Journal: Journal of Sport and Health Science

Article Title: Weightlifting outperforms voluntary wheel running for improving adiposity and insulin sensitivity in obese mice

doi: 10.1016/j.jshs.2025.101100

Figure Lengend Snippet: Resistance exercise exceeds the benefits of endurance exercise in ameliorating metabolic dysfunction. Following 8 weeks of diet and exercise interventions, all mice were assessed for their metabolic function by GTT, ITT, and skeletal muscle response of Akt and AS160 phosphorylation to injection of insulin measured by Western blot. (A–C) HOMA-IR taken after an overnight fast for baseline glucose and insulin. (D and E) GTT from 0–120 min and calculated AUC; colored * indicates significant difference from NC-SED. (F and G) ITT from 0–60 min and calculated AUC; colored * indicates significant difference from NC-SED. (H–N) pAkt stimulation, AS160 S318, and AS160 T642 in hindlimb muscles before and after insulin injection and the pre–post ∆ in phosphorylation. (O and P) Total and phosphorylated 4E-BP1. (Q–T) Western results for Raptor, COX4, LC3 II/I, and ubiquitin staining. Representative western blot images inset right. Data presented as mean ± standard error of the mean. Statistical analysis performed by analysis of variance between groups: * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. NC-SED n : 8–16 (white); HFD-SED n : 8–18 (red); HFD-R EX n : 8–16 (blue); HFD-E EX n : 8–15 (green). 4E-BP1 = Eukaryotic translation initiation factor 4E binding protein; Akt = protein kinase B; AS160 = Akt substrate 160; COX4 = cytochrome c oxidase 4; CS = citrate sythase; E EX = endurance exercise; GAPDH = glyceraldehyde 3 phosphate dehydrogenase; GTT = glucose tolerance test; HFD = high fat diet; HOMA-IR = homeostatic model assessment for insulin resistance; iAUC = integrated area under the curve; ITT = insulin tolerance test; LC3 II/I = microtubule-associated protein light chain 3; NC = normal chow; pAkt = phospho-Akt; R EX = resistance exercise; SED = sedentary; Ub = ubiquitin.

Article Snippet: Primary antibodies used for analysis were from Cell Signaling Technologies (Danvers, MA, USA) and diluted 1:1000 unless otherwise stated as follows: protein kinase B (Akt; 1:500; #4691; Cell Signaling Technologies), phospho-Akt (pAkt) S473 (1:500; #9271; Cell Signaling Technologies), Ubiquitin (#3933; Cell Signaling Technologies), microtubule-associated protein light chain 3 (LC3 II/I; #4018; Cell Signaling Technologies), cytochrome c oxidase subunit 4(COX4; #11967; Cell Signaling Technologies), Akt substrate 160 (AS160 S318; #8619; Cell Signaling Technologies), AS160 T642 (#8881; Cell Signaling Technologies), eukaryotic translation initiation factor 4E binding protein (4E-BP1; #9452; Cell Signaling Technologies), and glyceraldehyde 3 phosphate dehydrogenase (GAPDH; #2118; Cell Signaling Technologies).

Techniques: Phospho-proteomics, Injection, Western Blot, Muscles, Ubiquitin Proteomics, Staining, Binding Assay

Journal: Journal of Sport and Health Science

Article Title: Exercise training-induced extracellular miR-136-3p modulates glucose uptake and myogenesis through targeting of NRDC in human skeletal muscle

doi: 10.1016/j.jshs.2025.101091

Figure Lengend Snippet: miR-136-3p-induced increase in glucose uptake is independent of changes in canonical GLUT4 signaling pathways. The mRNA expression of GLUT4, TBC1D4, and AMPKα in primary human myotubes (A) transfected with miR-136-3p. Representative immunoblot and quantification of (B) AMPKα, (C) TBC1D4, (D) P-TBC1D4, (E) AKT, and (F) P-AKT in primary human myotubes transfected with miR-136-3p and subsequently incubated under basal or insulin-stimulated (120 nM, 1 h) conditions. Insets show representative Western blot image and total ponceau staining for loading control. Results are expressed as mean ± standard error of the mean. * p < 0.05, ** p < 0.005. AKT = protein kinase B; AMPKα = AMP-activated protein kinase α; GLUT4 = glucose transporter 4; miR = microRNA; NC = negative control; ns = no significance; P-AKT = phosphorylated AKT; P-TBC1D4 = phosphorylated TBC1D4; TBC1D4 = Tre-2/BUB2/CDC16 domain family member 4.

Article Snippet: Membranes were incubated with primary antibodies directed to NRDC (sc-137199; Santa Cruz Biotechnology, Dallas, TX, USA), AMP-activated protein kinase α (AMPKα) (#2532; Cell Signaling Technology, Danvers, MA, USA), Akt substrate of 160 kDa (AS160) (#2670; Cell Signaling Technology), phospho-AS160 (#8730; Cell Signaling Technology), protein kinase B (AKT) (#9272; Cell Signaling Technology), phospho-AKT (Ser473) (#9271; Cell Signaling Technology), or puromycin (MABE343; Merck Burlington, MA, USA).

Techniques: Protein-Protein interactions, Expressing, Transfection, Western Blot, Incubation, Staining, Control, Negative Control

Journal: Acta Pharmaceutica Sinica. B

Article Title: Neutralizing dentin sialophosphoprotein facilitates tumor vascular normalization in colorectal cancer by blocking the crosstalk between tumor cells and endothelial cells

doi: 10.1016/j.apsb.2026.06.011

Figure Lengend Snippet: DSPP/ α v β 3/MAPK signaling axis promotes tumor vessel abnormalization. (A, B) Investigating the potential regulatory functions of DSPP in CRC by the WiKi (A) and KEGG (B) pathway enrichment analysis. (C) The mitogen-activated protein kinase (MAPK)-related pathways were enriched in CRC with high DSPP expression by GSEA analysis. (D) Western blot assays showing the expression of the FAK/ERK pathway components in HUVEC treated with CM from the indicated CRC cells (E, F) Representative tubular structures formed by HUVECs treated with indicated CM from indicated HCT8/Caco-2 cells. Data are presented as mean ± SD ( n = 3). (G) Heat map demonstrates the differentially expressed genes related to angiogenesis and matrix metalloproteinase family in HUVEC treated with CM from control and sg DSPP HCT116 cells. (H) Detecting the effect of AZD6244 on the DSPP-upregulated expression of angiogenesis and matrix metalloproteinase family-related genes by real-time quantitative PCR. Data are presented as mean ± SD ( n = 4). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.

Article Snippet: Inhibitors, including the mitogen-activated protein kinase (MAPK) kinase inhibitor selumetinib (AZD6244, MCE, Monmouth Junction, NJ, USA) or cyclo (-RGDfK) TFA (HY-P0023A, MCE), were introduced into the cultured cells.

Techniques: Expressing, Western Blot, Control, Real-time Polymerase Chain Reaction

Journal: Acta Pharmaceutica Sinica. B

Article Title: Neutralizing dentin sialophosphoprotein facilitates tumor vascular normalization in colorectal cancer by blocking the crosstalk between tumor cells and endothelial cells

doi: 10.1016/j.apsb.2026.06.011

Figure Lengend Snippet: A schematic diagram shows the action mechanism of DSPP in regulating tumor vascular abnormalization to induce tumor metastasis. In the tumor microenvironment, IL-7F enhances the expression and secretion of DSPP in CRC. The CRC-secreted DSPP binds to the integrin α v β 3 on the endothelial cell surface and activates the downstream FAK/MAPK signaling to induce tumor vascular abnormalization, finally promote tumor metastasis.

Article Snippet: Inhibitors, including the mitogen-activated protein kinase (MAPK) kinase inhibitor selumetinib (AZD6244, MCE, Monmouth Junction, NJ, USA) or cyclo (-RGDfK) TFA (HY-P0023A, MCE), were introduced into the cultured cells.

Techniques: Expressing

Journal: Journal of Cell Science

Article Title: Apical-out polarity in epithelial spheroids requires α6β4 integrins, cell proliferation and anchorage independence

doi: 10.1242/jcs.264323

Figure Lengend Snippet: Anchorage independence is required for apical-out polarity. (A) MDCK cells were seeded into soft agar. Cells were left untreated or were treated with RhoA activator II. (B) Quantification of colonies formed in the agar assay. Each data point represents the mean (from a minimum of three field of view) from each experimental replicate (three replicate experiments were performed in total) (error bars are overall mean±s.d.). * P <0.05 (paired two-tailed t -test). (C) MDCK cysts were grown in Matrigel for 7 days and then treated with RhoA activator II for 72 h, pre-treated with FAK inhibitor Y15 24 h followed by Y15+Rho Activator II for an additional 48 h, or treated with Rho activator II for 24 h, followed by Y15+Rho activator II for an additional 48 h (post treatment). (D) Quantification of normal, disrupted lumen and eversion for each condition. Each data point represents the mean (expressed as a percentage) of each condition per replicate experiment (minimum of 10 cysts analyzed per condition per experiment, five replicate experiments performed in total; error bars are overall mean±s.d.). ** P <0.01; ns, not significant (two-way ANOVA with Tukey's multiple comparison test).

Article Snippet: Focal adhesion kinase (FAK) inhibitor Y15 (also known as FAK inhibitor 14) was used at a final concentration of 2.5 μM (Medchem express, catalog HY-12444).

Techniques: Two Tailed Test, Comparison