Proliferative phenotype of pulmonary microvascular endothelial cells plays a critical role in the overexpression of CTGF in the bleomycin-injured rat

Yan, Lin‐Feng; Wei, Yuying; Nan, Hai-Yan; Yin, Qian; Qin, Ying; Zhao, Xin; Chen, Baoying; Zhao, Guisen; Wei, Jing-Guo; Cui, Guang-Bin

doi:10.1016/j.etp.2013.08.004

Cited by 8 publications

(8 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CTGF is involved in various biological processes, including extracellular matrix production, proliferation, apoptosis, chemotaxis, and angiogenesis. Many cell types express CTGF, including endothelial cells, vascular smooth muscle cells, fibroblasts, and cardiac myocytes . CTGF is upregulated by stimuli involved in cardiovascular damage, including oxidative stress .…”

Section: Resultsmentioning

confidence: 99%

“…Many cell types express CTGF, including endothelial cells, vascular smooth muscle cells, fibroblasts, and cardiac myocytes. 43 CTGF is upregulated by stimuli involved in cardiovascular damage, including oxidative stress. 44,45 Our research group has previously reported that fermented goat milk induces a significant elevation of some antioxidant endogenous enzymes, together with an increase in TAS, a decrease in 8-hydroxy-2 ′ -deoxyguanosine, reducing DNA strand breaks, hydroperoxides, 15-F2t-isoprostanes and protein carbonyl groups in tissues, revealing an improvement in both systemic and cellular antioxidant activity of plasma and tissues due to fermented goat milk consumption.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Fermented goat milk consumption improves cardiovascular health during anemia recovery

et al. 2018

View full text Add to dashboard Cite

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Fermented goat milk consumption improves cardiovascular health during anemia recovery

et al. 2018

View full text Add to dashboard Cite

show abstract

“…These genes are important in blood vessel formation ( ACVRL1 ) [ 32 ], endothelial cell migration and angiogenesis ( RhoJ ) [ 33 ], endothelial cell proliferation, smooth muscle cell recruitment, and vascular remodeling ( ENG ) [ 34 , 35 ], as well as endothelial cell adhesion and survival ( CTGF ) [ 36 ]. Furthermore, several genes that were significantly co-expressed with PEAR1 have also been previously implicated in endothelial-related pathological conditions including pulmonary fibrosis ( CTGF ) [ 37 ] and hemorrhagic telangiectasia ( ACVRL1 and ENG ) [ 38 ]. While, to date, no investigation has evaluated the potential relationship between PEAR1 and any of these genes and conditions, our results suggest that future studies may be warranted.…”

Section: Discussionmentioning

confidence: 99%

Genetic Variation in the Platelet Endothelial Aggregation Receptor 1 Gene Results in Endothelial Dysfunction

et al. 2015

View full text Add to dashboard Cite

Platelet Endothelial Aggregation Receptor 1 (PEAR1) is a newly identified membrane protein reported to be involved in multiple vascular and thrombotic processes. While most studies to date have focused on the effects of this receptor in platelets, PEAR1 is located in multiple tissues including the endothelium, where it is most highly expressed. Our first objective was to evaluate the role of PEAR1 in endothelial function by examining flow-mediated dilation of the brachial artery in 641 participants from the Heredity and Phenotype Intervention Heart Study. Our second objective was to further define the impact of PEAR1 on cardiovascular disease computationally through meta-analysis of 75,000 microarrays, yielding insights regarding PEAR1 function, and predictions of phenotypes and diseases affected by PEAR1 dysregulation. Based on the results of this meta-analysis we examined whether genetic variation in PEAR1 influences endothelial function using an ex vivo assay of endothelial cell migration. We observed a significant association between rs12041331 and flow-mediated dilation in participants of the Heredity and Phenotype Intervention Heart Study (P = 0.02). Meta-analysis results revealed that PEAR1 expression is highly correlated with several genes (e.g. ANG2, ACVRL1, ENG) and phenotypes (e.g. endothelial cell migration, angiogenesis) that are integral to endothelial function. Functional validation of these results revealed that PEAR1 rs12041331 is significantly associated with endothelial migration (P = 0.04). Our results suggest for the first time that genetic variation of PEAR1 is a significant determinant of endothelial function through pathways implicated in cardiovascular disease.

show abstract

“…The atherosusceptible endothelium is characterized by elevated expression of proatherogenic genes as well as consequential aberrant proliferation, migration, and pro-inflammatory responses 1 . The proatherogenic genes that can be induced by application of disturbed flow or OS to ECs include cyclin A (CCNA2) 22 , 23 and connective tissue growth factor (CTGF) 10 , 24 , those have been found to be highly expressed in atherosclerotic plaques 25 – 27 . Cyclin A promotes both G1/S and G2/M transitions of the cell cycle in somatic cells.…”

Section: Introductionmentioning

confidence: 99%

“…Cyclin A promotes both G1/S and G2/M transitions of the cell cycle in somatic cells. CTGF has been associated with proliferation and inflammation in ECs and it enhances the chemosensory adhesion and migration of monocytes into atherosclerotic lesions 26 , 27 . Promoter DNA methylation contributes to the regulatory mechanisms of cyclin A and CTGF by various stimuli such as homocysteine 21 or high glucose 28 .…”

Section: Introductionmentioning

confidence: 99%

The Mammalian Target of Rapamycin and DNA methyltransferase 1 axis mediates vascular endothelial dysfunction in response to disturbed flow

Zhang

Huang

et al. 2017

Sci Rep

View full text Add to dashboard Cite

The earliest atherosclerotic lesions preferentially develop in arterial regions experienced disturbed blood flow, which induces endothelial expression of pro-atherogenic genes and the subsequent endothelial dysfunction. Our previous study has demonstrated an up-regulation of DNA methyltransferase 1 (DNMT1) and a global hypermethylation in vascular endothelium subjected to disturbed flow. Here, we determined that DNMT1-specific inhibition in arterial wall ameliorates the disturbed flow-induced atherosclerosis through, at least in part, targeting cell cycle regulator cyclin A and connective tissue growth factor (CTGF). We identified the signaling pathways mediating the flow-induction of DNMT1. Inhibition of the mammalian target of rapamycin (mTOR) suppressed the DNMT1 up-regulation both in vitro and in vivo. Together, our results demonstrate that disturbed flow influences endothelial function and induces atherosclerosis in an mTOR/DNMT1-dependent manner. The conclusions obtained from this study might facilitate further evaluation of the epigenetic regulation of endothelial function during the pathological development of atherosclerosis and offer novel prevention and therapeutic targets of this disease.

show abstract

Proliferative phenotype of pulmonary microvascular endothelial cells plays a critical role in the overexpression of CTGF in the bleomycin-injured rat

Cited by 8 publications

References 39 publications

Fermented goat milk consumption improves cardiovascular health during anemia recovery

Fermented goat milk consumption improves cardiovascular health during anemia recovery

Genetic Variation in the Platelet Endothelial Aggregation Receptor 1 Gene Results in Endothelial Dysfunction

The Mammalian Target of Rapamycin and DNA methyltransferase 1 axis mediates vascular endothelial dysfunction in response to disturbed flow

Contact Info

Product

Resources

About