Effect of Trimethyltin chloride on proliferation and cell cycle of intestinal porcine epithelial cells

Background/Aim: Aspergillus is often detected in respiratory samples from patients with chronic respiratory diseases, including pulmonary fibrosis, suggesting that it can easily colonize the airways. To determine the role of Aspergillus colonization in pulmonary fibrosis, we cultured human lung epithelial A549 cells or murine embryo fibroblast NIH/3T3 cells with Aspergillus conidia in 3D floating culture representing the microenvironment. Materials and Methods: Cells were cultured in two-dimensional (2D) and three-dimensional floating (3DF) culture with heat-inactivated Aspergillus fumigatus (AF) 293 conidia at an effector-to-target cell ratio of 1:10 (early-phase model) and 1:100 (colonization model), and RNA-sequencing and Western blots (WB) were performed. Results: AF293 conidia reduced A549 cell growth in 2D and 3DF cultures and induced apoptosis in A549 spheroids in 3DF culture. RNA-sequencing revealed the increased expression of genes associated with interferon-mediated antiviral responses including MX dymamin-like GTPase 1 (MX1). Interestingly, the decreased expression of genes associated with the cell cycle was observed with a high concentration of AF293 conidia. WB revealed that epithelial-mesenchymal transition was not involved. Notably, AF293 conidia increased NIH/3T3 growth only in 3DF culture without inducing an apoptotic reaction. RNA-sequencing revealed the increased expression of genes associated with interferon signalling, including MX2; however, the decreased expression of genes associated with the cell cycle was not observed. Conclusions: AF affects both apoptosis of epithelial cells and the growth of fibroblasts. A deeper understanding of the detailed mechanisms underlying Aspergillus-mediated signaling pathway in epithelial cells and fibroblasts will help us to understand the lung microenvironment.

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C/EBP β mediates the aberrant inflammatory response and cell cycle arrest in LPS-stimulated human renal tubular epithelial cells by regulating NF-κB pathway

Archives of Medical Research ◽

10.1016/j.arcmed.2021.03.008 ◽

2021 ◽

Author(s):

Ni Yang ◽

Hai Wang ◽

Rui Zhang ◽

Zequn Niu ◽

Shaowei Zheng ◽

...

Keyword(s):

Cell Cycle ◽

Epithelial Cells ◽

Inflammatory Response ◽

Cell Cycle Arrest ◽

Tubular Epithelial Cells ◽

Renal Tubular Epithelial Cells ◽

Cycle Arrest ◽

Renal Tubular

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Spirulina Crude Protein Promotes the Migration and Proliferation in IEC-6 Cells by Activating EGFR/MAPK Signaling Pathway

Marine Drugs ◽

10.3390/md17040205 ◽

2019 ◽

Vol 17 (4) ◽

pp. 205

Author(s):

Su-Jin Jeong ◽

Jeong-Wook Choi ◽

Min-Kyeong Lee ◽

Youn-Hee Choi ◽

Taek-Jeong Nam

Keyword(s):

Cell Cycle ◽

Epithelial Cells ◽

Signaling Pathway ◽

Crude Protein ◽

Cell Cycle Progression ◽

Intestinal Epithelial Cells ◽

Mapk Signaling ◽

S Phase ◽

Intestinal Epithelial ◽

Cycle Progression

Spirulina is a type of filamentous blue-green microalgae known to be rich in nutrients and to have pharmacological effects, but the effect of spirulina on the small intestine epithelium is not well understood. Therefore, this study aims to investigate the proliferative effects of spirulina crude protein (SPCP) on a rat intestinal epithelial cells IEC-6 to elucidate the mechanisms underlying its effect. First, the results of wound-healing and cell viability assays demonstrated that SPCP promoted migration and proliferation in a dose-dependent manner. Subsequently, when the mechanisms of migration and proliferation promotion by SPCP were confirmed, we found that the epidermal growth factor receptor (EGFR) and mitogen-activated protein (MAPK) signaling pathways were activated by phosphorylation. Cell cycle progression from G0/G1 to S phase was also promoted by SPCP through upregulation of the expression levels of cyclins and cyclin-dependent kinases (Cdks), which regulate cell cycle progression to the S phase. Meanwhile, the expression of cyclin-dependent kinase inhibitors (CKIs), such as p21 and p27, decreased with SPCP. In conclusion, our results indicate that activation of EGFR and its downstream signaling pathway by SPCP treatment regulates cell cycle progression. Therefore, these results contribute to the research on the molecular mechanism for SPCP promoting the migration and proliferation of rat intestinal epithelial cells.

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Cell cycle regulation of mammary epithelial cell detachment byStaphylococcus aureus

Journal of Dairy Research ◽

10.1017/s0022029900032088 ◽

1996 ◽

Vol 63 (4) ◽

pp. 543-553 ◽

Cited By ~ 1

Author(s):

Boris Zavizion ◽

Andrew J. Bramley ◽

Ioannis Politis

Keyword(s):

Cell Cycle ◽

Epithelial Cells ◽

Culture Medium ◽

Mammary Epithelial Cells ◽

Mammary Epithelial ◽

Cell Detachment ◽

Staph Aureus ◽

Bovine Mammary Epithelial Cells ◽

Isogenic Mutants ◽

Cycle Regulation

SummaryThe effect ofStaphylococcus aureuson detachment of bovine mammary epithelial cells in culture was examined. Mammary epithelial cells became detached from fresh monolayers following a 3 h incubation in the presence ofStaph. aureusM60. Two different procedures indicated that cell detachment coincided with the S-phase of the cell cycle. The roles of proteinases, toxins and Ca availability in inducing cell detachment were examined. Addition of the proteinase inhibitor phenyl-methylsulphonyl fluoride (1 mM) to the culture medium prevented cell detachment. Addition of a combination of purified staphylococcal proteinases XVI and XVII-B to the culture medium of mammary epithelial cells induced cell detachment in the absence ofStaph. aureus. Cell detachment may be caused by a staphylococcal proteinase. However, addition of Ca (10 mM) to the culture medium abolishedStaph. aureus-induced cell detachment, despite the fact that proteinase activity was still apparently present. Isogenic mutants ofStaph. aureusM60, expressing either ± or β toxins but not both, induced cell detachment, but to a lesser extent than the wild type. Thus, Ca and toxins play some role during cell detachment. Clones established from detached cells that were washed and replated showed the same susceptibility toStaph. aureus-induced cell detachment as the parental cells. This indicated that there is no subclone of mammary epithelial cells more sensitive to this effect.

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The proliferative effect of cortisol on bovine endometrial epithelial cells

Reproductive Biology and Endocrinology ◽

10.1186/s12958-019-0544-1 ◽

2019 ◽

Vol 17 (1) ◽

Author(s):

Junsheng Dong ◽

Jun Li ◽

Jianji Li ◽

Luying Cui ◽

Xia Meng ◽

...

Keyword(s):

Cell Cycle ◽

Growth Factors ◽

Growth Factor ◽

Epithelial Cells ◽

Signaling Pathways ◽

Akt Signaling ◽

Tissue Growth ◽

Mrna Levels ◽

Physiological Level ◽

Endometrial Epithelial Cells

Abstract Background Bovine endometrial epithelial cells (BEECs) undergo regular regeneration after calving. Elevated cortisol concentrations have been reported in postpartum cattle due to various stresses. However, the effects of the physiological level of cortisol on proliferation in BEECs have not been reported. The aim of this study was to investigate whether cortisol can influence the proliferation properties of BEECs and to clarify the possible underlying mechanism. Methods BEECs were treated with different concentrations of cortisol (5, 15 and 30 ng/mL). The mRNA expression of various growth factors was detected by quantitative reverse transcription-polymerase chain reaction (qPCR), progression of the cell cycle in BEECs was measured using flow cytometric analysis, and the activation of the Wnt/β-catenin and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathways was detected with Western blot and immunofluorescence. Results Cortisol treatment resulted in upregulated mRNA levels of vascular endothelial growth factor (VEGF) and connective tissue growth factor (CTGF); however, it had no influence on transforming growth factor-beta1 (TGF-β1). Cortisol (15 ng/mL) accelerated the cell cycle transition from the G0/G1 to the S phase. Cortisol upregulated the expression of β-catenin, c-Myc, and cyclinD1 and promoted the phosphorylation of PI3K and AKT. Conclusions These results demonstrated that cortisol may promote proliferation in BEECs by increasing the expression of some growth factors and activating the Wnt/β-catenin and PI3K/AKT signaling pathways.

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Down-regulation of Orai3 arrests cell-cycle progression and induces apoptosis in breast cancer cells but not in normal breast epithelial cells

Journal of Cellular Physiology ◽

10.1002/jcp.22363 ◽

2010 ◽

Vol 226 (2) ◽

pp. 542-551 ◽

Cited By ~ 109

Author(s):

Malika Faouzi ◽

Frederic Hague ◽

Marie Potier ◽

Ahmed Ahidouch ◽

Henri Sevestre ◽

...

Keyword(s):

Breast Cancer ◽

Cell Cycle ◽

Epithelial Cells ◽

Cancer Cells ◽

Breast Cancer Cells ◽

Cell Cycle Progression ◽

Normal Breast ◽

Cycle Progression ◽

Breast Epithelial Cells ◽

Normal Breast Epithelial Cells

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Inflammatory Response Elicited by Ureaplasma parvum colonization in human cervical epithelial, stromal, and immune cells

Reproduction ◽

10.1530/rep-21-0308 ◽

2021 ◽

Author(s):

Ourlad Alzeus Gaddi Tantengco ◽

Talar Kechichian ◽

Kathleen L Vincent ◽

Richard B Pyles ◽

Paul Mark B Medina ◽

...

Keyword(s):

Cell Cycle ◽

Cell Death ◽

Epithelial Cells ◽

Inflammatory Response ◽

Stromal Cells ◽

Female Reproductive Tract ◽

Ureaplasma Parvum ◽

Cervical Epithelial Cells ◽

Anti Inflammatory ◽

The Impact

Ureaplasma parvum is a commensal bacterium in the female reproductive tract but has been associated with pregnancy complications such as preterm prelabor rupture of membranes and preterm birth (PTB). However, the pathologic effects of U. parvum in the cervix, that prevents ascending infections during pregnancy, are still poorly understood. To determine the impact of U. parvum on the cervix, ectocervical (ecto) and endocervical (endo) epithelial and stromal cells were incubated with U. parvum. Macrophages were also tested as a proxy for cervical macrophages to determine the antigenicity of U. parvum. The effects of U. parvum, including influence on cell cycle and cell death, antimicrobial peptide production, epithelial-to-mesenchymal transition (EMT), and inflammatory cytokine levels, were assessed. U. parvum colonized cervical epithelial and stromal cells 4 hours post-infection. Like uninfected control, U. parvum neither inhibited cell cycle progression and nor caused cell death in cervical epithelial and stromal cells. U. parvum increased the production of the antimicrobial peptides (AMPs) cathelicidin and human β-defensin 3 and exhibited weak signs of EMT evidenced by decreased cytokeratin 18 and increased vimentin expression in cervical epithelial cells. U. parvum induced a pro-inflammatory environment (cytokines) and increased MMP-9 in cervical epithelial cells but promoted pro- and anti-inflammatory responses in cervical stromal cells and macrophages. U. parvum may colonize the cervical epithelial layer, but induction of AMPs and anti-inflammatory response may protect the cervix and may prevent ascending infections that can cause PTB. These findings suggest that U. parvum is a weak inducer of inflammation in the cervix.

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