The aim of this study was to investigate the effect of intracellular acidification on accumulation of rhodamine 123 (rh123) in non-mature cells with none or low expression of multidrug resistance MDR1. The expression of MDR1 mRNA was detected by real-time quantitative RT-PCR. Confocal laser microscopy was used to determine the calibration curve of intracellular acidification (pHi). MTT assay was used to detect the cytotoxicity of intracellular acidification on HL-60, MSC and CD34(+) cells from umbilical cord blood. Flow cytometry was applied to measure the influence of intracellular acidification. The results indicated that the intracellular acidification had no obvious cytotoxicity on HL-60, MSC and CD34(+) cells. The acidification resulted in the increased rhodamine 123 accumulation in HL-60, MSC and CD34(+) cells without P-gp activity. Moreover, the more primitive cells, the less accumulation of intracellular Rh123 were observed. It is concluded that the intracellular acidification can reverse the MDR of HL-60, MSC and CD34(+) cells.
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Microbiol Res
December 2024
School of Medical Laboratory, Shandong Second Medical University, Weifang 261053, China. Electronic address:
Non-tuberculous Mycobacteria (NTM) are found extensively in various environments, yet most are non-pathogenic. Only a limited number of these organisms can cause various infections, including those affecting the lungs, skin, and central nervous system, particularly when the host's autoimmune function is compromised. Among these, Non-tuberculous Mycobacteria Pulmonary Diseases (NTM-PD) are the most prevalent.
View Article and Find Full Text PDFHistochem Cell Biol
January 2025
Departamento de Diagnóstico en Patología y Medicina Oral, Facultad de Odontología, Universidad de La República, General Las Heras 1925, Montevideo, Uruguay.
The tumor microenvironment is an altered milieu that imposes multiple selective pressures leading to the survival and dissemination of aggressive and fit tumor cell subpopulations. How pre-tumoral and tumoral cells respond to changes in their microenvironment will determine the subsequent evolution of the tumor. In this study, we have subjected pre-tumoral and tumoral cells to coverslip-induced hypoxia, which recapitulates the intracellular hypoxia and extracellular acidification characteristic of the early tumor microenvironment, and we have used a combination of quantitative phase microscopy and epifluorescence to analyze diverse cellular responses to this altered environment.
View Article and Find Full Text PDFFront Immunol
January 2025
Department of Biophysics and Cell Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
The human voltage-gated proton channel (H1) provides an efficient proton extrusion pathway from the cytoplasm contributing to the intracellular pH regulation and the oxidative burst. Although its pharmacological inhibition was previously shown to induce cell death in various cell types, no such effects have been examined in polarized macrophages albeit H1 was suggested to play important roles in these cells. This study highlights that 5-chloro-2-guanidinobenzimidazole (ClGBI), the most widely applied H1 inhibitor, reduces the viability of human THP-1-derived polarized macrophages at biologically relevant doses with M1 macrophages being the most, and M2 cells the least sensitive to this compound.
View Article and Find Full Text PDFRMD Open
December 2024
The First Department of Internal Medicine, University of Occupational and Environmental Health Japan, Kitakyushu, Japan
Objective: To elucidate the association between the changes in intracellular metabolism in the early stage of B cell activation and systemic lupus erythematosus (SLE) pathogenesis.
Methods: CD19 or CD19CD27 (naïve) cells from the peripheral blood of healthy controls and lupus patients were cultured under different stimuli. The changes in intracellular metabolism and signalling pathways in these cells were evaluated.
Zhongguo Dang Dai Er Ke Za Zhi
December 2024
Children's Medical Center, Xiangya Hospital, Central South University, Changsha 410008, China.
Objectives: To explore the mechanism by which Wiskott-Aldrich syndrome protein family verprolin-homologous protein 1 (WAVE1) regulates lipopolysaccharide (LPS)-induced mitochondrial metabolic abnormalities and inflammatory responses in macrophages.
Methods: Macrophage cell lines with overexpressed WAVE1 (mouse BMDM and human THP1 cells) were prepared. The macrophages were treated with LPS (500 ng/mL) to simulate sepsis-induced inflammatory responses.
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