Dataset Information

Berberine Ameliorates High Glucose-Induced Cardiomyocyte Injury via AMPK Signaling Activation to Stimulate Mitochondrial Biogenesis and Restore Autophagic Flux.

ABSTRACT: Background: Type II diabetes (T2D)-induced cardiomyocyte hypertrophy is closely linked to the impairment of mitochondrial function. Berberine has been shown to be a promising effect for hypoglycemia in T2D models. High glucose-induced cardiomyocyte hypertrophy in vitro has been reported. The present study investigated the protective effect and the underlying mechanism of berberine on high glucose-induced H9C2 cell line. Methods: High glucose-induced H9C2 cell line was used to mimic the hyperglycemia resulting in cardiomyocyte hypertrophy. Berberine was used to rescue in this model and explore the mechanism in it. Confocal microscopy, immunofluorescence, RT-PCR, and western blot analysis were performed to evaluate the protective effects of berberine in high glucose-induced H9C2 cell line. Results: Berberine dramatically alleviated hypertrophy of H9C2 cell line and significantly ameliorated mitochondrial function by rectifying the imbalance of fusion and fission in mitochondrial dynamics. Furthermore, berberine further promoted mitogenesis and cleared the damaged mitochondria via mitophagy. In addition, berberine also restored autophagic flux in high glucose-induced cardiomyocyte injury via AMPK signaling pathway activation. Conclusion: Berberine ameliorates high glucose-induced cardiomyocyte injury via AMPK signaling pathway activation to stimulate mitochondrial biogenesis and restore autophagicflux in H9C2 cell line.

SUBMITTER: Hang W

PROVIDER: S-EPMC6178920 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Berberine Ameliorates High Glucose-Induced Cardiomyocyte Injury via AMPK Signaling Activation to Stimulate Mitochondrial Biogenesis and Restore Autophagic Flux.

Hang Weijian W He Benhong B Chen Jiehui J Xia Liangtao L Wen Bing B Liang Tao T Wang Xu X Zhang Qianying Q Wu Yue Y Chen Qingjie Q Chen Juan J

Frontiers in pharmacology 20181003

Background: Type II diabetes (T2D)-induced cardiomyocyte hypertrophy is closely linked to the impairment of mitochondrial function. Berberine has been shown to be a promising effect for hypoglycemia in T2D models. High glucose-induced cardiomyocyte hypertrophy in vitro has been reported. The present study investigated the protective effect and the underlying mechanism of berberine on high glucose-induced H9C2 cell line. Methods: High glucose-induced H9C2 cell line was used t ...[more]

PMID: 30337876

Similar Datasets

Project description:Arabidopsis Lon1 serves dual roles as a mitochondrial protease and chaperone. Loss of Lon1 function reduced autophagy flux at transcriptional, protein and cellular levels. Meanwhile, changes occurred in the levels of cellular subunit proteins, especially a significant upregulation of mitochondrial proteins overall in lon1 mutants. Lon1 is a key enzyme in maintaining mitochondrial protein homeostasis. In lon1 mutants, other mitochondrial proteases including mitochondrial autophagy receptor proteins showed significant increases in abundance. Mitophagy is an important mechanism for cellular quality control. lon1-2atg5-1 double mutant were constructed to investigate how they cooperatively regulate mitochondrial protein homeostasis. Transcriptome sequencing results revealed that Lon1 inactivation led to widespread unfolded protein responses (UPRs) pathway activation in lon1-2atg5-1, consistent with lon1-2, while loss function of ATG5 inactivation did not affect mitochondrial homeostasis. The double mutant also exhibited independent plant phenotypes from single parents, yet more severe seed number and embryo development issues, suggesting an additive effect of lon1-2 and atg5-1. Protein Storage Vacuole (PSV) and oil body phenotypes also showed more severe developmental damage in the double mutants. Brassinosteroid (BR) acts as a key plant hormone controlling seed and embryo development. GO and KEGG analysis of genes simultaneously downregulated in lon1-2, atg5-1, and lon1-2atg5-1 revealed significant downregulation of genes involved in BR biosynthesis and its homeostasis, indicating that this may be one of the key factors leading to abnormal seed and embryo development in the mutants. In general, the loss function of Lon1 reduces autophagy flux and induces UPRs to regulate protein homeostasis. Meanwhile, the simultaneous absence of Lon1 and autophagy significantly down-regulates the expression of genes related to BR biosynthesis and homeostasis, thereby leading to pronounced blockage in the development of double mutant seeds and embryos.

Dataset Information

Berberine Ameliorates High Glucose-Induced Cardiomyocyte Injury via AMPK Signaling Activation to Stimulate Mitochondrial Biogenesis and Restore Autophagic Flux.

Publications

Berberine Ameliorates High Glucose-Induced Cardiomyocyte Injury via AMPK Signaling Activation to Stimulate Mitochondrial Biogenesis and Restore Autophagic Flux.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure