Search

Your search keyword '"Sun, Minli"' showing total 33 results
Start Over Author "Sun, Minli" Search Limiters Academic (Peer-Reviewed) Journals
33 results on '"Sun, Minli"'

15. Trimethylamine N-oxide promotes atherosclerosis via regulating the enriched abundant transcript 1/miR-370-3p/signal transducer and activator of transcription 3/flavin-containing monooxygenase-3 axis

Author

Liu, Aijun, Zhang, Yonglin, Xun, Shucan, and Sun, Minli

Subjects
Male, STAT3 Transcription Factor, trimethylamine n-oxide, Bioengineering, Diet, High-Fat, Applied Microbiology and Biotechnology, stat3, Methylamines, Mice, excessive proliferation, Human Umbilical Vein Endothelial Cells, Animals, Humans, Aged, Feedback, Physiological, General Medicine, Middle Aged, Disease Models, Animal, MicroRNAs, Case-Control Studies, neat1, Oxygenases, Female, RNA, Long Noncoding, atherosclerosis, TP248.13-248.65, Research Article, Research Paper, Biotechnology
Abstract

Atherosclerosis (AS) is one of the main causes of cardiovascular diseases (CVDs). Trimethylamine N-oxide (TMAO) exacerbates the development of AS. This study aimed to investigate the roles of TMAO in AS. In this study, mice were fed with high fat food (HF) and/or injected with TMAO. Oil red O staining was applied for histological analysis. ELISA, qRT-PCR, and Western blot were conducted to determine the TMAO, serum, mRNA, and protein levels. CCK-8, colony formation assay, and flow cytometry assays were performed to detect the functions of human aortic endothelial cells (HUVECs). The results showed that TMAO induced thick internal and external walls and intimal plaques in vivo, and HUVEC dysfunction in vitro. TMAO and lncRNA enriched abundant transcript 1 (NEAT1) were increased in AS clinical samples and TMAO-HUVECs. Downregulated NEAT1 inhibited proliferation and promoted the apoptosis of HUVECs. NEAT1 regulated the expression of signal transducer and activator of transcription 3 (STAT3) via sponging miR-370-3p. Overexpression of miR-370-3p facilitated the effects of NEAT1 on the cellular functions of HUVECs, while STAT3 exerted opposing effects. The activation of STAT3 promoted the expression of flavin-containing monooxygenase-3 (FMO3). Taken together, our results show that TMAO-NEAT1/miR-370-3p/STAT3/FMO3 forms a positive feedback loop to exacerbate the development of AS. This novel feedback loop may be a promising therapeutic target for AS.

Published
2022

21. mRNAsi-related metabolic risk score model identifies poor prognosis, immunoevasive contexture, and low chemotherapy response in colorectal cancer patients through machine learning

Author

Weng, Meilin, primary, Li, Ting, additional, Zhao, Jing, additional, Guo, Miaomiao, additional, Zhao, Wenling, additional, Gu, Wenchao, additional, Sun, Caihong, additional, Yue, Ying, additional, Zhong, Ziwen, additional, Nan, Ke, additional, Liao, Qingwu, additional, Sun, Minli, additional, Zhou, Di, additional, and Miao, Changhong, additional

Published
2022
Full Text
View/download PDF

25. Association of Mu-Opioid Receptor Expression With Long-Term Survival and Perineural Nerve Invasion in Patients Undergoing Surgery for Ovarian Cancer

Author

Zhang, Hao, primary, Qu, Mengdi, additional, Sun, Caihong, additional, Wang, Yanghanzhao, additional, Li, Ting, additional, Xu, Wei, additional, Sun, Zhirong, additional, Zhang, Xiaoguang, additional, Guo, Kefang, additional, Chen, Wankun, additional, Sun, Minli, additional, and Miao, Changhong, additional

Published
2022
Full Text
View/download PDF

29. Tailored Chemodynamic Nanomedicine Improves Pancreatic Cancer Treatment via Controllable Damaging Neoplastic Cells and Reprogramming Tumor Microenvironment

Author

Chen, Yu, primary, Huang, Yukun, additional, Zhou, Songlei, additional, Sun, Minli, additional, Chen, Liang, additional, Wang, Jiahao, additional, Xu, Minjun, additional, Liu, Shanshan, additional, Liang, Kaifan, additional, Zhang, Qian, additional, Jiang, Tianze, additional, Song, Qingxiang, additional, Jiang, Gan, additional, Tang, Xuyi, additional, Gao, Xiaoling, additional, and Chen, Jun, additional

Published
2020
Full Text
View/download PDF

33. Depletion of Gsdma1/2/3 alleviates PMA-induced epidermal hyperplasia by inhibiting the EGFR-Stat3/Akt pathway.

Author

Liu Q, Li M, Sun M, Xin R, Wang Y, Chen Q, Gao X, and Lin Z

Subjects
Animals, Mice, Mice, Inbred C57BL, Gasdermins, STAT3 Transcription Factor metabolism, ErbB Receptors metabolism, ErbB Receptors genetics, Hyperplasia, Proto-Oncogene Proteins c-akt metabolism, Tetradecanoylphorbol Acetate pharmacology, Signal Transduction drug effects, Mice, Knockout, Epidermis pathology, Epidermis metabolism, Epidermis drug effects, Keratinocytes metabolism, Keratinocytes pathology
Abstract

Homeostasis of the skin barrier is essential for maintaining normal skin function. Gasdermin A (GSDMA) is highly expressed in the skin and associated with many skin diseases, such as melanoma and psoriasis. In mice, GSDMA is encoded by three gene homologues, namely Gsdma1, Gsdma2, and Gsdma3. Although Gsdma3 gain-of-function mutations cause hair loss and skin inflammation, Gsdma3-deficient mice do not show any visible phenotypes in skin and hair structures. To explore the physiological function of GSDMA, we generated conventional Gsdma1/2/3 knockout (KO) mice. These mice showed significantly alleviated epidermal hyperplasia and inflammation induced by phorbol 12-myristate 13-acetate (PMA). Furthermore, the alleviation of epidermal hyperplasia depended on the expression of Gsdma1/2/3 specifically in keratinocytes. Mechanistically, Gsdma1/2/3 depletion downregulated epidermal growth factor receptor (EGFR) ligands, leading to the decreased EGFR-Stat3/Akt signalling. These results demonstrate that depletion of Gsdma1/2/3 alleviates PMA-induced epidermal hyperplasia partially by inhibiting the EGFR-Stat3/Akt pathway., (© The Author(s) (2023). Published by Oxford University Press on behalf of Journal of Molecular Cell Biology, CEMCS, CAS.)

Published
2024
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results