MicroRNA-17-5p aggravates lipopolysaccharide-induced injury in nasal epithelial cells by targeting Smad7

Abstract

BackgroundGlobally, rhinitis is one of the most common chronic disorders. Despite availability of drugs to manage the symptomatology of rhinitis, researchers still focus on identification of novel molecular targets for better management. MicroRNAs are implicated in many biological and pathological processes. However, the role of miR-17-5p in rhinitis remains unexplored. This study aimed to explore the role of miR-17-5p in lipopolysaccharide (LPS)-induced injury of nasal epithelial RPMI2650 cells and to elucidate the possible underlying molecular mechanism.ResultsLPS damaged RPMI2650 cells by inhibiting cell proliferation, promoting apoptosis, and stimulating the release of inflammatory cytokines. miR-17-5p expression was significantly increased in RPMI2650 cells following treatment with LPS. Furthermore, it was found that overexpression of miR-17-5p led to aggravation of LPS-induced injury. miR-17-5p negatively regulated expression of Smad7; overexpression of Smad7 protected the RPMI2650 cells by inactivating NF-κB and Wnt/β catenin pathways and vice versa.ConclusionsOverexpression of miR-17-5p aggravated LPS-induced damage of RPMI2650 cells. Expression of Smad7 was negatively regulated by miR-17-5p; Smad7 expression inactivated NF-κB and Wnt/β catenin pathways.

MiR-581/SMAD7 Axis Contributes to Colorectal Cancer Metastasis: A Bioinformatic and Experimental Validation-Based Study

“…The miR-581/SMAD7 axis we investigated here could also be a supplement to SMAD7 epigenetic modification. A variety of onco-miRNAs were discovered targeting SMAD7 [10,23,[31][32][33][34]. Since the miRNA-target network is complex and not a 'one to one' model, the core miRNA that regulates SMAD7 level still needs to be further explored.…”

microRNA‐148a‐3p in extracellular vesicles derived from bone marrow mesenchymal stem cells suppresses SMURF1 to prevent osteonecrosis of femoral head

“…15 SMAD7 elevates the expression of B-cell CLL/lymphoma 2 (BCL2). 16 EVs that are derived from human platelet-rich plasma promote the expression of BCL2 to prevent the cell apoptosis in ONFH. 17 At present, few studies have explored the combined regulatory role of BMSC-EV-miR-148a-3p/SMURF1/SMAD7/BCL2 axis in ONFH.…”

“…Furthermore, up‐regulated SMAD7 is closely related to the proliferation of BMSCs 15 . SMAD7 elevates the expression of B‐cell CLL/lymphoma 2 (BCL2) 16 . EVs that are derived from human platelet‐rich plasma promote the expression of BCL2 to prevent the cell apoptosis in ONFH 17 .…”

Structure of the C-terminal guanine nucleotide exchange factor module of Trio in an autoinhibited conformation reveals its oncogenic potential

“…Although the WT α6-αN region in Tgat is entirely present, the lack of the core PH domain fold in this variant could mean that the αN helix is disordered and thus cannot confer full autoinhibition as we see in the 2153Δ and 2152Δ variants. Alternatively, the 15 residue extension could drive an activated conformation of the α6-αN hinge region by making unique contacts within the protein, with other signaling partners, or with the cell membrane (27-29).…”