Objectives: Diesel exhaust particles (DEP)s are notorious ambient pollutants composed of a complex mixture of a carbon core and diverse chemical irritants. Several studies have demonstrated significant relationships between DEP exposure and serious nasal inflammatory response , but available information regarding underlying networks in terms of gene expression changes has not sufficiently explained potential mechanisms of DEP-induced nasal damage, especially .
Methods: In the present study, we identified DEP-induced gene expression profiles under short-term and long-term exposure, and identified signaling pathways based on microarray data for understanding effects of DEP exposure in the mouse nasal cavity.
Results: Alteration in gene expression due to DEP exposure provokes an imbalance of the immune system via dysregulated inflammatory markers, predicted to disrupt protective responses against harmful exogenous substances in the body. Several candidate markers were identified after validation using qRT-PCR, including S100A9, CAMP, IL20, and S100A8.
Conclusions: Although further mechanistic studies are required for verifying the utility of the potential biomarkers suggested by the present study, our results may provide meaningful suggestions for understanding the complex cellular signaling pathways involved in DEP-induced nasal damages.
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http://dx.doi.org/10.1177/0003489419883289 | DOI Listing |
Dig Dis Sci
January 2025
Ningxia Medical University, Xing Qing Block, Shengli Street No.1160, Yin Chuan City, 750004, Ningxia Province, People's Republic of China.
Background: Colon adenocarcinoma (COAD) is a leading cause of cancer-related mortality worldwide. Transient receptor potential vanilloid 4 (TRPV4), a calcium-permeable non-selective cation channel, has been implicated in various cancers, including COAD. This study investigates the role of TRPV4 in colon adenocarcinoma and elucidates its potential mechanism via the ferroptosis pathway.
View Article and Find Full Text PDFClin Rheumatol
January 2025
Guizhou University of Traditional Chinese Medicine, Guiyang, Guizhou Province, China.
Objective: Rheumatoid arthritis (RA) is an autoimmune condition that causes severe joint deformities and impaired functionality, affecting the well-being and daily life of individuals. Consequently, there is a pressing demand for identifying viable therapeutic targets for treating RA. This study aimed to explore the molecular mechanisms of osteoclast differentiation in PBMC from patients with RA through transcriptome sequencing and bioinformatics analysis.
View Article and Find Full Text PDFBiochem Genet
January 2025
Department of Gynecology, Women's Hospital, Zhejiang University School of Medicine, Hangzhou, China.
This study aimed to identify shared gene expression related to circadian rhythm disruption in polycystic ovary syndrome (PCOS) and non-alcoholic fatty liver disease (NAFLD) to discover common diagnostic biomarkers. Visceral fat RNA samples were collected from 12 PCOS and 14 non-PCOS patients, a sample size representing the clinical situation and sufficient to capture PCOS gene expression profiles. Along with liver transcriptome profiles from NAFLD patients, these data were analyzed to identify crosstalk circadian rhythm-related genes (CRRGs) between the diseases.
View Article and Find Full Text PDFClin Exp Med
January 2025
Department of Thoracic Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China.
Introduction Recently, immune cells within the tumor microenvironment (TME) have become crucial in regulating cancer progression and treatment responses. The dynamic interactions between tumors and immune cells are emerging as a promising strategy to activate the host's immune system against various cancers. The development and progression of hepatocellular carcinoma (HCC) involve complex biological processes, with the role of the TME and tumor phenotypes still not fully understood.
View Article and Find Full Text PDFArch Dermatol Res
January 2025
Department of Physiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
We have recently shown that fluoxetine (FX) suppressed polyinosinic-polycytidylic acid-induced inflammatory response and endothelin release in human epidermal keratinocytes, via the indirect inhibition of the phosphoinositide 3-kinase (PI3K)-pathway. Because PI3K-signaling is a positive regulator of the proliferation, in the current, highly focused follow-up study, we assessed the effects of FX (14 µM) on the proliferation and differentiation of human epidermal keratinocytes. We found that FX exerted anti-proliferative actions in 2D cultures (HaCaT and primary human epidermal keratinocytes [NHEKs]; 48- and 72-h; CyQUANT-assay) as well as in 3D reconstructed epidermal equivalents (48-h; Ki-67 immunohistochemistry).
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