Inhibition of miR-203 Ameliorates Osteoarthritis Cartilage Degradation in the Postmenopausal Rat Model: Involvement of Estrogen Receptor α

Tian, Lijun; Su, Zhiyong; Ma, Xiuli; Wang, Feng; Guo, Yusong

doi:10.1089/humc.2019.101

“…The role of miR-203 in the regulation of ERα and cartilage degradation in IL-1β-stimulated chondrocytes has been verified in another study [98]. The suppression of miR-203 expression has improved osteoarthritis cartilage degradation in an animal model [99]. A number of miRNAs such as miR-26b-3p are involved in the regulation of osteoblast differentiation [100].…”

Section: Mirnas and Er Function In Other Disordersmentioning

confidence: 86%

Perspectives on the Role of Non-Coding RNAs in the Regulation of Expression and Function of the Estrogen Receptor

Taheri

¹

,

Shoorei

²

,

Dinger

³

et al. 2020

Cancers

View full text Add to dashboard Cite

Estrogen receptors (ERs) comprise several nuclear and membrane-bound receptors with different tissue-specific functions. ERα and ERβ are two nuclear members of this family, whereas G protein-coupled estrogen receptor (GPER), ER-X, and Gq-coupled membrane estrogen receptor (Gq-mER) are membrane-bound G protein-coupled proteins. ERα participates in the development and function of several body organs such as the reproductive system, brain, heart and musculoskeletal systems. ERβ has a highly tissue-specific expression pattern, particularly in the female reproductive system, and exerts tumor-suppressive roles in some tissues. Recent studies have revealed functional links between both nuclear and membrane-bound ERs and non-coding RNAs. Several oncogenic lncRNAs and miRNAs have been shown to exert their effects through the modulation of the expression of ERs. Moreover, treatment with estradiol has been shown to alter the malignant behavior of cancer cells through functional axes composed of non-coding RNAs and ERs. The interaction between ERs and non-coding RNAs has functional relevance in several human pathologies associated with estrogen regulation, such as cancers, intervertebral disc degeneration, coronary heart disease and diabetes. In the current review, we summarize scientific literature on the role of miRNAs and lncRNAs on ER-associated signaling and related disorders.

show abstract

“…demonstrated that miR-140-5p was related with chondrocyte proliferation, apoptosis and inflammation in OA 32 . MiR-203 inhibition could ameliorate OA cartilage degradation in postmenopausal rat model 33 . We used starBase to forecast the target miRNA of MEG3 and found that miR-361-5p was a target of MEG3.…”

Section: Discussionmentioning

confidence: 99%

MEG3 promotes proliferation and inhibits apoptosis in osteoarthritis chondrocytes by miR-361-5p/FOXO1 axis

Wang

¹

,

Hu

²

,

Zhang

³

et al. 2019

Preprint

View full text Add to dashboard Cite

Background: This study aimed to investigate the role of long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) and related molecular mechanisms in osteoarthritis (OA). Methods: Patients with OA and patients undergoing thigh amputation were involved in OA group and normal group, respectively. Cartilage tissues of all patients were isolated and cultured. Based on different transfection, MEG3 cells were grouped into Blank, pcDNA3.1-NC, pcDNA3.1-MEG3, si-NC, si-MEG3, pcDNA3.1-NC + mimics NC, pcDNA3.1-MEG3 + mimics NC, pcDNA3.1-NC + miR-361-5p mimics and pcDNA3.1-MEG3 + miR-361-5p mimics group. The RT-qPCR was used to detect the expression of MEG3, miR-361-5p and FOXO1. Moreover, western blot, luciferase reporter assay, RIP, CCK-8 and flow cytometry analysis were performed to reveal the morphology, proliferation and apoptosis in cartilage cells. Finally, the histological analysis and immunostaining were performed on OA rat model. Results: The expression of MEG3 and FOXO1 in OA was significantly decreased while miR-361-5p was increased compared with the normal group. MEG3 might serve as a ceRNA of miR-361-5p in OA chondrocytes. Moreover, the western blot and CCK-8 assay showed that MEG3, targeted miR-361-5p/FOXO1, might elevate cell proliferation and impair cell apoptosis. Finally, rat model analysis showed that MEG3 suppressed the cartilage matrix degradation. Conclusion: Taken together, MEG3 can contribute to cell proliferation, inhibit cell apoptosis and extracellular matrix (ECM) degradation via miR-361-5p/FOXO1 axis in OA chondrocytes.

show abstract

“…demonstrated that miR-140-5p was related with chondrocyte proliferation, apoptosis and inflammation in OA 30 . MiR-203 inhibition could ameliorate OA cartilage degradation in postmenopausal rat model 31 . We used StarBase to forecast the target miRNA of MEG3 and found that miR-361-5p was a target of MEG3.…”

Section: Discussionmentioning

confidence: 99%

MEG3 promotes proliferation and inhibits apoptosis in osteoarthritis chondrocytes by miR-361-5p/FOXO1 axis

Wang

¹

,

Hu

²

,

Zhang

³

et al. 2019

Preprint

0

View full text Add to dashboard Cite

Background: This study aimed to investigate the role of long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) and related molecular mechanisms in osteoarthritis (OA). Methods: Patients with OA and patients undergoing thigh amputation were enrolled in OA group and normal group, respectively. Cartilage tissues of all patients were isolated and cultured. After different transfections, chondrocytes were classified into Blank, pcDNA3.1-NC, pcDNA3.1-MEG3, si-NC, si-MEG3, pcDNA3.1-NC + mimics NC, pcDNA3.1-MEG3 + mimics NC, pcDNA3.1-NC + miR-361-5p mimics and pcDNA3.1-MEG3 + miR-361-5p mimics groups. The qRT-PCR was used to detect the expression of MEG3, miR-361-5p and FOXO1. Western blot, luciferase reporter assay, RIP, CCK-8 and flow cytometry analysis were performed to reveal the morphology, proliferation and apoptosis of cartilage cells. Histological analysis and immunostaining were conducted in OA rat model. Results: The expression of MEG3 and FOXO1 in OA was significantly decreased while miR-361-5p was increased compared with the normal group. MEG3 might serve as a ceRNA of miR-361-5p in OA chondrocytes. Moreover, the western blot and CCK-8 assay showed that MEG3, targeted miR-361-5p/FOXO1, might elevate cell proliferation and impair cell apoptosis. Functional analysis in vivo showed that MEG3 suppressed the cartilage matrix degradation. Conclusion: Taken together, MEG3 can contribute to cell proliferation, inhibit cell apoptosis and extracellular matrix (ECM) degradation via miR-361-5p/FOXO1 axis in OA chondrocytes. BackgroundOsteoarthritis (OA) is a disease increasing with age and even induces serious pain and disability 1 , which characterized by various pathological changes, such as articular cartilage degradation, synovial inflammation and subchondral osteoblast activation 2 . Although various genetic, biological, and biomechanical components have been proved to be associated with OA 3 , the underlying molecular mechanisms of OA progression remains unclear and the efficacious cure is still not available.Accumulating reports have indicated that lncRNAs are implicated in the various cancerogenesisrelated signaling pathways 4-8 . Moreover, lncRNAs have also been reported to be associated with knee OA progression 9 . As a member of lncRNA, maternally expressed 3 (MEG3) has been regarded as an important factor in the development of tumors 10 . Increasing publications have found that MEG3 is

show abstract

Inhibition of miR-203 Ameliorates Osteoarthritis Cartilage Degradation in the Postmenopausal Rat Model: Involvement of Estrogen Receptor α

Cited by 19 publications

References 29 publications

Perspectives on the Role of Non-Coding RNAs in the Regulation of Expression and Function of the Estrogen Receptor

Perspectives on the Role of Non-Coding RNAs in the Regulation of Expression and Function of the Estrogen Receptor

MEG3 promotes proliferation and inhibits apoptosis in osteoarthritis chondrocytes by miR-361-5p/FOXO1 axis

MEG3 promotes proliferation and inhibits apoptosis in osteoarthritis chondrocytes by miR-361-5p/FOXO1 axis

Contact Info

Product

Resources

About