scholarly journals Cytochrome P450 2S1 Depletion Enhances Cell Proliferation and Migration in Bronchial Epithelial Cells, in Part, through Modulation of Prostaglandin E2 Synthesis

2012 ◽  
Vol 40 (11) ◽  
pp. 2119-2125 ◽  
Author(s):  
T. W. Madanayake ◽  
T. P. Fidler ◽  
T. M. Fresquez ◽  
N. Bajaj ◽  
A. M. Rowland
Keyword(s):  
Cell Proliferation ◽  
Cytochrome P450 ◽  
Epithelial Cells ◽  
Prostaglandin E2 ◽  
Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Chitinase-like protein YKL-40 regulates human bronchial epithelial cells proliferation, apoptosis, and migration through TGF-β1/Smads pathway

2019 ◽  
Vol 39 (4) ◽  
pp. 451-463 ◽  
Author(s):  
R Guan ◽  
R Lin ◽  
R Jin ◽  
L Lu ◽  
X Liu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Biological Behavior ◽  
Control Group ◽  
Bronchial Epithelial ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Tgf Β1 ◽  
Cells Cultured ◽  
Proliferation And Migration

In order to study the effects of chitinase-like protein YKL-40 on proliferation, apoptosis, and migration of human bronchial epithelial cell line (BEAS-2B), and the underlying mechanisms, we cultured BEAS-2B alone or with different concentrations of YKL-40. thiazolyl blue tetrazolium bromide (MTT) assay was used to examine the cell proliferation. Annexin V-fluorescein isothiocyanate isomer (FITC)/propidium iodide staining and scratch assay were performed to test the cell apoptosis and migration. The concentrations of transforming growth factor-β1 (TGF-β1), Smad3, Smad7, alpha-smooth muscle actin (α-SMA), interleukin-4 (IL-4), IL-6, and IL-8 in the cell culture supernatant were detected by enzyme-linked immunosorbent assay. The messenger RNA and protein levels of YKL-40, TGF-β1, Smad3, Smad7, and α-SMA were detected by reverse transcription polymerase chain reaction and Western blot. BEAS-2B cells cultured with different concentrations of YKL-40 showed significantly higher cell proliferation and migration and inflammatory cytokines compared with that of control group, while the cell apoptosis was significantly lower than that of control group ( p < 0.05). In addition, BEAS-2B cells cultured with YKL-40 had increased TGF-β1, Smad3, Smad7, and α-SMA levels in the supernatant, compared with that of BEAS-2B cells cultured alone ( p < 0.05). Furthermore, LY364947, as TGF-β1/Smads signaling pathway inhibitor, decreased cell proliferation and migration ability and enhanced cell apoptosis of BEAS-2B cells compared with control group ( p < 0.05). However, YKL-40 administration reversed the effect of LY364947 on the biological behavior of BEAS-2B cells. YKL-40 could affect the biological behaviors of BEAS-2B cells, which might be related to the TGF-β1/Smads pathway.

scholarly journals Exosomal miR-380 derived from alveolar macrophages in COPD is involved in enhanced proliferation of human bronchial epithelial cells

2020 ◽  
Author(s):  
Yunxin Fan ◽  
Xiumin Feng ◽  
Jingxi Zhang ◽  
Chong Bai
Keyword(s):  
Lung Cancer ◽  
Epithelial Cells ◽  
Alveolar Macrophages ◽  
Proliferative Activity ◽  
Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Tnf Α ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background Chronic obstructive pulmonary disease (COPD) is closely related to the occurrence of lung cancer. Both diseases involve changes in the biological function and structure of bronchial epithelial cells. Recently, the role of exosomes in intercellular communication has attracted increasing attention from researchers. As an important molecule carried by exosomes, the role of exosomal miRNAs in diseases such as COPD and lung cancer has also been gradually confirmed. The aim of this study is to investigate the effect of exosomal miRNA derived from macrophages on the proliferation of bronchial epithelial cells. Results After co-culture with alveolar macrophages from COPD, the proliferative activity and migration capacity of 16HBE was significantly enhanced compared with those from healthy controls. Alveolar macrophages from COPD promoted the production of MUC5AC, MUC5B and MUC2 as well as TNF - α and IL-6 in 16HBE. MiR-380 was up-regulated miRNA in exosomes derived from alveolar macrophages through miRNA array analysis. Exosomal miR-380 enhanced the proliferation and migration of 16HBE, promoted the expression of mucins such as MUC5AC, MUC5B and MUC2 of 16HBE, but inhibited the expression of CFTR protein. The target gene of miR-380 was CFTR. The proliferative activity and migration ability of 16HBE was enhanced by blocking CFTR. Conclusions Alveolar macrophages from COPD can enhance the proliferation and migration of 16HBE and promote the expression of mucin and proinflammatory mediators such as IL-6 and TNF-α. Exosomal miR-380 derived from macrophages in COPD was significantly up-regulated. The enhancement of proliferation and migration may be related to the down regulation of CFTR by exosomes delivering miR-380 to bronchial epithelial cells, opening a new way for the therapy and prevention in COPD and its complication.

scholarly journals Netrin-1 increases proliferation and migration of renal proximal tubular epithelial cells via the UNC5B receptor

2009 ◽  
Vol 296 (4) ◽  
pp. F723-F729 ◽  
Author(s):  
Weiwei Wang ◽  
W. Brian Reeves ◽  
Ganesan Ramesh
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cells ◽  
Tubular Epithelial Cell ◽  
Tubular Epithelial Cells ◽  
Renal Tubular Epithelial Cell ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Renal Tubular ◽  
Proliferation And Migration

The cellular hallmark of kidney repair is a rapid proliferation of renal tubular epithelial cells ultimately leading to the restoration of nephron structure and function. Netrin-1 was discovered as a neural guidance cue and found to be expressed outside the nervous system, including in kidney. Previous work showed that netrin-1 is upregulated in response to ischemic injury and ameliorates ischemic injury. The objectives of this study were to determine the role of netrin-1 in renal tubular epithelial cell proliferation and migration in vitro. Real-time RT-PCR analysis showed that netrin-1 and its receptors UNC5B and neogenin are highly expressed in cultured mouse renal epithelial cells (TKPTS), whereas the expression of the Deleted in Colon Cancer (DCC), UNC5A, UNC5C, and UNC5D receptors is negligible or undetectable. Netrin-1 protein was induced in the edges of mechanical wounds in vitro. Netrin-1 increased TKPTS cell proliferation in a dose-dependent manner. The netrin-1-induced increase in TKPTS cell proliferation was completely prevented by small interfering RNA (siRNA) inhibition of UNC5B receptor but not UNC5C receptor expression. Netrin-1 also increased TKPTS cell migration in vitro, and this was also mediated through the UNC5B receptor. Netrin-1 increased the phosphorylation of Akt and ERK. Inhibition of phosphatidylinositol 3-kinase and MEK1/2 completely inhibited netrin-1-induced cell proliferation but not migration. These results indicate that netrin-1 increases renal tubular epithelial cell proliferation and migration through the UNC5B receptor. Moreover, the increase in cell proliferation, but not migration, was mediated via activation of Akt and ERK pathways.

scholarly journals MiR-21 in Substance P-induced exosomes promotes cell proliferation and migration in human colonic epithelial cells

2019 ◽  
Vol 317 (6) ◽  
pp. G802-G810 ◽  
Author(s):  
Kyriaki Bakirtzi ◽  
Ivy Ka Man Law ◽  
Kai Fang ◽  
Dimitrios Iliopoulos ◽  
Charalabos Pothoulakis
Keyword(s):  
Cell Proliferation ◽  
Substance P ◽  
Epithelial Cells ◽  
Colonic Epithelial Cells ◽  
Cell Proliferation And Migration ◽  
Exosome Biogenesis ◽  
And Migration ◽  
Proliferation And Migration

Exosomes are cellular vesicles involved in intercellular communication via their specialized molecular cargo, such as miRNAs. Substance P (SP), a neuropeptide/hormone, and its high-affinity receptor, NK-1R, are highly expressed during colonic inflammation. Our previous studies show that SP/NK-1R signaling stimulates differential miRNA expression and promotes colonic epithelial cell proliferation. In this study, we examined whether SP/NK-1R signaling regulates exosome biogenesis and exosome-miRNA cargo sorting. Moreover, we examined the role of SP/NK-1R signaling in exosome-regulated cell proliferation and migration. Exosomes produced by human colonic NCM460 epithelial cells overexpressing NK-1R (NCM460-NK1R) were isolated from culture media. Exosome abundance and uptake were assessed by Western blot analysis (abundance) and Exo-Green fluorescence microscopy (abundance and uptake). Cargo-miRNA levels were assessed by RT-PCR. Cell proliferation and migration were assessed using xCELLigence technology. Colonic epithelial exosomes were isolated from mice pretreated with SP for 3 days. Cell proliferation in vivo was assessed by Ki-67 staining. SP/NK-1R signaling in human colonic epithelial cells (in vitro) and mouse colons (in vivo) increased 1) exosome production, 2) the level of fluorescence in NCM460s treated with Exo-Green-labeled exosomes, and 3) the level of miR-21 in exosome cargo. Moreover, our results showed that SP/NK-1R-induced cell proliferation and migration are at least in part dependent on intercellular communication via exosomal miR-21 in vitro and in vivo. Our results demonstrate that SP/NK-1R signaling regulates exosome biogenesis and induces its miR-21 cargo sorting. Moreover, exosomal miR-21 promotes proliferation and migration of target cells. NEW & NOTEWORTHY Substance P signaling regulates exosome production in human colonic epithelial cells and colonic crypts in wild-type mice. MiR-21 is selectively sorted into exosomes induced by Substance P stimulation and promotes cell proliferation and migration in human colonocytes and mouse colonic crypts.

scholarly journals HB-EGF-induced IL-8 secretion from airway epithelium leads to lung fibroblast proliferation and migration

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yanyu Li ◽  
Guomei Su ◽  
Yu Zhong ◽  
Zhilin Xiong ◽  
Tong Huang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Epithelium ◽  
Bronchial Epithelial Cells ◽  
Lung Fibroblast ◽  
Lung Fibroblasts ◽  
Bronchial Epithelial ◽  
Airway Fibrosis ◽  
And Migration ◽  
Culture Supernatants ◽  
Proliferation And Migration

Abstract Background We have reported that heparin-binding epidermal growth factor (HB-EGF) is increased in patients with chronic obstructive pulmonary disease (COPD) and associated with collagen deposition, but the mechanisms remain unclear. In the present study, we aimed to investigated the inflammatory cytokines secreted by bronchial epithelial cells following exposure to HB-EGF that promoted proliferation and migration of human lung fibroblast. Methods HB-EGF–induced inflammatory cytokines were assayed in two airway epithelial cells (primary human bronchial epithelial cells [HBECs] and BEAS-2B cells). Moreover, the culture supernatants derived from HB-EGF-treated HBECs and BEAS-2B cells were added to human primary lung fibroblasts. The effect of culture supernatants on proliferation and migration of fibroblasts was assessed. Results IL-8 expression was significantly increased in bronchial epithelial cells treated with HB-EGF, which was at least partially dependent on NF-kB pathways activation. HB-EGF–induced IL-8 was found to further promote lung fibroblasts proliferation and migration, and the effects were attenuated after neutralizing IL-8. Conclusions These findings suggest that HB-EGF may be involved in the pathology of airway fibrosis by induction of IL-8 from airway epithelium, subsequently causing lung fibroblasts proliferation and migration. Thus, inhibition of HBEGF and/or IL-8 production could prevent the development of airway fibrosis by modulating fibroblast activation.

ARFGAP3 an androgen target gene promotes prostate cancer cell proliferation and migration.

2020 ◽  
Author(s):  
Lungwani Muungo
Keyword(s):  
Cell Proliferation ◽  
Cancer Cell ◽  
Cell Biology ◽  
Adaptor Protein ◽  
Cancer Cell Proliferation ◽  
Lncap Cells ◽  
Gtpase Activating Protein ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

ADP ribosylation factor GTPase-activating protein 3 (ARFGAP3) is a GTPase-activating protein that associates with the Golgiapparatus and regulates the vesicular trafficking pathway. In the present study, we examined the contribution of ARFGAP3 toprostate cancer cell biology. We showed that ARFGAP3 expression was induced by 100 nM of dihydrotestosterone (DHT) atboth the mRNA and protein levels in androgen-sensitive LNCaP cells. We generated stable transfectants of LNCaP cells withFLAG-tagged ARFGAP3 or a control empty vector and showed that ARFGAP3 overexpression promoted cell proliferation andmigration compared with control cells. We found that ARFGAP3 interacted with paxillin, a focal adhesion adaptor protein thatis important for cell mobility and migration. Small interfering RNA (siRNA)-mediated knockdown of ARFGAP3 showed thatARFGAP3 siRNA markedly reduced LNCaP cell growth. Androgen receptor (AR)-dependent transactivation activity on prostatespecificantigen (PSA) enhancer was synergistically promoted by exogenous ARFGAP3 and paxillin expression, as shown byluciferase assay in LNCaP cells. Thus, our results suggest that ARFGAP3 is a novel androgen-regulated gene that can promoteprostate cancer cell proliferation and migration in collaboration with paxillin.

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