Change of extracellular signal-regulated kinase expression in pulmonary arteries from smokers with and without chronic obstructive pulmonary disease

Liu, Kui; Liu, Xiansheng; Yu, Muqing; Xu, Yongjian

doi:10.3109/01902148.2013.788234

Cited by 6 publications

(7 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Low concentrations of CSE (1, 2 and 5%) increased cell proliferation, while high concentrations exhibited a significant inhibition on cell proliferation. These results were in accordance with previous studies (34)(35)(36).…”

Section: Discussionsupporting

confidence: 94%

Inhibition of FHL1 inhibits cigarette smoke extract-induced proliferation in pulmonary arterial smooth muscle cells

Chen

et al. 2015

Molecular Medicine Reports

View full text Add to dashboard Cite

Cigarette smoke can induce pulmonary vascular remodeling, which involves pulmonary artery smooth muscle cell (PASMC) proliferation, resulting in pulmonary hypertension in chronic obstructive pulmonary disease. FHL1 is a member of the FHL subfamily, characterized by an N‑terminal half LIM domain, followed by four complete LIM domains, and has been suggested to be critical in cell proliferation. However, the effects of FHL1 on cigarette smoke‑induced PASMC proliferation and the precise molecular mechanism remain to be elucidated. The present study demonstrated that the protein expression of FHL1 correlated with cigarette smoke extract (CSE)‑induced PASMC proliferation. Knockdown of the expression of FHL1 using siRNA significantly suppressed cell proliferation and inhibited the cell cycle transition between the G1 and S phase by regulating the cyclin‑dependent kinase pathway at the basal level and following CSE stimulation. By contrast, overexpressing FHL1 using an adenovirus increased cell proliferation and promoted the cell cycle transition between the G1 and S phase. Furthermore, CSE significantly increased the protein expression of FHL1, however, exerted no effect on the mRNA expression levels. This alteration was due to the prolonged FHL1 half‑life, leading to the antagonizing of protein degradation. Collectively, these data suggested that FHL1 may be involved in excessive cell proliferation and may represent a potential therapeutic target for pulmonary hypertension.

show abstract

Section: Discussionsupporting

confidence: 94%

Inhibition of FHL1 inhibits cigarette smoke extract-induced proliferation in pulmonary arterial smooth muscle cells

Chen

et al. 2015

Molecular Medicine Reports

View full text Add to dashboard Cite

show abstract

“…The ERK/MAPK signaling pathway regulates multiple biological processes including development, apoptosis, autophagy, oncogenesis, and inflammation ( 9 ). Several studies have described upregulation of the ERK pathway following CS exposure both in vivo and in vitro ( 12 , 17 ). In agreement, our present results revealed that the expression and phosphorylation of ERK1/2 were increased in COPD patients and in endothelial cells treated with CSE.…”

Section: Discussionmentioning

confidence: 99%

“…Overexpression of constituted active form of Notch1 (N1ICD) suppressed Toll-like receptor-triggered extracellular signal-regulated kinase (ERK) activation in macrophages, suggesting that Notch1 should be an ERK regulator ( 39 ). The ERK pathway, a regulator of cellular processes, has been shown to increase following exposure to CS both in vivo and in vitro ( 12 , 17 ). In addition, ERK activation plays an active role in CS-induced apoptosis ( 17 ).…”

Section: Introductionmentioning

confidence: 99%

Notch1 regulates endothelial apoptosis via the ERK pathway in chronic obstructive pulmonary disease

Zong

Cai

et al. 2018

American Journal of Physiology-Cell Physiology

View full text Add to dashboard Cite

The Notch signaling pathway plays critical role for determining cell fate by controlling proliferation, differentiation, and apoptosis. In the current study, we investigated the roles of the Notch signaling pathway in cigarette smoke (CS)-induced endothelial apoptosis in chronic obstructive pulmonary disease (COPD). We obtained surgical specimens from 10 patients with COPD and 10 control participants. Notch1, 2, and 4 express in endothelial cells, whereas Notch3 mainly localizes in smooth muscle cells. Compared with control groups, we found that the expression of Notch1, 3, and 4 decreased, as well as their target genes Hes1 and Hes2, while the expression of Notch2 and extracellular signal-regulated kinase (ERK)1/2 increased in COPD patients compared with controls, as well as in human pulmonary microvascular endothelial cells (HPMECs) when exposed to CS extract (CSE). Overexpression of Notch1 with N1ICD in HPMECs markedly alleviated the cell apoptosis induced by CSE. The ERK signaling pathway was significantly activated by CSE, which correlated with CSE-induced apoptosis. However, this activation can be abolished by N1ICD overexpression. Furthermore, treatment of PD98059 (ERK inhibitor) significantly alleviated CSE-induced apoptosis, as well as reduced the methylation of mitochondrial transcription factor A (mtTFA) promoter, which was correlated with CS-induced endothelial apoptosis. These results suggest that CS alters Notch signaling in pulmonary endothelial cells. Notch1 protects against CS-induced endothelial apoptosis in COPD through inhibiting the ERK pathway, while the ERK pathway further regulates the methylation of mtTFA promotor.

show abstract

“…Cell proliferation, differentiation, and survival are all controlled by the mitogen-activated protein kinase (MAPK) superfamily, of which extracellular signal-regulated kinase (ERK) is a subfamily (163,164). The expression of ERK was shown to be considerably higher in smokers in both in vivo and in vitro experiments (165,166). Ginkgo biloba extract protects human pulmonary artery endothelial cells (HPAECs) against cigarette smoke extract-induced apoptosis through ERK signalling, as shown by Hsu et al (167).…”

Section: Dna Methylationmentioning

confidence: 89%

The Function of Histone Modifications in Chronic Obstructive Pulmonary Disease

Nezhad¹

2022

Preprint

View full text Add to dashboard Cite

Numerous genes expression lead to inflammation in the individuals’ lungs that have chronic obstructive pulmonary disease (COPD) may be affected by epigenetic alteration. Important epigenetic processes include methylation of DNA and different histones post-translational changes, including ubiquitination, phosphorylation, methylation, SUMOylation and acetylation. Smoking can trigger the enzymes that control these epigenetic changes. According to the majority of publications, both environmental and genetic variables have a substantial role in the development of COPD. Although, the information about COPD epigenetic is not much but, a better perception of the disease pathophysiology and identifying new markers to create novel therapeutics for patients can be achieved via a better understanding of the epigenetic processes involved.

show abstract

Change of extracellular signal-regulated kinase expression in pulmonary arteries from smokers with and without chronic obstructive pulmonary disease

Abstract: Increased expression of ERK might be involved in the pathogenesis of abnormal proliferation of PASMCs in smokers with and without COPD.

Cited by 6 publications

References 27 publications

Inhibition of FHL1 inhibits cigarette smoke extract-induced proliferation in pulmonary arterial smooth muscle cells

Inhibition of FHL1 inhibits cigarette smoke extract-induced proliferation in pulmonary arterial smooth muscle cells

Notch1 regulates endothelial apoptosis via the ERK pathway in chronic obstructive pulmonary disease

The Function of Histone Modifications in Chronic Obstructive Pulmonary Disease

Contact Info

Product

Resources

About