Journal: Journal of Nanobiotechnology

Article Title: RVG-targeted extracellular vesicles loaded with echinatin attenuate dopaminergic neurodegeneration via the IGF-2/PI3K/Akt pathway in Parkinson’s disease mice

doi: 10.1186/s12951-025-03997-5

Figure Lengend Snippet: RVG-EVs@Echi attenuate oxidative stress in the in vitro PD models. ( a ) Representative blots and ( b ) quantification of the expression levels of IGF2, P-PI3K, PI3K, P-Akt, Akt, and Nrf2 in MN9D cells. ( c ) Representative blots and ( d ) quantification of Bcl-2, Bax, and the resulting Bcl-2/Bax ratio in MN9D cells. ( e , g ) Representative blots and ( f , h ) quantification showing the effects of the IGF-1R/IR inhibitor NVP-AEW541 in MN9D cells. ( i ) Representative graphs of ROS generation in control or MPP+-treated cells upon RVG-EVs@Echi treatment. Scale bars, 50 μm and 10 μm for the original and magnified images, respectively. ( k ) MitoSOX was used to stain live control or MPP+-treated cells upon treatment with RVG-EVs@Echi. Scale bars, 50 μm and 10 μm for the original and magnified images, respectively. ( j , l ) Quantification of the relative ROS and MitoSOX fluorescence intensity. n = 6 per group. ( m ) Representative flow cytometry histograms and ( n ) quantification of mean fluorescence intensity (MFI) showing intracellular ROS levels in MN9D cells. n = 3 per group. Statistical Analysis: For (a-d): Groups are Control, MPP+, and MPP + + RVG-EVs@Echi. n = 3 per group. * p < 0.05, ** p < 0.01 vs. Control group; # p < 0.05, ## p < 0.01 vs. MPP + group. For (e-h): Groups are Control, MPP + + RVG-EVs@Echi, and MPP + + RVG-EVs@Echi + NVP-AEW541. n = 3 per group. * p < 0.05, ** p < 0.01 vs. Control group; # p < 0.05, ## p < 0.01 vs. MPP + + RVG-EVs@Echi group. For (i-n): Groups are Control, RVG-EVs@Echi, MPP+, and MPP + + RVG-EVs@Echi. * p < 0.05, ** p < 0.01 vs. Control group; # p < 0.05, ## p < 0.01 vs. RVG-EVs@Echi group; & p < 0.05, && p < 0.01 vs. MPP + group

Article Snippet: To assess the effects of RVG-EVs@Echi, MN9D cells were treated with MPP+ (600 μM) or RVG-EVs@Echi (1 μM) for 24 h. For the IGF-1R inhibition experiment, cells were pre-treated with the IGF-1R/IR inhibitor NVP-AEW541 (0.2 μM; MCE, HY-50866) [ ] for 2 h, followed by co-incubation with MPP + and RVG-EVs@Echi for 24 h.

Techniques: In Vitro, Expressing, Control, Staining, Fluorescence, Flow Cytometry

Journal: PLoS ONE

Article Title: Comparative mRNA and miRNA transcriptome analysis of a mouse model of IGFIR-driven lung cancer

doi: 10.1371/journal.pone.0206948

Figure Lengend Snippet: (A) Schematic of doxycycline inducible expression of IGFIR in the mouse lung via the SPC promoter. (B) Unsupervised hierarchical clustering dendrogram of RNA-Seq data from tumor (T, red) and non-transgenic normal lung (N, grey) samples. (C) Volcano plot of log2 fold changes and differential expression p values between tumor and normal lung tissue. (D) Pie chart illustrating percentage of genes up and down-regulated in IGFIR-driven tumors. (E) Dot plots of endogenous murine Igf1r (padj = 5.71E-11) and human IGFIR transgene (padj = 5.65E-249) mRNA expression following mapping to a hybrid genome. (F) Heatmap showing differential expression of markers of AT2 and Club cells as well as subtypes of non-small cell lung cancer. ADC, adenocarcinoma, SCC, squamous cell carcinoma, mADC, mucinous adenocarcinoma. Adjusted p-values for (C) and (E) were obtained from DESeq2.

Article Snippet: To further enrich for tumor cells, a biotinylated anti-human IGF1R antibody (1:10, clone REA271, Miltenyi Biotech) was added to the epithelial enriched fraction for 30 min on ice followed by positive selection and separation as above.

Techniques: Expressing, RNA Sequencing, Transgenic Assay, Quantitative Proteomics

Journal: Nature communications

Article Title: FoxK1 and FoxK2 in insulin regulation of cellular and mitochondrial metabolism.

doi: 10.1038/s41467-019-09418-0

Figure Lengend Snippet: Fig. 8 Schematic model of insulin regulation of FoxK1/K2 and FoxOs in cellular function. The FoxK Forkhead transcription factors translocate from the cytoplasm to nucleus reciprocally to the translocation of FoxO1. FoxK translocation to the nucleus is dependent on the Akt-mTOR pathway, while its localization to the cytoplasm in the basal state is dependent on GSK3. Once in the nucleus, FoxKs play important roles in regulation of genes, fatty acid oxidation, mitochondrial biogenesis, cell proliferation and survival. Where other unknown proteins (named here X) are in the FoxK and IR/IGF1R protein- protein complexes remains to be determined

Article Snippet: Mouse IR (MC224356) and IGF1R (MC224342) cDNA clones were from Origene.

Techniques: Cell Function Assay, Translocation Assay