RESUMO
During investigations of invertebrate-associated fungi in Yunnan Province of China, a new species, Sporodiniella sinensis sp. nov., was collected. Morphologically, S. sinensis is similar to Sporodiniella umbellata; however, it is distinguished from S. umbellata by its greater number of sporangiophore branches, longer sporangiophores, larger sporangiospores, and columellae. The novel species exhibits similarities of 91.62â% for internal transcribed spacer (ITS), 98.66-99.10â% for ribosomal small subunit (nrSSU), and 96.36-98.22â% for ribosomal large subunit (nrLSU) sequences, respectively, compared to S. umbellata. Furthermore, phylogenetic analyses based on combined sequences of ITS, nrLSU and nrSSU show that it forms a separate clade in Sporodiniella, and clusters closely with S. umbellata with high statistical support. The phylogenetic and morphological evidence support S. sinensis as a distinct species. Here, it is formally described and illustrated, and compared with other relatives.
Assuntos
Ácidos Graxos , Mucorales , Animais , Filogenia , China , Análise de Sequência de DNA , Composição de Bases , RNA Ribossômico 16S/genética , DNA Bacteriano/genética , Técnicas de Tipagem Bacteriana , Ácidos Graxos/química , InvertebradosRESUMO
Diabetic retinopathy (DR) has become the leading cause of blindness among adults at working age. Previous studies have implicated circ_0001897 in the development of DR. In this study, we investigated the functional roles and mechanisms of circ_0001897 in high glucose-induced angiogenesis and inflammation. Peripheral blood samples from DR patients and healthy controls were collected to examine circ_0001897 expression, which demonstrated a significant upregulation of circ_0001897 in DR patients. To investigate the functional role and mechanisms of circ_0001897, human retinal microvascular endothelial cells (HRECs) were treated with high glucose (HG) to establish an in vitro DR model of endothelial cells. HG treatment induced the upregulation of circ_0001897 in HRECs, and enhanced cell proliferation, inflammatory responses, as well as in vitro angiogenesis. Circ_0001897 knockdown significantly attenuated the cell proliferation, inflammatory responses, and angiogenesis induced by HG treatment. Mechanistically, circ_0001897 sponged and inhibited the activity of mir-29c-3p, which in turn regulates the downstream target transforming growth factor beta 2 (TGFB2). The effects of circ_0001897 knockdown could be rescued by mir-29c-3p inhibitor or TGFB2 overexpression. Collectively, our data demonstrated the novel role of circ_0001897/mir-29c-3p/TGFB2 axis in regulating HG-induced inflammation and angiogenesis of HRECs. These findings suggest that targeting circ_0001897 could serve as an intervention strategy to ameliorate DR.
Assuntos
Retinopatia Diabética , MicroRNAs , Adulto , Proliferação de Células/genética , Retinopatia Diabética/genética , Retinopatia Diabética/metabolismo , Células Endoteliais/metabolismo , Glucose/metabolismo , Glucose/toxicidade , Humanos , Inflamação/genética , Inflamação/metabolismo , MicroRNAs/metabolismo , Neovascularização Patológica/genéticaRESUMO
AIM: To study the effect of miR-26b on lens epithelial cells induced by transforming growth factor beta (TGF-ß) 2 and the underlying signaling pathways. METHODS: Human lens epithelial cell line B-3 (HLE-B3) was incubated with TGF-ß2 (5 ng/mL) and then transfected with miR-26b mimics. The expression of miR-26b was determined using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR), while 5'-bromodeoxyuridine (BrdU) and wound-healing assays were used to measure the growth and migration of HLE-B3 cells, respectively. The expression of epithelial-mesenchymal transition (EMT) markers and the activity of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway were measured by Western blotting assay and immunofluorescence staining. Electron microscopy was also used to observe cellular morphology. RESULTS: The expression levels of miR-26b were significantly reduced in human posterior capsular opacification-attached lens tissue and TGF-ß2-stimulated HLE-B3 cells. In the presence of TGF-ß2, the growth, migration, and EMT of HLE-B3 cells were distinctly enhanced; these effects were attenuated by the administration of miR-26b mimics. Furthermore, the overexpression of miR-26b significantly reduced upregulation of the PI3K/Akt pathway when stimulated by TGF-ß2 in HLE-B3 cells. Moreover, the addition of an activator (740 Y-P) led to the upregulation of the PI3K/Akt pathway and abolished the protective effect of miR-26b on the HLE-B3 cells that was mediated by TGF-ß2. CONCLUSION: The miR-26b suppresses TGF-ß2-induced growth, migration, and EMT in HLE-B3 cells by regulating the PI3K/Akt signaling pathway.