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CircPan3 Promotes the Ghrelin System and Chondrocyte Autophagy by Sponging miR-667-5p During Rat Osteoarthritis Pathogenesis.

ABSTRACT: This study aimed to investigate the potential roles of circRNAs in regulating osteoarthritis (OA)-related ghrelin synthesis, autophagy induction, and the relevant molecular mechanisms. Results showed that Col2a1, Acan, ghrelin, and autophagy-related markers expression were downregulated, while matrix metalloproteinase 13 (MMP13) and a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5) expressions increased in both IL-1β-induced rat chondrocytes and cartilage tissues of OA rats. A total of 130 circRNAs and 731 mRNAs were differentially expressed in IL-1β-induced rat chondrocytes. Among them, we found that circPan3 expression was significantly decreased in both cellular and animal OA models. CircPan3 directly targeted miR-667-5p. CircPan3 overexpression promoted Col2a1, Acan, ghrelin, beclin 1, and LC3-II expression but reduced MMP13 and ADAMTS5 expression in rat chondrocytes, whereas overexpression of miR-667-5p exhibited opposite effects on the above markers. Furthermore, we found that miR-667-5p bound directly to the 3'-UTR sequence of ghrelin gene. Moreover, the circPan3-induced alterations in chondrocytes were antagonized by miR-667-5p overexpression. Taken together, our findings demonstrate that circPan3 promotes ghrelin synthesis and chondrocyte autophagy via targeting miR-667-5p, protecting against OA injury. This study provided experimental evidence that circPan3/miR-667-5p/ghrelin axis might serve as targets of drug development for the treatment of OA.

SUBMITTER: Zeng J

PROVIDER: S-EPMC8640465 | biostudies-literature |

REPOSITORIES: biostudies-literature

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CircPan3 Promotes the Ghrelin System and Chondrocyte Autophagy by Sponging miR-667-5p During Rat Osteoarthritis Pathogenesis

Project description:This SuperSeries is composed of the SubSeries listed below.

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CircPan3 Promotes the Ghrelin System and Chondrocyte Autophagy by Sponging miR-667-5p During Rat Osteoarthritis Pathogenesis [circRNA-Seq]

Project description:This study aimed to investigate the potential roles of circRNAs in regulating osteoarthritis (OA)-related ghrelin synthesis, autophagy induction, and the relevant molecular mechanisms.

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CircPan3 Promotes the Ghrelin System and Chondrocyte Autophagy by Sponging miR-667-5p During Rat Osteoarthritis Pathogenesis [RNA-seq]

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CircPan3 Promotes the Ghrelin System and Chondrocyte Autophagy by Sponging miR-667-5p During Rat Osteoarthritis Pathogenesis

Project description:CircPan3 Promotes the Ghrelin System and Chondrocyte Autophagy by Sponging miR-667-5p During Rat Osteoarthritis Pathogenesis

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CircPan3 Promotes the Ghrelin System and Chondrocyte Autophagy by Sponging miR-667-5p During Rat Osteoarthritis Pathogenesis [circRNA-Seq]

Project description:CircPan3 Promotes the Ghrelin System and Chondrocyte Autophagy by Sponging miR-667-5p During Rat Osteoarthritis Pathogenesis [circRNA-Seq]

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CircPan3 Promotes the Ghrelin System and Chondrocyte Autophagy by Sponging miR-667-5p During Rat Osteoarthritis Pathogenesis [RNA-seq]

Project description:CircPan3 Promotes the Ghrelin System and Chondrocyte Autophagy by Sponging miR-667-5p During Rat Osteoarthritis Pathogenesis [RNA-seq]

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circRNA.33186 Contributes to the Pathogenesis of Osteoarthritis by Sponging miR-127-5p.

Project description:Osteoarthritis (OA), the most prevalent age-related joint disorder, is characterized by chronic inflammation, progressive articular cartilage destruction, and subchondral bone sclerosis. Accumulating evidences indicate that circular RNAs (circRNAs) play a critical role in various diseases, but the function of circRNAs in OA remains largely unknown. Here we showed that circRNA.33186 was significantly upregulated in IL-1β)-treated chondrocytes and in cartilage tissues of a destabilized medial meniscus (DMM)-induced OA mouse model. Knockdown of circRNA.33186 increased anabolic factor (type II collagen) expression and decreased catabolic factor (MMP-13) expression. Knockdown of circRNA.33186 also promoted proliferation and inhibited apoptosis in IL-1β-treated chondrocytes. Silencing of circRNA.33186 in vivo markedly alleviated DMM-induced OA. Mechanistic study showed that circRNA.33186 directly binds to and inhibits miR-127-5p, thereby increasing MMP-13 expression, and contributes to OA pathogenesis. Taken together, our findings demonstrated a fundamental role of circRNA.33186 in OA progression and provide a potential drug target in OA therapy.

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miR-10a-5p Promotes Chondrocyte Apoptosis in Osteoarthritis by Targeting HOXA1.

Project description:Osteoarthritis (OA) is a common joint disease characterized by degradation of the articular cartilage and joint inflammation. Studies have revealed the importance of microRNAs in the regulation of chondrocyte apoptosis. MicroRNA deep sequencing of control and osteoarthritic cartilage has revealed that miR-10a-5p is significantly upregulated in osteoarthritic tissues. However, its role in these tissues remains unknown. The present study was conducted to investigate the effect of miR-10a-5p in promoting OA. miR-10a-5p expression was increased in chondrocytes after interleukin-1? treatment in vitro. Transfection with a miR-10a-5p inhibitor abrogated interleukin-1?-induced apoptosis. A luciferase activity assay showed that miR-10a-5p targeted the 3' UTR of the homeobox gene HOXA1, inhibiting its expression. Treatment with HOXA1 siRNA reversed the rescuing effect of the miR-10a-5p inhibitor on chondrocyte apoptosis. Additionally, an OA model was established in mice by anterior cruciate ligament transection. AntagomiR-10a-5p improved the cartilage surfaces of osteoarthritic mice, whereas agomiR-10a-5p worsened them. A terminal deoxynucleotidyl transferase dUTP nick-end labeling assay indicated reduced apoptosis and increased HOXA1 expression in osteoarthritic mice after miR-10a-5p knockdown. These findings reveal a novel mechanism regulating OA progression and demonstrate the potential of miR-10a-5p and homeobox protein HOXA1 as therapeutic targets.

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Project description:Chondrocyte apoptosis is an important factor in the development and progression of osteoarthritis (OA). Cryptotanshinone (CTS) can inhibit chondrocyte apoptosis, but the specific mechanism remains unknown. The aim of the present study was to explore how CTS may affect chondrocyte apoptosis. Reverse transcription‑quantitative PCR and western blotting were used to validate microRNA (miR)‑574‑5p, YY1‑associated factor 2 (YAF2), Bcl‑2 and Bax expression levels. H&E, Safranin O and TUNEL staining assays were used to evaluate the apoptosis of arthritic chondrocytes in vivo. A Cell Counting Kit‑8 assay and flow cytometry were performed to detect cell proliferation and apoptosis of chondrocytes in vitro. The methylation level of the miR‑574‑5p promoter was measured via methylation specific PCR. The degree of chondrocyte apoptosis and the expression levels of YAF2 and Bcl‑2 were decreased in the mice with OA, and were increased in the OA + CTS mice, while the expression levels of miR‑574‑5p and Bax showed opposite changes. Furthermore, the degree of chondrocyte apoptosis and the expression levels of the aforementioned key factors in chondrocytes were consistent with those observed in vivo. The methylation degree of the miR‑574‑5p promoter was increased by the addition of CTS, and was reduced after the addition of a methylation inhibitor, 5‑aza‑CdR, indicating that CTS could regulate the methylation of miR‑574‑5p promoter. The present study suggested that CTS could downregulate the expression of miR‑574‑5p by regulating its methylation, and thus, could improve YAF2 expression and affect chondrocyte apoptosis.

| S-EPMC8047883 | biostudies-literature

Excessive MiR-365b-5p Maturation via N6-methyladenosine Regulates Chondrocyte Apoptosis and Phenotype by NCL/MiR-365b-5p/FHL1 Axis in Osteoarthritis

Project description:RNA pull-down assays were performed as the protocol of the PureBinding RNA-Protein pull-down Kit (Geneseed, Guangzhou, China). Specific biotinylated probes that hybridize to target pri-miR-365 were obtained from Ribobio. The probes (200pmol) targeting pri-miR-365 or control probes and RNA samples of chondrocytes were added to the pull-down system. After the mixture of RNA and probes was denaturated at 85°C for 5 minutes, and hybridized at room temperature for 2 hours, 100 µl streptavidin-coated magnetic beads were added to the mixture. Non-specifically bound RNAs were removed by hybridization, capture, and washing. The proteins that interacted with pri-miR-365 were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Then, pri-miR-365-interacting bands were subjected to mass spectrometry (Beijing Genomics Institute, Shenzhen, China). The result was gained to establish a proteomic library.

2022-11-21 | PXD038257 |

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