Journal: Journal of Advanced Research

Article Title: Negative pressure mechanical signal increases the phosphorylation of eNOS Ser1177 by upregulating HSP90 expression to promote wound angiogenesis

doi: 10.1016/j.jare.2025.07.041

Figure Lengend Snippet: NPWT modulates the biological behavior of HDMECs by regulating HSP90. (A) Volcano plot of differentially expressed proteins in the different groups of HDMECs. (B) Pie chart of differential protein cellular localization. (C) Heatmap of differentially expressed proteins in HDMECs from various groups. (D) GO analysis of upregulated proteins in HDMECs treated with NPWT. (E) mRNA expression of HSP90 after the application of siRNA. (F) CCK8 assay was used to measure the proliferation rate of HDMECs across different groups. n = 8. (G, H) Migration and lumen formation of HDMECs in each group after the application of the HSP90 inhibitor 17-AAG or siHSP90. n = 3. Scale bar = 200 µm. (I) Changes in NO levels in HDMECs across different groups. n = 3. Scale bar = 50 µm. (J) Variations in ROS levels across different groups. n = 3. Scale bar = 50 µm. (K, L) Apoptosis and necrosis levels of HDMECs in different groups. n = 3. Scale bar = 100 µm.

Article Snippet: Primary human dermal microvascular endothelial cells (HDMECs) were isolated from cryopreserved human dermal tissue via established methods [ ] and cultured in ECM (Sciencell) at 37 °C with 5 % CO 2 for 24 h. The cells in the corresponding groups were treated with 0.5 mM 17-AAG (MCE) or 0.5 mM 666–15 (MCE).

Techniques: Expressing, CCK-8 Assay, Migration

Journal: Cellular & Molecular Biology Letters

Article Title: The promoting roles of GLP1R and GIPR in stemness maintenance and multiple lineage-specific differentiation of PDLSCs

doi: 10.1186/s11658-026-00867-2

Figure Lengend Snippet: Enhanced cell growth of PDLSCs facilitated by GIPRA/MAPK/ERK axis. a Western blot assay showing the expression of Ki-67, PCNA, and CCND3 affected by GIPRA as well as inhibition of cAMP/PKA/CREB, MAPK/ERK, Wnt/β-catenin, or JAK/STAT3 signaling pathways. The interpretation of bubble colors in the line chart is illustrated in Fig. a. b CCK-8 assay indicating the cell growth enhanced by GIPRA, but suppressed by ERK Inh ( n = 5 in each group). The interpretation of line colors in the line chart is illustrated in Fig. b. c Venn diagram showing the intersection of differentially binding genes by p-CREB, p-ERK1/2, TCF4, and p-STAT3 (log FC > 1, P < 0.05) compared between GIPRA and NC group. d The bubble plot displays the top ten functions of cell division and cell cycle (GO biological process) associated with the 5994 (red color highlighted) specifically binding genes by p-ERK1/2 in c . e – g IGV showing the binding peaks of p-ERK1/2 on MKI67 ( e ), PCNA ( f ), and CCND3 genes ( g ). The differential binding peaks of p-ERK1/2 on these gene promoters are highlighted by blue boxes. h – k Line plot illustrates the distribution of ChIP-seq signal intensity of p-ERK1/2 ( h ), p-CREB ( i ), TCF4 ( j ), and p-STAT3 ( k ) across the transcription start sites (±3 kb) of differentially binding genes in PDLSCs treated with GIPRA as well as GIPRA plus ERK Inh. NC, normal PDLSCs as negative control; Inh., inhibitor

Article Snippet: The in vitro treatment conditions for the small-molecule compound were as follows: GLP1RA semaglutide acetate (10 nM, 24 h), GIPRA (Pro3) GIP (0.5 nM, 24 h), GLP-1R/GIPR agonist-1 (10 nM, 24 h) also termed as 2GRA in this study, BGM0504 (2 nM, 24 h, BrightGene Pharmaceutical Co., Ltd., China) [ ], CREB inhibitor 666-15 (1 μM, 2 h, HY-101120, MCE), Akt inhibitor MK-2206 (5 μM, 24 h, HY-108232, MCE), ERK1/2 inhibitor SCH772984 (0.5 μM, 24 h, HY-50846, MCE), β-catenin inhibitor IN-3 (5 μM, 24 h, HY-147007, MCE), STAT3-IN-14 (5 μM, 2 h, HY-N10472, MCE).

Techniques: Western Blot, Expressing, Inhibition, Protein-Protein interactions, CCK-8 Assay, Binding Assay, ChIP-sequencing, Negative Control