C-Kit/c-Kit ligand interaction of bone marrow endothelial progenitor cells is influenced in a cigarette smoke extract-induced emphysema model

He, Shengdong; He, Zhijun; Chen, Yan; Ye, Jiru; Zong, Dandan; Zhang, Yan; Chen, Ping

doi:10.3109/01902148.2013.802828

Cited by 21 publications

(21 citation statements)

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“…However, the inhibition of COX-2 expression by (26)(27)(28)(29)(30)(31). Tobacco consumption plays a critical role in the pathogenesis of pulmonary vascular abnormalities in COPD, of which the pulmonary vascular endothelial dysfunction is characteristically exhibited (32).…”

Section: Discussionmentioning

confidence: 99%

The role of cyclooxygenase-2 in the protection against apoptosis in vascular endothelial cells induced by cigarette smoking

et al. 2017

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Background: Apoptosis has been demonstrated to be an important upstream event in the pathogenesis of chronic obstructive pulmonary disease (COPD). Cyclooxygenase-2 (COX-2) seems to be biologically relevant in COPD. However, the role of COX-2 in the apoptosis in vascular endothelial cells induced by cigarette smoke extract (CSE) remains to be elucidated. Our recent study found that the prostacyclin, one of the COX products in the microvascular endothelium, inhibited apoptosis in the emphysematous lungs of rats induced by CSE. In order to clarify the role of COX-2 in the apoptosis of vascular endothelial cells induced by CSE, we performed the present experiment to elucidate it. Methods: Twenty surgical lung specimens were obtained from 6 patients with COPD, 7 smoking controls and seven nonsmoking controls. The apoptotic index (AI) and COX-2 protein expression were detected in lung tissues. To further investigate the effects of CSE on the apoptosis and COX-2 expression in a human vascular endothelial cell line, the apoptosis rate and COX-2 expression were examined in human umbilical vein endothelial cells (ECV304) under exposure to varied concentrations of CSE as well as under exposure to 5.0% CSE for varied durations. Repeatedly, the apoptosis rate and COX-2 expression in ECV304 cells under 5.0% CSE were examined after exposing to varied concentrations of celecoxib, a highly selective COX-2 inhibitor. Results: Significantly increased AI and expression of COX-2 were found both in the lungs of patients with COPD and smoking controls compared with nonsmoking controls. The CSE induced apoptosis in ECV304 cells in means of both dose-dependent and time-dependent manners. The COX-2 was slightly expressed in the cells after exposing to 5% CSE for 3 and 6 h, and markedly expressed after the exposure time for 9 and 12 h, but vanished after 24 h of the exposure. Of interest, with the completely block of the COX-2 expression by celecoxib at 50.0 μmol/L, the apoptosis rate was markedly increased again in ECV304 cells under exposure to 5.0% CSE. Conclusions: Endothelial cell apoptosis and the expression of COX-2 protein were increased in both COPD patients and CSE-induced vascular endothelial cells. Of interest, it seems that the COX-2 probably had a protective role against the apoptosis in the vascular endothelial cells induced by cigarette smoking.

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Section: Discussionmentioning

confidence: 99%

The role of cyclooxygenase-2 in the protection against apoptosis in vascular endothelial cells induced by cigarette smoking

et al. 2017

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“…30 C-Kit/c-Kit ligand interaction of bone marrow-derived EPCs was influenced in a CSE-induced emphysema model. 33 EPCs with normal self-renew, proliferatory capacity, differentiative potential are essential for their own trans-endothelia shift, homing to injured location, repairment, and regeneration of various tissues and organs. Oxidative stress could lead to premature EPCs ''aging''.…”

Section: Discussionmentioning

confidence: 99%

Decitabine enhances stem cell antigen-1 expression in cigarette smoke extract-induced emphysema in animal model

Chen

et al. 2015

Exp Biol Med (Maywood)

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Stem cell antigen-1 (Sca-1) is a mouse glycosyl phosphatidylinositol-anchored protein and a cell surface marker found on hematopoietic stem cells (HSCs). Despite decades of study, its biological functions remain little known. Sca-1 is a typical marker of bone marrow-derived HSCs, it is also expressed by a mixture of tissue-resident stem, progenitor cells in nonhematopoietic organs. Endothelial progenitor cell (EPC) is a subtype of HSC and contributes to endothelial repair by homing in on locations of injury. Abnormal genetic methylation has been detected in smoking-related diseases. The present study aimed to investigate the lung function and histomorphology, the expression of Sca-1 gene in lung tissues, and bone marrow-derived EPCs in cigarette smoke extract (CSE)-induced emphysema mice, and to further determine whether Decitabine (Dec), the most widely used inhibitor of DNA methylation, could protect against the damages caused by CSE. The results of the present study demonstrated that Dec could partly protect against CSE-induced emphysema in mice, enhance Sca-1 expression in lung tissue, and bone marrowderived EPCs. The results suggested that the depletion of the progenitor cell pool and DNA methylation of Sca-1 gene may be involved in the progression of emphysema in mice.

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“…As one of the most momentous risk factor of COPD, cigarette smoke could initiate apoptosis in macrophages, fibroblasts, vascular endothelial cells and epithelial cells. 22,23 Multiple evidence indicates that direct exposure to CSE affects miRNA expression in various lung diseases, including COPD. 24 A recent study reported that miR-34a was correlated with CSE-stimulated lung endothelial cell apoptosis in COPD.…”

Section: Discussionmentioning

confidence: 99%

“…9 In addition to the key genes related to COPD pathogenesis, non-coding RNAs containing microRNAs (miRNAs) have been shown to be concerned with COPD. 10,11 miRNAs, with [19][20][21][22][23][24][25] nucleotides, are a series of small endogenous nucleotide RNAs that participate in various biological processes by negatively modulate genes expression under post-transcriptional level. 12,13 The dysregulation of miRNAs are involved in multifarious diseases including COPD, which are often utilized as biomarkers for exposure to environmental factors.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐497 functions as an inflammatory suppressor via targeting DDX3Y and modulating toll‐like receptor 4/NF‐κB in cigarette smoke extract‐stimulated human bronchial epithelial cells

Jia

Zhao

2019

The Journal of Gene Medicine

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Background:We aimed to investigate the biological effect of miR-497 in cigarette smoke extract (CSE)-damaged human bronchial epithelial (HBE) cells and the underlying molecular mechanism.Methods: MiR-497 mimic was transfected into HBE cells to up-regulate miR-497 expression. Cigarette smoke extract (CSE, 20 μg/mL) was utilized to treat HBE cells to form the injury model. Cell proliferation and apoptosis were detected by CCK8 and flow cytometry assays. DDX3Y mRNA expression was determined by a quantitative reverse transcriptase-polymerase chain reaction. The interaction between miR-497 and DDX3Y was verified by a luciferase reporter assay. Protein expression levels were tested by western blotting.Results: CSE treatment decreased miR-497 level in HBE cells. CSE exposure restrained cell proliferation, promoted cell apoptosis and enhanced the relative expression of TLR4 and p-NF-κB p65. DDX3Y was predicted as a target of miR-497. The mRNA and protein expression of DDX3Y was negatively modulated by miR-497 in CSE-injured HBE cells. Up-regulation of miR-497 by miR-497 mimic increased cell proliferation and reduced cell apoptosis in CSE-treated HBE cells, which were rescued by DDX3Y high expression in CSE-treated HBE cells. Consistently, Bcl-2 protein level was heightened, whereas Bax and actived caspase-3/9 protein levels were decreased by miR-497 mimic in CSE-stimulated HBE cells, which was reversed by DDX3Y over-expression in CSE-stimulated HBE cells. The relative expression of TLR4 and p-NF-κB p65 was decreased by miR-497 mimic, whereas they were rescued by DDX3Y over-expression in CSE-damaged HBE cells. Conclusions:The results of the present study demonstrate that up-regulation of miR-497 exhibits a protective effect on CSE-damaged HBE cells, which might be achieved by targeting DDX3Y and regulating the TLR4/NF-κB pathway. KEYWORDSchronic obstructive pulmonary disease, cigarette smoke extract, DEAD-box helicase 3 Y-linked, human bronchial epithelial cells, miR-497, Toll-like receptor 4/NF-ĸB pathway

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C-Kit/c-Kit ligand interaction of bone marrow endothelial progenitor cells is influenced in a cigarette smoke extract-induced emphysema model

Abstract: The interaction between c-Kit and sKitL in bone marrow EPCs, a critical step in endothelial repair, is negatively affected in a CSE-induced emphysema model.

Cited by 21 publications

References 35 publications

The role of cyclooxygenase-2 in the protection against apoptosis in vascular endothelial cells induced by cigarette smoking

The role of cyclooxygenase-2 in the protection against apoptosis in vascular endothelial cells induced by cigarette smoking

Decitabine enhances stem cell antigen-1 expression in cigarette smoke extract-induced emphysema in animal model

MicroRNA‐497 functions as an inflammatory suppressor via targeting DDX3Y and modulating toll‐like receptor 4/NF‐κB in cigarette smoke extract‐stimulated human bronchial epithelial cells

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