Pitavastatin up‐regulates <scp>eNOS</scp> production by suppressing miR‐155 expression in lipopolysaccharide‐stimulated human umbilical vein endothelial cells

Jing, Changqin; Guo, Menglong; Bao, Xiaodan; Li, Tianhan; Lin, Juntang; Lu, Xinjie; Wang, Wenfeng

doi:10.1111/1755-5922.12282

Cited by 10 publications

(3 citation statements)

References 27 publications

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“…Following ER stress in diabetic rats, the expression of CHOP‐10 was significantly increased by regulating the eNOS gene promoter, thereby inhibiting eNOS mRNA expression. Second, Regulation of eNOS expression at the Transcriptional and Post‐transcriptional levels to regulate eNOS promotor activity and mRNA stability (Jing et al., 2017). The control of mRNA stabilisation has become an important mechanism for regulating the expression of target genes.…”

Section: Discussionmentioning

confidence: 99%

Probucol improves erectile function by regulating endoplasmic reticulum stress in rats with streptozotocin‐induced diabetes

et al. 2021

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This study was to explore the effect and mechanism of Probucol on STZ‐induced erectile dysfunction in diabetic rats. Thirty SD male rats aged 12 weeks were given intraperitoneal injection of STZ after fasting for 12 hr. Diabetic rats were haphazardly partitioned under two assemblies and administered 0 or 500 mg/kg probucol by oral gavage to 12 weeks. Control group was intraperitoneally injected with physiological saline, and saline was administered by oral gavage daily. Intracorporeal pressure was used to evaluate erectile function. Levels of proteins were detected using immunohistochemistry and Western blotting. α‐SMA and vWF were detected using immunofluorescence staining. After treatment, erectile function in probucol group was significantly improved. Endoplasmic reticulum stress‐related proteins were expressed higher in DM group than in sham group, while expression of these proteins decreased significantly in probucol group. However, α‐SMA and vWF were expressed at lower levels in DM group than in sham group, and probucol treatment reversed this phenomenon. Finally, Bax and Caspase3 were expressed at higher levels and Bcl‐2 was expressed at lower levels in DM group, while the opposite result was obtained in probucol group. In conclusions, probucol improves erectile function by reducing endothelial dysfunction and inhibiting PERK/ATF4/CHOP pathway in STZ‐induced diabetic rats.

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Section: Discussionmentioning

confidence: 99%

Probucol improves erectile function by regulating endoplasmic reticulum stress in rats with streptozotocin‐induced diabetes

et al. 2021

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“…LPS increased expression levels of miR-155 in rat primary synovial fibroblasts, an in-vitro model for rheumatoid arthritis [ 116 ]. Treating human primary umbilical vein endothelial cells with LPS (0.05–1 μg/L) for 24 h enhanced the expression of miR-155 in a dose-dependent manner [ 117 ]. In mouse primary osteoblasts and osteoclasts, miR-155 expression was found to be upregulated in a time-dependent manner upon LPS stimulation [ 118 , 119 ].…”

Section: Inductive Effect Of Tlr4 Activation On Mir-155mentioning

confidence: 99%

TLR4 signaling in the development of colitis-associated cancer and its possible interplay with microRNA-155

2021

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Ulcerative colitis (UC) has closely been associated with an increased risk of colorectal cancer. However, the exact mechanisms underlying colitis-associated cancer (CAC) development remain unclear. As a classic pattern-recognition receptor, Toll like receptor (TLR)4 is a canonical receptor for lipopolysaccharide of Gram-negative bacteria (including two CAC-associated pathogens Fusobacterium nucleatum and Salmonella), and functions as a key bridge molecule linking oncogenic infection to colonic inflammatory and malignant processes. Accumulating studies verified the overexpression of TLR4 in colitis and CAC, and the over-expressed TLR4 might promote colitis-associated tumorigenesis via facilitating cell proliferation, protecting malignant cells against apoptosis, accelerating invasion and metastasis, as well as contributing to the creation of tumor-favouring cellular microenvironment. In recent years, considerable attention has been focused on the regulation of TLR4 signaling in the context of colitis-associated tumorigenesis. MicroRNA (miR)-155 and TLR4 exhibited a similar dynamic expression change during CAC development and shared similar CAC-promoting properties. The available data demonstrated an interplay between TLR4 and miR-155 in the context of different disorders or cell lines. miR-155 could augment TLR4 signaling through targeting negative regulators SOCS1 and SHIP1; and TLR4 activation would induce miR-155 expression via transcriptional and post-transcriptional mechanisms. This possible TLR4-miR-155 positive feedback loop might result in the synergistic accelerating effect of TLR4 and miR-155 on CAC development.

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“…52,53 Additional miRNAs targeted by atorvastatin also include miRNA-22, which is involved in angiotensin II-mediated cardiac hypertrophy, 54 miRNA-29a-3p, miRNA-29b-3p, miRNA-454-39, miRNA-300m, miRNA33b-5p and miRNA-33a-5p. 55 When miRNA-155 is considered, its suppression induced by statins determines an upregulated transcription of eNOS gene in HUVECs, 56 whereas in human beings an increased expression of Src homology 2-containing-inositol-phosphatase-1 (SHIP1) was observed and associated with lower rate of cardiovascular injuries in patients receiving percutaneous coronary intervention. 14 MiRNAs would also mediate some anti-cancer properties of statins.…”

Section: Histone Modificationmentioning

confidence: 99%

Statins: Epidrugs with effects on endothelial health?

Mohammadzadeh

Montecucco

et al. 2020

Eur J Clin Investigation

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Background: Epigenetic events involving the methylation of CpG cites in DNA, histone modifications and noncoding RNAs correlated with many essential processes in human cells and diseases, such as cancer and cardiovascular diseases. HMG-CoA reductase inhibitors (statins)-the LDL cholesterol-lowering drugs-are broadly used in cardio-and cerebro-vascular diseases. It is well established that statins exert pleiotropic functions, but how they exert effects on epigenetic modifications independently of HMG-CoA reductase inhibition is not yet clear. Thereby, understanding these mechanisms may pave the way for further clinical application of statin therapy. Design: Following and electronic database search, studies reporting substantial effects of statins on epigenetic reprogramming in both cultured cells and in vivo models were retrieved and reviewed. Results: Epigenetic mechanisms play an essential role in cellular development and function, and data collected in the past few years have revealed that many of the pleiotropic properties of statins are mediated by epigenetic mechanisms. Furthermore, those 'nonclassical' effects are not limited to CV field but they would extend to other conditions such as malignancies. Conclusion: This review suggests that the epigenetic effects of statins mediate, at least in part, the pleiotropic actions of these drugs but further validation of such effects in clinical studies is yet to be provided.

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Pitavastatin up‐regulates eNOS production by suppressing miR‐155 expression in lipopolysaccharide‐stimulated human umbilical vein endothelial cells

Abstract: Pitavastatin increases eNOS expression and inhibits of LPS-induced miR-155 expression.

Cited by 10 publications

References 27 publications

Probucol improves erectile function by regulating endoplasmic reticulum stress in rats with streptozotocin‐induced diabetes

Probucol improves erectile function by regulating endoplasmic reticulum stress in rats with streptozotocin‐induced diabetes

TLR4 signaling in the development of colitis-associated cancer and its possible interplay with microRNA-155

Statins: Epidrugs with effects on endothelial health?

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