Role of the ciRS-7/miR-7 axis in the regulation of proliferation, apoptosis and inflammation of chondrocytes induced by IL-1β

Zhou, Xindie; Jiang, Lifeng; Fan, Guoming; Yang, Haoyu; Wu, Lidong; Huang, Yong; Xu, Nanwei; Jin, Li

doi:10.1016/j.intimp.2019.03.037

Cited by 72 publications

(56 citation statements)

References 27 publications

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“…[ 27 ] According to previous Zhou's research, ciRS‐7 was illuminated to be involved in regulating interleukin‐1β (IL‐1β)‐evoked C28/I2 chondrocytes' proliferation, apoptosis, and inflammation. [ 28 ] Huang et al 29 demonstrated that ciRS‐7 promoted esophageal squamous cell carcinoma cells' migration and invasion through the nuclear factor kappa B pathway via targeting miR‐7. However, the function of ciRS‐7 in atherosclerosis remains extensively unclear.…”

Section: Discussionmentioning

confidence: 99%

Retracted: Circular RNA ciRS‐7 promotes tube formation in microvascular endothelial cells through downregulation of miR‐26a‐5p

Cui

Shen

Qin

et al. 2020

J Biochem & Molecular Tox

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Atherosclerosis is one of the most common and crucial heart diseases involving the heart and brain. At present, atherosclerosis and its major complications comprise the leading causes of death worldwide. Our purpose was to identify the role of ciRS-7 in atherosclerosis. Tubulogenesis of HMEC-1 cell was evaluated utilizing tube formation assay. CellCounting Kit-8 assay and flow cytometry were utilized to test viability and apoptosis.Migration assay was utilized to determine the migration capacity of experimental cells.Western blot was applied to examine apoptosis and tube formation-associated protein expression. In addition, the above experiments were repeated when silencing ciRS-7, overexpressing ciRS-7, and upregulating miR-26a-5p. HMEC-1 cells formed tube-like structures over time. Silencing ciRS-7 suppressed viability, migration, and tube formation but promoted apoptosis. Oppositely, overexpressing ciRS-7 reversed the effect in HMEC-1 cells. miR-26a-5p expression was elevated by silencing ciRS-7 and reduced by overexpressing ciRS-7. Moreover, overexpressing ciRS-7 facilitated viability, migration, and tube formation via upregulating miR-26a-5p. Conclusively, overexpressing ciRS-7 mobilized phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pathway and suppressed c-Jun N-terminal kinase (JNK)/p38 pathway. ciRS-7 exerted influence on apoptosis, viability, migration, and tube formation through mediating PI3K/AKT and JNK/p38 pathways by miR-26a-5p downregulation in HMEC-1 cells.

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Section: Discussionmentioning

confidence: 99%

Retracted: Circular RNA ciRS‐7 promotes tube formation in microvascular endothelial cells through downregulation of miR‐26a‐5p

Cui

Shen

Qin

et al. 2020

J Biochem & Molecular Tox

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“…Our previous studies already proved that miR-7 was down-regulated in normal chondrocytes and thereby exacerbated the course of OA through aggravating cartilage degradation (12). Nonetheless, the downstream regulatory target gene still remains unknown.…”

Section: Resultsmentioning

confidence: 99%

“…Nevertheless, as the research development of the regulatory function of microRNAs in various types of diseases, the pathological association of miRNAs and OA has become a research hotspot, and accumulating researches reported that miRNAs function as key factor in mediating the development of OA. Simultaneously, our previous studies discovered that miR-7 was signi cantly overexpressed in OA chondrocytes, and served as a promoting factor in mediating the course of OA (12). For further exploration of the down-stream regulatory pathway, multiple databases including Targetscan, starBase v3.0 and miRanda were utilized to calculate the target gene of miR-7, of which SEMA6D was a target gene with highest score.…”

Section: Discussionmentioning

confidence: 99%

“…To date, research report elucidated that miRNA regulatory network, chondrocytes autophagy and alteration of epigenetics would be the targeting therapeutic strategies for osteoarthritis (11). Additionally, our previous research discovered that miR-7 was overexpressed in IL-1β induced OA chondrocytes via activating PI3K/AKT/mTOR and thereby worsen the course the OA (12). However, the speci c molecular mechanism of miR-7 still remained unknown, which makes it a hindrance in developing novel curing method of osteoarthritis.…”

Section: Introductionmentioning

confidence: 99%

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SEMA6D, Negatively Regulated by miR-7, Contributing to Chondrocyte Catabolic and Anabolic Activities via p38 Signaling Pathway

Zhou

Zhang

et al. 2020

Preprint

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Background: MiR-7 has been recognized as a promoting factor of osteoarthritis (OA), but the specific down-stream pathway of miR-7 still remains unknown. Further investigation of the molecular regulatory mechanism of miR-7 might help develop a novel therapeutic method for OA.Results: Here we revealed that Semaphorin 6D (SEMA6D) was a direct target gene of miR-7, of which presented a negatively regulatory relation in vitro and in vivo. Lucubration of SEMA6D suggested that SEMA6D is validated to promote the anabolic metabolism and reduce the catabolism of chondrocytes via inhibiting the activation of p38 pathway.Conclusions: Present research illustrated that SEMA6D is a negatively regulatory factor of miR-7 and a pivotal mediator of the catabolism and anabolism of chondrocytes. SEMA6D exerts its function via inhibiting the activation of p38 pathway.

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“…To date, four circRNAs have been shown to have reduced expression levels in OA development, which inhibit chondrocyte apoptosis by regulating the expression of miRNAs and their downstream proteins. For instance, ciRS‐7 promoted the proliferation of chondrocytes in an IL‐1β‐induced OA model via negatively regulating miR‐7 (Zhou, Jiang, et al, ). circRNA‐CER, hsa_circ_0045714, and circSERPINE2 regulate the biosynthesis of the ECM and promote the proliferation of chondrocytes by negatively regulating miR‐136, and activating the miR‐193b/IGF1R and miR‐1271‐5p/ERG axes (Li, Zhang, Xiao, et al, ; Liu, Zhang, et al, ; Shen et al, ).…”

Section: Chondrocyte Injuriesmentioning

confidence: 99%

Noncoding RNAs: New regulatory code in chondrocyte apoptosis and autophagy

Jiang

Liu

et al. 2020

WIREs RNA

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Osteoarthritis (OA) is a bone and joint disease characterized by progressive cartilage degradation. In the face of global trends of population aging, OA is expected to become the fourth most common disabling disease by 2020. Nevertheless, the detailed pathogenesis of OA has not yet been elucidated. Noncoding RNAs (ncRNAs), including long noncoding RNAs, microRNAs, and circular RNAs, do not encode proteins but have recently emerged as important regulators of apoptosis and autophagy of chondrocytes, thereby highlighting a potential role in chondrocyte injury leading to OA onset and progression. We here review recent findings on these regulatory roles of ncRNAs to provide new directions for research on the pathogenesis of OA and offer new therapeutic targets for prevention and treatment. This article is categorized under: RNA in Disease and Development > RNA in Disease RNA in Disease and Development > RNA in Development

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Role of the ciRS-7/miR-7 axis in the regulation of proliferation, apoptosis and inflammation of chondrocytes induced by IL-1β

Cited by 72 publications

References 27 publications

Retracted: Circular RNA ciRS‐7 promotes tube formation in microvascular endothelial cells through downregulation of miR‐26a‐5p

Retracted: Circular RNA ciRS‐7 promotes tube formation in microvascular endothelial cells through downregulation of miR‐26a‐5p

SEMA6D, Negatively Regulated by miR-7, Contributing to Chondrocyte Catabolic and Anabolic Activities via p38 Signaling Pathway

Noncoding RNAs: New regulatory code in chondrocyte apoptosis and autophagy

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