Journal: Life Metabolism

Article Title: Deletion of hepatic growth hormone receptor contributes to the pathogenesis of lean MAFLD by elevating CD36

doi: 10.1093/lifemeta/loaf037

Figure Lengend Snippet: LGHRKO mice contain excessive hepatic lipids with impaired liver function, similar to DIO mice. (a) Microscopic appearance of the livers in control, DIO, and LGHRKO mice. (a’–c’) H&E-stained liver section at 200× magnification. (d’–f’) H&E-stained liver section at 400× magnification. (g’–i’) Oil Red O-stained liver section at 200× magnification. (j’–l’) Oil Red O-stained liver section at 400× magnification. (b) Hepatic TG content of control, DIO, and LGHRKO mice. (c) Serum AST and ALT levels of control, DIO, and LGHRKO mice. (d) Relative hepatic mRNA levels of lipogenesis genes Acc1 and Fas . (e) Relative hepatic mRNA levels of lipolysis genes Atgl , Hsl , and Mgl . n = 6–8 mice in each group. Data are presented as mean ± SEM.

Article Snippet: Protein lysates (50 μg) were separated by SDS-PAGE, transferred onto nitrocellulose (NC) membranes (#66485; PALL), and blotted with the indicated primary antibodies at 1:1000 dilution: ACC1 (#A15606; ABclonal, RRID: AB_2763012), FAS (#A0461; ABclonal, RRID: AB_2757202), PPARγ (#A0270; ABclonal, RRID: AB_2757083), ATGL (#A6245; ABclonal, RRID: AB_2766852), HSL (#A15686; ABclonal, RRID: AB_2763096), MGL (#A6654; ABclonal, RRID: AB_2767241), CD36 (#A5792, Abclonal, RRID: AB_2766544), β-actin (#AC026, Abclonal, RRID: AB_2768234), and GAPDH (#10494-1-AP; Proteintech, RRID: AB_2263076).

Techniques: Control, Staining

Journal: Scientific Reports

Article Title: Sox11 overexpression restores embryonic pro-growth transcription in mature corticospinal tract neurons

doi: 10.1038/s41598-025-33479-5

Figure Lengend Snippet: Single-nucleus profiling detects a large transcriptional response to Sox11 overexpression. ( a ) Experimental design in which CST neurons of adult male and female mice were retrogradely labeled by nuclear-localized AAV2-Retro-H2B-mGreenlantern, AAV2-Retro-Sox11, and a unique molecular barcode. Fluorescently labeled tissue from each group was dissected after one, two, four, or six weeks and pooled for single-nucleus profiling. ( b ) UMAP visualization shows separation of Sox11-treated nuclei from control and co-clustering of all Sox11 time points. ( c ) MA plots showing the relationship between transcript abundance and differential gene expression at the four time points, comparing Sox11-treated to control nuclei (non-parametric Wilcoxon rank sum test, p_adj < 0.05), which reveal numerous transcripts are significantly up-regulated (green) and down-regulated (red). ( d ) Gene ontology analysis of transcripts that are significantly upregulated in Sox11-treated nuclei shows enrichment for terms such as neuron development and cytoskeletal organization ( e ) Gene ontology analysis of transcripts that are significantly downregulated in Sox11-treated nuclei shows enrichment for terms including ion transport and synaptic signaling (p-values indicated in plots, Benjamini-Hochberg test).

Article Snippet: Fig. 2 Fluorescence in situ hybridization confirms upregulation of Sox11, Dpysl3, and Dpysl5 in Sox11-treated animals. ( a ) Experimental design involving retrograde transduction of CST neurons with nuclear-localized AAV2-Retro-H2B-mGreenlantern (H2B-mGl) alone or in combination with AAV2-Retro-Sox11, followed 2 weeks later by in situ hybridization to detect candidate genes. ( b – g ) Coronal sections of cortex with CST nuclei labeled by H2B-mGl (green) and in situ hybridization detection of Sox11 ( b , c ), Dpysl3 ( d , e ), and Dpysl5 ( f , g ) in red.

Techniques: Over Expression, Labeling, Control, Gene Expression

Journal: Scientific Reports

Article Title: Sox11 overexpression restores embryonic pro-growth transcription in mature corticospinal tract neurons

doi: 10.1038/s41598-025-33479-5

Figure Lengend Snippet: Fluorescence in situ hybridization confirms upregulation of Sox11, Dpysl3, and Dpysl5 in Sox11-treated animals. ( a ) Experimental design involving retrograde transduction of CST neurons with nuclear-localized AAV2-Retro-H2B-mGreenlantern (H2B-mGl) alone or in combination with AAV2-Retro-Sox11, followed 2 weeks later by in situ hybridization to detect candidate genes. ( b – g ) Coronal sections of cortex with CST nuclei labeled by H2B-mGl (green) and in situ hybridization detection of Sox11 ( b , c ), Dpysl3 ( d , e ), and Dpysl5 ( f , g ) in red. Panels ( b , d , f ) show control tissue and ( c , e , g ) show Sox11-overexpressing samples with elevated target expression (arrows). ( h – j ) Quantification of average signal intensity in CST nuclei shows significant increases in Sox11 ( h ), Dpysl3 ( i ), and Dpysl5 ( j ). N > 50 neurons from three replicate animals, **** p < 0.0001, unpaired t-test.

Article Snippet: Fig. 2 Fluorescence in situ hybridization confirms upregulation of Sox11, Dpysl3, and Dpysl5 in Sox11-treated animals. ( a ) Experimental design involving retrograde transduction of CST neurons with nuclear-localized AAV2-Retro-H2B-mGreenlantern (H2B-mGl) alone or in combination with AAV2-Retro-Sox11, followed 2 weeks later by in situ hybridization to detect candidate genes. ( b – g ) Coronal sections of cortex with CST nuclei labeled by H2B-mGl (green) and in situ hybridization detection of Sox11 ( b , c ), Dpysl3 ( d , e ), and Dpysl5 ( f , g ) in red.

Techniques: Fluorescence, In Situ Hybridization, Transduction, Labeling, Control, Expressing