Identification of Genes Differentially Expressed in Simvastatin‐Induced Alveolar Bone Formation

Liu, Jingpeng; Chanumolu, S. K.; Krei, Z; Albahrani, Mustafa; Akhtam, A; Jia, Zhenshan; Wang, X; Wang, Dezhen; Otu, H. H.; Reinhardt, RA; Nawshad, Ali

doi:10.1002/jbm4.10122

Cited by 9 publications

(10 citation statements)

References 66 publications

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“…Also, simvastatin could recover the impaired Wnt/β‐catenin signalling caused by the effect of elevated glucose in mesangial cells and prevent their apoptosis 74 . These findings suggest that simvastatin can activate the Wnt/β‐catenin signalling pathway, thereby modulating several cell functions, including osteogenic differentiation 75 …”

Section: Statins Play Roles In Osteoblast Differentiation and Activitymentioning

confidence: 86%

The role of statins in the differentiation and function of bone cells

Chamani

Liberale

Mobasheri

et al. 2021

Eur J Clin Investigation

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Background Statins are 3‐Hydroxy‐3‐methylglutaryl coenzyme A (HMG‐CoA) reductase inhibitors blocking cholesterol biosynthesis in hepatic cells, thereby causing an increase in low‐density lipoprotein (LDL) receptors resulting in enhanced uptake and clearance of atherogenic LDL‐cholesterol (LDL‐C) from the blood. Accordingly, statins decrease the risk of developing atherosclerosis and its acute complications, such as acute myocardial infarction and ischaemic stroke. Besides the LDL‐C‐lowering impact, statins also have other so‐called pleiotropic effects. Among them, the ability to modulate differentiation and function of bone cells and exert direct effects on osteosynthesis factors. Specifically, earlier studies have shown that statins cause in vitro and in vivo osteogenic differentiation. Design The most relevant papers on the bone‐related ‘pleiotropic’ effects of statins were selected following literature search in databases and were reveiwed. Results Statins increase the expression of many mediators involved in bone metabolism including bone morphogenetic protein‐2 (BMP‐2), glucocorticoids, transforming growth factor‐beta (TGF‐β), alkaline phosphatase (ALP), type I collagen and collagenase‐1. As a result, they enhance bone formation and improve bone mineral density by modulating osteoblast and osteoclast differentiation. Conclusion This review summarizes the literature exploring bone‐related ‘pleiotropic’ effects of statins and suggests an anabolic role in the bone tissue for this drug class. Accordingly, current knowledge encourages further clinical trials to assess the therapeutic potential of statins in the treatment of bone disorders, such as arthritis and osteoporosis.

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Section: Statins Play Roles In Osteoblast Differentiation and Activitymentioning

confidence: 86%

The role of statins in the differentiation and function of bone cells

Chamani

Liberale

Mobasheri

et al. 2021

Eur J Clin Investigation

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“…Research. 8um-thick serial formalin-fixed paraffin-embedded sections and frozen sections were used to serve IHC and IF staining as previously described (22). Primary antibodies against Ki-67, IGF2BP3, E-Cadherin, SNAI, ZEB-2 and Caspase-3 were used in this study (see Supplementary file 1: Table S3).…”

Section: Immunohistochemistry (Ihc) and Immunofluorescent (If) Stainingmentioning

confidence: 99%

circIGHG-Induced Epithelial-to-Mesenchymal Transition Promotes Oral Squamous Cell Carcinoma Progression via miR-142-5p/IGF2BP3 Signaling

et al. 2021

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Circular RNAs (circRNA) are a new member of endogenously produced noncoding RNAs that have been characterized as key regulators of gene expression in a variety of malignances. However, the role of circRNA in oral squamous cell carcinoma (OSCC) remains largely unknown. In this study, we identified unique circRNA that regulate OSCC progression and metastasis and pave roads for future research in early diagnosis, prevention, and treatment of OSCC. Transcriptomic analyses identified a circRNA derived from IGHG locus (circIGHG) as significantly upregulated in OSCC and positively associated with poor prognosis of OSCC. circIGHG directly bound miR-142-5p and consequently elevated IGF2BP3 activity. Knockdown of circIGHG led to impaired expression of IGF2BP3 and attenuated aggressiveness of OSCC cells. Epithelial–mesenchymal transition was the main mechanism through which circIGHG/IGF2BP3 promotes metastasis of OSCC. Overall, these results demonstrate that circIGHG plays a pivotal role in OSCC development and metastasis and has potential to serve as a biomarker and therapeutic target for early-stage diagnosis and treatment of OSCC. Significance: These findings broaden our insights regarding regulation of OSCC progression by circular RNA and serve as a reference for future clinical research in OSCC diagnosis and treatment.

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“…Future study of temporal responses of plasma osteocrin in subjects presenting with ACS, and plasma levels of microRNA-100 and miRNA-143 (proven negative regulators of Npr3 expression in cardiac tissue 41,46 , can be expected to clarify these observations and contribute to our understanding of the adaptive responses to cardiac injury in humans. Although statins are reported to upregulate osteocrin gene expression in bone tissues 47 , any possible contribution of statins to the current findings seems unlikely in view of unchanging NTproCNP/CNP ratios from baseline values in days 1-7 in all three groups.…”

Section: Discussionmentioning

confidence: 60%

Effect of statin therapy on plasma C-type Natriuretic Peptides and Endothelin-1 in males with and without symptomatic coronary artery disease

Prickett

Troughton

Espiner

2020

Sci Rep

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C-type Natriuretic Peptide (CNP) and Endothelin-1 (ET-1) have reciprocal roles in maintaining vascular homeostasis and are acutely modulated by statins in human cultured endothelial cells. Whether these actions of statins in vitro are reflected in studies in vivo is unknown. In a prospective study of 66 subjects with or without post-acute coronary syndrome (ACS), plasma concentrations of bioactive CNP and bio-inactive aminoterminal proCNP (NTproCNP), ET-1, B-type Natriuretic Peptide (BNP) and high sensitivity C Reactive Protein (hsCRP) were measured together with lipids before and at intervals of 1, 2 and 7 days after commencing atorvastatin 40 mg/day-and for a further period of 6months in those with ACS. Plasma lipids fell significantly in all subjects but plasma CNP, NTproCNP and ET-1 were unchanged by atorvastatin. In ACS, baseline hsCRP, BNP and CNP but not NTproCNP or ET-1 were significantly raised compared to values in age-matched controls. The ratio of NTproCNP to CNP was significantly lower in ACS throughout the study and was unaffected by statin therapy. We conclude that conventional doses of atorvastatin do not affect plasma CNP products or ET-1. Elevated CNP after cardiac injury likely results from regulated changes in clearance, not enhanced production. Statin therapy is widely employed to prevent coronary artery disease and stroke. Statins reduce serum cholesterol and have contributed to reduced morbidity and mortality of cardiovascular disease in the last three decades. Independent of actions on lipids, numerous studies show potentially beneficial (pleiotropic) effects of statinsincluding anti-inflammatory actions within vascular tissues 1-which are important in maintaining endothelial integrity and preventing atherosclerosis 2. In vitro studies suggest that statins may have important beneficial effects on important regulators of vascular structure and function. Among these are the endothelial peptides, C-type Natriuretic Peptide (CNP) and Endothelin-1 (ET-1) both of which are modulated by statins in studies using human vascular endothelial cells in tissue culture 3. CNP is a growth factor expressed in the vascular endothelium wherein anti-inflammatory, anti-proliferative and vaso-dilator actions of the mature peptide have vasoprotective roles by reducing intimal injury 4. While evidence supports a largely paracrine mode of action of CNP, clinical studies show that products of proCNP in plasma (aminoterminal proCNP, NTproCNP, and bio active CNP) are increased in settings of vascular stress in both young adults 5 and at mid-life 6-possibly as an adaptive response to inflammation and/or shear stress 7,8. These results together with other findings suggest that tissue changes in CNP or ET-1 production 9 may be captured by concurrent changes in plasma if studied under well standardised conditions. Since the CNP gene (NPPC) expression is upregulated by statins in at least three different tissues-human umbilical vein endothelial cells 10 , porcine aortic valve interstitial cells 11 and hepatic endothelial ...

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Identification of Genes Differentially Expressed in Simvastatin‐Induced Alveolar Bone Formation

Cited by 9 publications

References 66 publications

The role of statins in the differentiation and function of bone cells

The role of statins in the differentiation and function of bone cells

circIGHG-Induced Epithelial-to-Mesenchymal Transition Promotes Oral Squamous Cell Carcinoma Progression via miR-142-5p/IGF2BP3 Signaling

Effect of statin therapy on plasma C-type Natriuretic Peptides and Endothelin-1 in males with and without symptomatic coronary artery disease

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