jiang

Zhang

et al. 2022

Parasites Vectors

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“…Although some studies have suggested an association between H3K14 acetylation and microRNA (miR)-134–5p expression in cardiac fibroblasts, the specific role of H3K14 remains unknown due to the lack of comparisons with the normal state ( 33 ). Acetylation of H3K14 at the miR-30a-5p promoter in H9c2 cells is associated with c-Myc expression ( 34 ). However, whether H3K14 acetylation is directly involved in cardiac hypertrophy and HF remains unclear.…”

Section: Histone Acetylation In Cardiac Hypertrophy and Heart Failurementioning

confidence: 99%

Roles of histone acetylation sites in cardiac hypertrophy and heart failure

Funamoto

Imanishi

Tsuchiya

et al. 2023

Front. Cardiovasc. Med.

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Heart failure results from various physiological and pathological stimuli that lead to cardiac hypertrophy. This pathological process is common in several cardiovascular diseases and ultimately leads to heart failure. The development of cardiac hypertrophy and heart failure involves reprogramming of gene expression, a process that is highly dependent on epigenetic regulation. Histone acetylation is dynamically regulated by cardiac stress. Histone acetyltransferases play an important role in epigenetic remodeling in cardiac hypertrophy and heart failure. The regulation of histone acetyltransferases serves as a bridge between signal transduction and downstream gene reprogramming. Investigating the changes in histone acetyltransferases and histone modification sites in cardiac hypertrophy and heart failure will provide new therapeutic strategies to treat these diseases. This review summarizes the association of histone acetylation sites and histone acetylases with cardiac hypertrophy and heart failure, with emphasis on histone acetylation sites.

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H3K14 hyperacetylation‑mediated c‑Myc binding to the miR‑30a‑5p gene promoter under hypoxia postconditioning protects senescent cardiomyocytes from hypoxia/reoxygenation injury

Cited by 2 publications

References 35 publications

Cryptosporidium parvum regulates HCT-8 cell autophagy to facilitate survival via inhibiting miR-26a and promoting miR-30a expression

Cryptosporidium parvum regulates HCT-8 cell autophagy to facilitate survival via inhibiting miR-26a and promoting miR-30a expression

Roles of histone acetylation sites in cardiac hypertrophy and heart failure

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