Circular RNA circNID2 Promotes Bovine Adipogenesis via miR-339a/NNAT

Bta-Novel-miR-357 Inhibits the Proliferation and Promotes Apoptosis of Bovine Myoblasts by Targeting S100A2.

Findings reveal a novel epigenetic regulatory axis (novel-miR-357/S100A2 mRNA) involved in early muscle development and provide an important molecular mechanism for deeper understanding of the epigenetic regulatory processes underlying heterosis in cattle.

A novel circular RNA hsa_circ_0079474 facilitates intrauterine adhesion by targeting miR-630/YAP1 axis to stimulate epithelial-mesenchymal transition.

Emerging evidence highlights the critical role of circular RNAs (circRNAs) in regulating pathological processes in various diseases, including organ fibrosis. Endometrial fibrosis, commonly referred to as intrauterine adhesions (IUA), is a major cause of uterine infertility. However, the involvement of circRNAs in the pathogenesis of IUA remains largely unexplored, necessitating further research. This study aimed to identify a specific circRNA that may serve as a diagnostic biomarker and therapeutic target for IUA. CircRNA microarray analysis was performed to compare circRNA expression profiles between paired fibrotic and normal endometrial samples from patients with IUA. The expression of hsa_circ_0079474 was significantly upregulated in fibrotic tissues compared with normal tissues. Functional analyses demonstrated that hsa_circ_0079474 enhanced cell proliferation, promoted cell cycle progression, and facilitated epithelial-mesenchymal transition (EMT) in vitro, as assessed by qRT-PCR, CCK-8 assays, EdU assays, flow cytometry, and Masson staining. Mechanistically, dual-luciferase reporter assays and RNA immunoprecipitation confirmed that hsa_circ_0079474 acted as a molecular sponge for miR-630, leading to the upregulation of YAP1. In an IUA rat model, hsa_circ_0079474 was found to drive EMT, whereas miR-630 administration reversed this process and ameliorated endometrial fibrosis. Consequently, these findings indicate that hsa_circ_0079474 contributes to the progression of IUA by modulating the miR-630/YAP1 axis, providing new insights into circRNA-mediated mechanisms in IUA and highlighting hsa_circ_0079474 as a potential therapeutic target.

CircRNA hsa_circ_0001946 promotes hypertrophic scar pathogenesis via the miR-514a-3p/COL5A2 axis.

Hypertrophic scars (HSs) represent a fibroproliferative disorder characterized by excessive extracellular matrix deposition. However, the underlying regulatory mechanisms involving circular RNAs (circRNAs) have not yet been fully elucidated. This study aimed to delineate the circRNA expression landscape in HS and reveal the functional roles of a specific candidate circRNA through the competing endogenous RNA (ceRNA) network. Eighty-one differentially expressed circRNAs (DEcircRNAs) were identified in five paired HS and normal skin samples by high-throughput sequencing. Functional enrichment analysis of host genes highlighted pathways involving cell proliferation and ECM-receptor interactions. CircRNA-miRNA-mRNA network analysis revealed hsa_circ_0001946 as a significantly upregulated candidate circRNA. Subsequent RT-qPCR validated its elevation in human HS tissues and hypertrophic scar fibroblasts (HSFs). Subcellular fractionation and RNase R assays confirmed its cytoplasmic localization and circular stability. Functionally, knockdown of hsa_circ_0001946 significantly inhibited HSF proliferation, migration, and collagen gel contraction. Mechanistically, dual-luciferase reporter assays demonstrated that hsa_circ_0001946 acts as a sponge for miR-514a-3p; notably, silencing hsa_circ_0001946 attenuated the pro-fibrotic effects induced by miR-514a-3p inhibition. Furthermore, miR-514a-3p was shown to directly target and suppress COL5A2. Collectively, these findings establish that hsa_circ_0001946 promotes HS development by sequestering miR-514a-3p to derepress COL5A2 expression. This study identifies the hsa_circ_0001946/miR-514a-3p/COL5A2 axis as a novel pathogenic mechanism contributing to HS formation, suggesting hsa_circ_0001946 as a promising intervention target for mitigating pathological scarring.

Circ_0001495 promotes bladder cancer progression by regulating miR-1184 via MAPK signaling pathway

Bta-miR-380-3p regulates cell proliferation and adipogenesis in bovine intramuscular fat preadipocytes via targeting sterol O-acyltransferase 1.

A bta-miR-380-3p-SOAT1 regulatory axis linking post-transcriptional control with cholesterol metabolism, preadipocyte expansion, and IMF deposition is revealed, providing mechanistic insight and a potential molecular target for improving marbling and meat quality traits in cattle breeding programs.

circ_ATP5A1 sponges hsa-miR-145-5p to regulate ZFP36 and ferroptosis-associated signaling in acute kidney injury

Circular RNAs (circRNAs) are a novel class of non-coding RNAs that function as competing endogenous RNAs (ceRNAs) by sharing microRNA (miRNA) response elements with mRNAs, thereby modulating gene expression in various biological processes, including ferroptosis. Accumulating evidence has implicated circRNAs in the progression of acute kidney injury (AKI); however, whether circRNAs are involved in the regulation of ferroptosis during AKI and the underlying molecular mechanisms remain unclear. A circRNA-miRNA-mRNA interaction network was initially built via bioinformatics. Quantitative real-time PCR (RT-qPCR), Western blot, and immunohistochemistry were used to measure circ_ATP5A1, hsa-miR-145-5p, and ZFP36 expression. Dual-luciferase reporter assays combined with RNA immunoprecipitation verified the targeting relationships among the three molecules. In LPS-treated HK-2 cells, cell viability, inflammatory responses, and ferroptosis were evaluated using CCK-8, lactate dehydrogenase (LDH) release assay, flow cytometry, ELISA, and commercial reagent kits. An LPS-induced AKI mouse model was also established to assess the protective effect of circ_ATP5A1 expression. A ceRNA regulatory network comprising circ_ATP5A1/hsa-miR-145-5p/ZFP36 was established through bioinformatics prediction and experimental validation. Experimental findings revealed that expression of circ_ATP5A1 and ZFP36 was downregulated in both LPS-challenged HK-2 cells and AKI mice, whereas hsa-miR-145-5p was upregulated. Mechanistic studies demonstrated that circ_ATP5A1 acts as a ceRNA by sponging hsa-miR-145-5p, thereby relieving the repressive effect of hsa-miR-145-5p on its downstream target ZFP36. Functional assays showed that overexpression of circ_ATP5A1 restored the viability of LPS-exposed HK-2 cells, reduced inflammatory cytokine secretion (IL-1β, IL-6, TNF-α), increased the expression of ferroptosis-related markers glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11), and decreased acyl-CoA synthetase long-chain family member 4 (ACSL4) expression. In vivo, circ_ATP5A1 overexpression significantly ameliorated renal dysfunction and tissue injury in AKI mice. The circ_ATP5A1/hsa-miR-145-5p/ZFP36 axis attenuates AKI by inhibiting ferroptosis, providing a theoretical basis for AKI treatment.