Retracted: Effects of microRNA‐206 and its target gene IGF‐1 on sevoflurane‐induced activation of hippocampal astrocytes in aged rats through the PI3K/AKT/CREB signaling pathway

Abstract

The study aims to explore the effects of microRNA-206 (miR-206) targeting IGF-1 on the activation of hippocampal astrocytes in aged rats induced by sevoflurane through the PI3K/AKT/CREB signaling pathway. Wistar rats and astrocytes were divided into the normal/blank, sham/negative control (NC), sevoflurane (sevo), miR-206 mimics+sevo, miR-206 inhibitors+sevo, miR-206 NC+sevo, IGF-1 shRNA+sevo, and miR-206 inhibitors+IGF-1 shRNA+sevo groups. The Morris water maze test was exhibited to assess the cognitive functions. Glial fibrillary acidic protein (GFAP) expression was detected by immunofluorescence assay. Western blotting and RT-qPCR were used to detect the expression of miR-206, IGF-1, PI3K, AKT, CREB, pPI3K, pAKT, pCREB, cytochrome-c (Cyt-c), and caspase-3. Cell viability and apoptosis were detected by MTT assay and annexin V/PI double staining respectively. Mitochondrial transmembrane potential (MTP) were determined by flow cytometry. The IGF-1 shRNA+sevo group showed reduced miR-206 expression. Compared with the normal/blank group, the sevo, and miR-206 NC+sevo groups showed decreased miR-206 and GFAP expressions, cell viability and MTP but increased expressions of IGF-1, PI3K, AKT, CREB, pPI3K, pAKT, pCREB, Cyt-c and caspase-3, as well as cell apoptosis. Similar trends were observed in the miR-206 inhibitors+sevo group when compared with the sevo group. The study provides evidence that miR-206 alleviates the inhibition of activation of hippocampal astrocytes in aged rats induced by sevoflurane by targeting IGT-1 through suppressing the PI3K/AKT/CREB signaling pathway.

Baicalein inhibits proliferation and collagen synthesis of mice fibroblast cell line NIH/3T3 by regulation of miR-9/insulin-like growth factor-1 axis

“…miRNA normally exerts its functions in cells by targeting IGF-1. For instance, a study displayed miR-206 targeted IGF-1 in astrocytes [38]. Other study displayed miR-130b-3p worked in lung fibrosis by targeting IGF-1 [39].…”

Carbonic Anhydrase 12 Protects Endplate Cartilage From Degeneration Regulated by IGF-1/PI3K/CREB Signaling Pathway

“…In addition, we find that IGF-1 could activate and phosphorylate PI3K, RAC, MSK1, and CREB in HEPCC. Because the IGF-1/PI3K/RAC/MSK1/CREB signaling pathway is well established ( Wiggin et al, 2002 ; Stitt et al, 2004 ; Yuzugullu et al, 2015 ; Dillon et al, 2015 ; Zhang et al, 2015 ; Lien et al, 2017 ; Liu T.J. et al, 2018 ), we reveal an inevitable role of this pathway in promoting CA12 expression with PI3K and CREB inhibitors. Another downstream element of the IGF-1/PI3K/RAC/MSK1 pathway, p65 ( Vermeulen et al, 2003 ; Kefaloyianni et al, 2006 ) is excluded in its role of CA12 regulation by our study with p65 inhibitor QNZ.…”

Exogenous fibroblast growth factor 1 ameliorates diabetes-induced cognitive decline via coordinately regulating PI3K/AKT signaling and PERK signaling

“…Series of studies have shown that miR-206 is highly expressed in the brain of AD patients or AD animal models, which contribute to cognitive decline by inhibiting BDNF expression [47,48]. Additionally, miR-206 can regulate IGF-1 expression, and activate PI3K/AKT signaling [49,50]. Thus, we speculate that miR-206 could regulate IGF-1 expression, affect PI3K/AKT/CREB signaling during DICD.…”