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Idiopathic pulmonary fibrosis (IPF) is a progressive, chronic, and irreversible interstitial lung disease with unknown cause. To explore the role and regulatory mechanism of leucine-rich repeat-containing protein 15 (LRRC15) in IPF, bleomycin (BLM)-induced pulmonary fibrosis in mouse and A549 cells were constructed, and the expression of LRRC15 were detected. Then, MTT, GFP-RFP-LC3 dual fluorescent labeling system and Western blotting were used to investigate the effects of LRRC15 on cell activity and autophagy after transfection of siLRRC15, respectively. The results indicated that the expression of LRRC15 was significantly increased after the BLM treatment in mouse lung tissue and A549 cells. The designed and synthesized siLRRC15 followed by transfection into A549 cells resulted in a dramatic reduction in LRRC15 expression and partially restored the cell damage induced by BLM. Moreover, the expression of LC3-II and P62 were up-regulated, the amount of autophagosome were increased by GFP-RFP-LC3 dual fluorescent labeling assay after BLM treatment. Meanwhile, this study also showed that the key autophagy proteins LC3-II, ATG5 and ATG7 were up-regulated, P62 was down-regulated and autophagic flux were enhanced after further treatment of A549 cells with siLRRC15. The above findings suggest that LRRC15 is an indicator of epithelial cell damage and may participate in the regulation of fibrosis through autophagy mechanism in IPF. This study provides necessary theoretical basis for further elucidating the mechanism of IPF.
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http://dx.doi.org/10.16288/j.yczz.23-299 | DOI Listing |
Pathol Res Pract
March 2025
Department of Oncology, Xi'an International Medical Center Hospital, Xi'an 710100, China. Electronic address:
Background: Exosomes are released by most cell types, including tumor-associated macrophages (TAMs), transfer diverse macromolecules and participate in intercellular communication in cancer. However, whether M2-polarized TAMs (M2-TAMs)-derived exosomes (M2-exos) transmit the oncogenic protein malate dehydrogenase 1 (MDH1) to reprogram lung adenocarcinoma (LUAD) cancer cells is unknown.
Methods: THP-1-differentiated macrophages were co-cultured with A549 cells to generate TAMs (M0-TAMs and M2-TAMs).
Med Oncol
March 2025
National Engineering Research Center of Traditional Chinese Medicine Solid Preparation Manufacturing Technology, Jiangxi University of Traditional Chinese Medicine, Nanchang, 330004, China.
Recently, long non-coding RNAs have gained an increasing amount of attention in treating lung cancer. However, a full understanding of how CCAT1 lncRNA works against proliferation is not yet available. Therefore, we assess the impact of CCAT1 on the lung cancer cell proliferation, apoptosis, and doxorubicin (DOX) sensitivity, and the involvement of miR-181a/CPEB2 pathway.
View Article and Find Full Text PDFSci Rep
March 2025
Faculty of Engineering and Natural Sciences, Department of Industrial Engineering, Osmaniye Korkut Ata University, Osmaniye, 80000, Turkey.
In this study, the biological activities of the extracts obtained under optimum extraction conditions of the kernel part of Juglans regia L. were determined. Two different methods, Response Surface Method (RSM) and Artificial Neural Network-Genetic Algorithm (ANN-GA) integration, were used for optimization.
View Article and Find Full Text PDFAnn Clin Lab Sci
January 2025
Department of General Surgery, The Second People's Hospital of China Three Gorges University, Yichang, Hubei, China
Objective: We explored the mechanism of action of microRNA-146a in the lung cancer cell line A549 through the Noth1/Hes-1 signal pathway.
Methods: A549 cells were divided into a control NT group without transfection, NC group with transfection of miR-146a-NC, and MM group with transfection of miR-146a mimics. We employed qRT-PCR, MTT, Hoechst33258 fluorescence staining, Transwell assay, cell wound scratch assay, and Western blot for detection of the expression of miR-146a and Notch1/Hes-1, cell activity, apoptotic capacity, and invasion and migration abilities.
Microb Pathog
March 2025
Instituto Politécnico Nacional, Escuela Nacional de Ciencias Biológicas, Department of Microbiology, México City, México. Electronic address:
In recent years, Candida glabrata (C. glabrata) has emerged as a pathogen responsible for systemic mortal infections. C.
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