Objective: To explore the expression of miR-155 in patients with chronic lymphocytic leukemia (CLL) and its correlation with the clinical and biological features in CLL.
Methods: The expression of miR-155 was detected by quantitative real time polymerase chain reaction (qRT-PCR) in the peripheral mononuclear cells collected from 73 CLL patients and CD19 positive B cells collected from 60 healthy controls, respectively. The expression of miR-155 in CLL patients was compared with the healthy controls, and the correlation of miR-155 expression with the clinical characteristics of CLL patients such as age, sex, Binet stage, cytogenetic and molecular genetic, as well as the relationship of miR-155 expression level with time to treatment (TTT) and overall survival (OS) was further analysed.
Results: The expression of miR-155 was significantly elevated in CLL patients compared with the healthy controls. Further analysis showed that miR-155 expression decreased in the patients with the mutated immunoglobulin heavy chian variable region (IGHV) as compared with the patients unmutated (P<0.05), and its expression was significant higher in the IGHV-39 family (P<0.05). Fluorescence in situ hybridization (FISH) showed that the expression of miR-155 increased in patients with P53 mmutation/deletion and ATM deletion (P<0.05). However, OS and TTT were not different between the patients with high and low expression of miR-155.
Conclusion: MiR-155 is increasingly expresses in CLL patients and correlates with poor prognosis, suggesting its important role in the genesis and progress of CLL.
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http://dx.doi.org/10.19746/j.cnki.issn.1009-2137.2020.01.007 | DOI Listing |
Diabetes Metab Syndr Obes
January 2025
Department of Nursing, Indonesian Christian University of Maluku, Ambon, Maluku, Indonesia.
Heliyon
January 2025
Wolfson Sensory, Pain and Regeneration Centre, King's College London, London, United Kingdom.
Neuropathic pain following peripheral nerve injury results from maladaptive changes in neurons and immune cells contribution to mechanisms underlying chronic pain. Specifically, in dorsal root ganglia (DRG), sensory neuron cell bodies release extracellular vesicles (EVs) which promote pro-inflammatory macrophage accumulation that facilitates nociceptive signalling. Here, we show that macrophages shuttle EVs to neurons.
View Article and Find Full Text PDFRev Invest Clin
January 2025
Department of Immunology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.
Background: MiR-155 plays a role in inflammatory pathways and cardiovascular diseases, though its relationship with inflammation, atherosclerosis, and outcomes in ST-elevation myocardial infarction (STEMI) is not well established.
Objective: To investigate associations between miR-155 levels, inflammation, atherosclerotic burden, and major adverse cardiovascular events (MACE) in STEMI patients.
Methods: Sixty-nine STEMI patients and 16 healthy controls were recruited from a specialized university-affiliated cardiovascular center.
Chem Res Toxicol
January 2025
Department of Prenatal Diagnosis Center, The Second Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong 524000, China.
The widespread use of perfluorooctanesulfonic acid (PFOS) has raised concerns regarding its potential on pregnant women, particularly in relation to the development of pre-eclampsia (PE). This study investigates the impact of PFOS exposure on the LncRNA/Rnd3 axis in pregnant mice and its association with trophoblast cell functions in PE. Bioinformatics analysis revealed PFOS-related gene alterations in PE, with pathways enriched in apoptotic signaling and cytokine interactions.
View Article and Find Full Text PDFZhongguo Zhong Yao Za Zhi
December 2024
School of Traditional Chinese Medicine, Binzhou Medical College Yantai 264003, China Institute of Basic Medicine, Xiyuan Hospital, China Academy of Chinese Medical Sciences Beijing 100091, China.
This article explored the specific mechanism by which ginsenoside Rg_1 regulates cellular autophagy to attenuate hypoxia/reoxygenation(H/R) injury in HL-1 cardiomyocytes through the microRNA155(miR-155)/neurogenic gene Notch homologous protein 1(Notch1)/hairy and enhancer of split 1(Hes1) pathway. An HL-1 cell model with H/R injury was constructed, and ginsenoside Rg_1 and/or Notch1 inhibitor DAPT and miR-155 mimics were used to treat cells. Cell counting kit(CCK)-8 was used to detect the relative viability of HL-1 cells with H/R injury.
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