Mouse Anti-Human p27 monoclonal antibody, clone JID138

circRNAs (circular RNAs) play important roles in the development of endometriosis. This study aimed to explore the functions of circRNAs on endometriosis. Two ectopic, two paired eutopic, and two normal endometrial tissue samples were collected for RNA-seq to obtain circRNA profiles and construct a circRNA-miRNA-mRNA network. The validation of 9 circRNAs in 15 patients was assessed by qRT-PCR. We selected hsa_circ_0008433 as the potential biomarker, followed by examining cell proliferation, colony formation, migration, angiopoiesis, cell cycle, and apoptosis. Furthermore, the expression of apoptosis-related proteins was detected using immunofluorescence (IF) and Western blotting. Bioinformatic analysis was used to select the potential target miRNA and genes of hsa_circ_0008433. A total of 209 upregulated and 117 downregulated differentially expressed circRNAs were identified from the eutopic and ectopic endometrial tissue samples. Eight circRNA levels were significantly increased in ectopic endometrial tissue sample compared with eutopic endometrial tissue. The hsa_circ_0008433 knockdown inhibited endometrial stromal cell proliferation, migration, colony formation, and angiopoiesis; promoted cell apoptosis; and downregulated Ki67 and PCNA expression levels. Moreover, the hsa_circ_0008433 knockdown increased Bax and E-CAD expression and decreased Bcl2, CDKN1B, and CyclinD1 levels. Ten potential target miRNAs of hsa_circ_0008433 were selected, and six of them occur significantly aberrant in hsa_circ_0008433-expressing cells. Increased hsa_circ_0008433 levels regulate epithelial mesenchymal transition (EMT) in endometriosis through the circRNA-miRNA-mRNA axis.

Subarachnoid hemorrhage is a common disease in the neural system, which causes high fatality rate. Therefore, it is necessary to figure out inner mechanisms of factors related to this disease. RT-qPCR was applied for measuring expressions of CDKN1B and miR-502-5p and other factors of apoptosis and inflammation. Cell viabilities were detected through CCK-8. Binding conditions between miR-502-5p and CDKN1B were detected through luciferase report assay. Western blot was used for measuring levels of proteins in PPAR gamma/NF-kappa B signaling pathway. Apoptosis and inflammation of HT22 cell line, a kind of nerve cell line, were enhanced and viabilities were suppressed by oxyhemoglobin. CDKN1B expressed lower in induced HT22 cell line and overexpressed CDKN1B could promote viabilities and suppress apoptosis as well as inflammation. MiR-502-5p was the target gene of CDKN1B and enhanced apoptosis and inflammation of cells in HT22 cell line. Furthermore, miR-502-5p reversed functions of CKDN1B in induced cells through regulating proteins in PPAR gamma/NF-kappa B signaling pathway. CDKN1B was the gene that could inhibit SAH caused by apoptosis in nerve cells and inflammation by sponging miR-502-5p and regulating factors in PPAR gamma/NF-kappa B signaling pathway, suggesting it could be a factor for protecting functions of nerve cells after SAH.