Journal: Advanced Science

Article Title: PDIA6–SCD1 Axis Rewires Lipid Metabolism to Drive Gastric Cancer Progression

doi: 10.1002/advs.75923

Figure Lengend Snippet: CAF‐derived CXCL12 reinforces PDIA6 expression through CXCR4‐STAT3 signaling in GC. (A,B) Immunofluorescence staining and western blot analysis of the CAF markers FAP and α‐SMA in CAFs and paired NFs. (C,D) qRT‐PCR and western blot analyses of PDIA6 mRNA and protein expression in GC cells treated with CAF‐conditioned medium (CAF‐CM) or NF‐conditioned medium (NF‐CM). (E,F) Transwell migration and EdU incorporation assays evaluating the effects of PDIA6 knockdown on CAF‐CM‐induced GC cell phenotypes. (G) Western blot analysis of STAT3 and PDIA6 in GC cells treated with or without CAF‐CM and transfected with control or STAT3 siRNA. (H) RNA‐seq analysis identifying CXCL12 as a highly upregulated secreted factor in CAFs relative to NFs. (I) Correlation analysis of CXCL12 and PDIA6 expression in the TCGA‐STAD cohort. (J,K) Single‐cell RNA‐seq analysis showing fibroblast‐specific expression of CXCL12 in GC tissues. (L,M) Western blot analysis of CXCL12 protein expression and ELISA of CXCL12 secretion in CAFs, NFs, and GC cells. (N) Western blot analysis of p‐STAT3 (Tyr705), total STAT3, and PDIA6 in GC cells pretreated with AMD3100 (2.5 µg/mL) for 30 min and then incubated with or without CAF‐CM for 24 h. (O) Western blot analysis of p‐STAT3 (Tyr705), total STAT3, and PDIA6 in GC cells treated with CAF‐CM together with IgG control or αCXCL12 (10 µg/mL, 24 h). (P) Western blot analysis of p‐STAT3 (Tyr705) and PDIA6 in GC cells treated with CAF‐CM or recombinant human CXCL12 (rhCXCL12, 25/50/100 ng/mL) for 24 h, with or without AMD3100 pretreatment. (Q,R) Cell proliferation and migration assays evaluating the effects of rhCXCL12 stimulation and αCXCL12 neutralization on GC cell behavior. Data are presented as mean ± SD.

Article Snippet: CXCL12 levels in cell culture supernatants were quantified using a human CXCL12 ELISA kit (RK00266, Abclonal, China) according to the manufacturer's instructions.

Techniques: Derivative Assay, Expressing, Immunofluorescence, Staining, Western Blot, Quantitative RT-PCR, Migration, Knockdown, Transfection, Control, RNA Sequencing, Single Cell, Enzyme-linked Immunosorbent Assay, Incubation, Recombinant, Neutralization

Journal: Advanced Science

Article Title: PDIA6–SCD1 Axis Rewires Lipid Metabolism to Drive Gastric Cancer Progression

doi: 10.1002/advs.75923

Figure Lengend Snippet: CAF‐derived CXCL12 reinforces PDIA6 expression through CXCR4‐STAT3 signaling in GC. (A,B) Immunofluorescence staining and western blot analysis of the CAF markers FAP and α‐SMA in CAFs and paired NFs. (C,D) qRT‐PCR and western blot analyses of PDIA6 mRNA and protein expression in GC cells treated with CAF‐conditioned medium (CAF‐CM) or NF‐conditioned medium (NF‐CM). (E,F) Transwell migration and EdU incorporation assays evaluating the effects of PDIA6 knockdown on CAF‐CM‐induced GC cell phenotypes. (G) Western blot analysis of STAT3 and PDIA6 in GC cells treated with or without CAF‐CM and transfected with control or STAT3 siRNA. (H) RNA‐seq analysis identifying CXCL12 as a highly upregulated secreted factor in CAFs relative to NFs. (I) Correlation analysis of CXCL12 and PDIA6 expression in the TCGA‐STAD cohort. (J,K) Single‐cell RNA‐seq analysis showing fibroblast‐specific expression of CXCL12 in GC tissues. (L,M) Western blot analysis of CXCL12 protein expression and ELISA of CXCL12 secretion in CAFs, NFs, and GC cells. (N) Western blot analysis of p‐STAT3 (Tyr705), total STAT3, and PDIA6 in GC cells pretreated with AMD3100 (2.5 µg/mL) for 30 min and then incubated with or without CAF‐CM for 24 h. (O) Western blot analysis of p‐STAT3 (Tyr705), total STAT3, and PDIA6 in GC cells treated with CAF‐CM together with IgG control or αCXCL12 (10 µg/mL, 24 h). (P) Western blot analysis of p‐STAT3 (Tyr705) and PDIA6 in GC cells treated with CAF‐CM or recombinant human CXCL12 (rhCXCL12, 25/50/100 ng/mL) for 24 h, with or without AMD3100 pretreatment. (Q,R) Cell proliferation and migration assays evaluating the effects of rhCXCL12 stimulation and αCXCL12 neutralization on GC cell behavior. Data are presented as mean ± SD.

Article Snippet: CXCL12 levels in cell culture supernatants were quantified using a human CXCL12 ELISA kit (RK00266, Abclonal, China) according to the manufacturer's instructions.

Techniques: Derivative Assay, Expressing, Immunofluorescence, Staining, Western Blot, Quantitative RT-PCR, Migration, Knockdown, Transfection, Control, RNA Sequencing, Single Cell, Enzyme-linked Immunosorbent Assay, Incubation, Recombinant, Neutralization

Journal: Nature Communications

Article Title: Perivascular adipose single-cell atlas identifies CD55 + adipose-derived stem cells as vascular remodeling regulators in atherosclerosis

doi: 10.1038/s41467-026-72962-z

Figure Lengend Snippet: A Cell-cell crosstalk analysis among ADSC subsets and T cell subpopulation interaction weights in control v.s. CAS groups. B Outgoing-Incoming interaction strength analysis among ADSC subsets and T cell subpopulations in control v.s. CAS groups. C Interaction strength difference analysis among ADSC subsets and T cell subpopulations in control v.s. CAS groups. D Cell-cell crosstalk analysis among ADSC subsets and myeloid cell subpopulation interaction weights in control v.s. CAS groups. E Outgoing-Incoming interaction strength analysis among ADSC subsets and myeloid cell subpopulations in control v.s. CAS groups. F Interaction strength difference analysis among ADSC subsets and myeloid cell subpopulations in control v.s. CAS groups. G Ligand-receptor bubble plot of increased communication from ADSC subtypes to T cell subpopulations. H Ligand-receptor bubble plot of increased communication from ADSC subtypes to myeloid subtypes. I Chordal chart of CXCL12-CXCR4 pathway communication strength among ADSC subtypes, myeloid cell subtypes, NK cell subtypes, and T cell subtypes in CAS group and/or control group. J ELISA test detecting the expression level of CXCL12 in ADSC-conditioned medium. Experiments were performed with three biological replicates. K ELISA test detecting the expression level of CXCL14 in ADSC-conditioned medium. Experiments were performed with three biological replicates. L – N Representative images and statistical analysis of Transwell assay, examining whether CXCL14⁺ADSCs recruit macrophages via the CXCL12-CXCR4 pathway. Scale bar = 50 μm. Experiments were performed with six biological replicates. O Chordal chart of AREG-EGFR pathway communication strength among ADSC subtypes, myeloid cell subtypes, NK cell subtypes, and T cell subtypes in CAS group and/or control group. P –values in ( G ) and ( H ) were calculated using one-sided permutation tests without correction for multiple comparisons. Two-tailed unpaired t -test was used for ( J , K , and N ). Error bars show mean ± SD. CAS carotid artery stenosis, ADSC adipose-derived stem cell. Source data are provided as a Source Data file.

Article Snippet: The concentration of FGF2, CXCL12, and CXCL14 in conditioned medium of CD55 + ADSC and CXCL14 + ADSC were quantified using human FGF2 ELISA Kit (KE00129, Proteintech, China), human CXCL12/SDF-1 ELISA Kit (RK00266, ABclonal, China), and human CXCL14 (C-X-C motif chemokine 14) ELISA Kit (EH1843, FineTest, China), respectively, following the manufacturers’ protocols.

Techniques: Control, Enzyme-linked Immunosorbent Assay, Expressing, Transwell Assay, Two Tailed Test, Derivative Assay

Journal: Nature Communications

Article Title: Perivascular adipose single-cell atlas identifies CD55 + adipose-derived stem cells as vascular remodeling regulators in atherosclerosis

doi: 10.1038/s41467-026-72962-z

Figure Lengend Snippet: During carotid stenosis, the expanded ADSC population includes distinct functional subsets. The CD55 + ADSC subset promotes plaque instability by migrating into lesions, potentially differentiating into endothelial cells, and secreting FGF2 to concurrently stimulate angiogenesis and a synthetic phenotypic switch in smooth muscle cells, resulting in neointimal hyperplasia. Conversely, the CXCL14 + ADSC subset functions in inflammatory recruitment by leveraging pathways like CXCL12-CXCR4 to attract macrophages and other immune cells. Furthermore, extensive cell-cell interactions within PVAT, particularly between these ADSCs and lymphocytes/myeloid cells, orchestrate a synergistic effect that amplifies chemotaxis and angiogenesis, ultimately accelerating the formation of unstable, clinically significant plaques that predispose to stroke. This schematic was created in BioRender. Chen, J. (2026) https://BioRender.com/uf4cxuu .

Article Snippet: The concentration of FGF2, CXCL12, and CXCL14 in conditioned medium of CD55 + ADSC and CXCL14 + ADSC were quantified using human FGF2 ELISA Kit (KE00129, Proteintech, China), human CXCL12/SDF-1 ELISA Kit (RK00266, ABclonal, China), and human CXCL14 (C-X-C motif chemokine 14) ELISA Kit (EH1843, FineTest, China), respectively, following the manufacturers’ protocols.

Techniques: Functional Assay, Chemotaxis Assay