Upregulation of microRNA-320 decreases the risk of developing steroid-induced avascular necrosis of femoral head by inhibiting CYP1A2 both in vivo and in vitro

Wei, Jihua; Luo, Qunqiang; Tang, Yue; Chen, Ji-Xia; Huang, Chunlan; Lu, Dinggui; Tang, Qianli

doi:10.1016/j.gene.2018.03.045

Cited by 10 publications

(4 citation statements)

References 31 publications

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“…To find possible targets of miR-23b-3p, we predict the target of miR-23b-3p using the RNA22 website and finally focus on CYP1A2 to be investigated in the study. A previous study found that the expression of CYP1A2 was upregulated in the tissues of patients with SNFH [ 16 ]. Through the online prediction website of STRING, we found an association between CYP1A2 and the risk gene of SNFH.…”

Section: Discussionmentioning

confidence: 99%

“…It has been proved that miR-23b-3p can be regulated by lncRNA NEAT1, and miR-23b-3p can inhibit the progress of SNFH by inhibiting ZNF667 [ 15 ]. Wei et al found that CYP1A2 served as a downstream target of miR-23b-3p and was associated with the risk genes of SNFH, and upregulation of miR-320 could reduce the risk of SNFH by inhibiting CYP1A2 [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

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lncRNA NEAT1 regulates CYP1A2 and influences steroid-induced necrosis

Zhou

Zhang

et al. 2021

Open Life Sciences

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The main cause of steroid-induced necrosis of femoral head (SNFH) is excessive glucocorticoid (GC) intake. The aim of this article was to investigate the role of lncRNA NEAT1 as a molecular sponge to adsorb miR-23b-3p and regulate CYP1A2 in SNFH. Fluorescence in situ hybridization was used to localize lncRNA NEAT1. Human bone marrow mesenchymal stem cells (hBMSCs) were collected from patients with SNFH. The expression of lncRNA NEAT1, miR-23b-3p and CYP1A2 in hBMSCs were intervened. Compared to the control group, the lncRNA NEAT1 and CYP1A2 expression in the SNFH group was increased, while miR-23b-3p expression was decreased. GCs could inhibit the osteogenic differentiation of hBMSCs and upregulate the expression of lncRNA NEAT1. Knockdown of lncRNA NEAT1 could promote the proliferation and osteogenic differentiation of hBMSCs in the SNFH group. Overexpression of miR-23b-3p could partially counteract the effect of lncRNA NEAT1 on hBMSCs. CYP1A2 was confirmed to be a target of miR-23b-3p. Overexpression of CYP1A2 could partially rescue the effect of miR-23b-3p overexpression on hBMSCs. In conclusion, lncRNA NEAT1 as a ceRNA can adsorb miR-23b-3p and promote the expression of CYP1A2, which then inhibits the osteogenic differentiation of hBMSCs and promotes the progress of SNFH.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

lncRNA NEAT1 regulates CYP1A2 and influences steroid-induced necrosis

Zhou

Zhang

et al. 2021

Open Life Sciences

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“…Wei et al [29] found that the miR-320 expression level significantly decreased in patients with steroid-induced ONFH, accompanied by increased cytochrome P450 1A2 (CYP1A2) expression and activity. In animal models, luciferase reporter gene detection demonstrated that Cyp1a2 is the downstream target gene of miR-320, while hemodynamic and microcirculatory analyses indicated that upregulated CYP1A2 expression can greatly promote the occurrence and development of steroid-induced ONFH.…”

Section: Functions Of Mirnas In Animal Modelsmentioning

confidence: 99%

Noncoding RNAs in Steroid-Induced Osteonecrosis of the Femoral Head

Sun

Tan

2019

BioMed Research International

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Steroid-induced osteonecrosis of the femoral head (ONFH) is a severe orthopedic disease caused by the long-term administration of glucocorticoids. The main pathological feature of ONFH is the gradually progressive necrosis of bone cells and the bone marrow, ultimately resulting in structural changes or even complete collapse of the femoral head. However, the exact pathogenic mechanism of ONFH remains unknown. Noncoding RNAs (ncRNAs) have emerged as very powerful regulators of gene expression, functioning at both transcriptional and posttranscriptional levels in the pathogenesis of ONFH. Here, we review the current knowledge of the role of ncRNAs, including microRNAs, long noncoding RNAs, and circular RNAs, in the pathogenesis of steroid-induced ONFH. Further focus and validation of these associations can provide new insight into the pathogenic mechanisms at the molecular level to suggest targets for treatment and prevention.

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“…In the absence of any recognized ideal treatment strategies, most patients resort to artificial joint replacement surgery. However, post-surgery complications are frequent in corticosteroid-induced femoral head necrosis patients who are mostly young and middle-aged persons, with the attendant serious impact on them and their families [4]. Therefore, it is important to identify effective treatment methods at the early stage of the disease so as to prevent its occurrence.…”

Section: Introductionmentioning

confidence: 99%

Expression levels of apoptotic factors in a rat model of corticosteroid-induced femoral head necrosis

Fu¹,

Han²,

Xue³

et al. 2021

Trop. J. Pharm Res

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Purpose: To study the expression levels of apoptotic factors in corticosteroid-mediated femoral head necrosis (FHN) in rats. Methods: Sprague-Dawley (SD) rats (n = 60) bred adaptively for one week were randomly assigned to control and model groups (30 rats/group). A rat model of corticosteroid-induced femoral head necrosis was established. Then, 3 mL of blood drawn from the inferior vena cava of each rat was used for the assay of the expression levels of osteoprotegerin (OPG) and osteoclast differentiation factor (RANKL) in each group using enzyme-linked immunosorbent assay (ELISA). The caspase-3- and Bcl-2-+ve cells in each group were determined with immunohistochemical method. Results: Relative to control, serum OPG level of model group was significantly decreased, while the RANKL level was markedly raised (p < 0.05). The degree of empty lacunae in the model rats was markedly increased, relative to control. Caspase-3-+ve cells were more numerous in the model group than in control, while Bcl-2-positive cells were markedly decreased compared to control (p < 0.05). Conclusion: Apoptosis occurs in the rat model of femoral head necrosis. Glucocorticoids may regulate the apoptotic process by upregulating caspase-3 and inhibiting Bcl-2. This provides a novel lead for FHN therapy. Keywords: Femoral head necrosis, Corticosteroid, Glucocorticoid, Apoptosis

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Upregulation of microRNA-320 decreases the risk of developing steroid-induced avascular necrosis of femoral head by inhibiting CYP1A2 both in vivo and in vitro

Cited by 10 publications

References 31 publications

lncRNA NEAT1 regulates CYP1A2 and influences steroid-induced necrosis

lncRNA NEAT1 regulates CYP1A2 and influences steroid-induced necrosis

Noncoding RNAs in Steroid-Induced Osteonecrosis of the Femoral Head

Expression levels of apoptotic factors in a rat model of corticosteroid-induced femoral head necrosis

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