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Figure 6. MIF represses adipogenesis and activates ERK1/2 in vitro (A) Representative images of SVF cells and the corresponding culture dishes with oil red O staining. The SVF cells were induced to differentiate into Adi in the absence (control) or presence of MIF, CXCL11, or <t>CXCL12.</t> Scale bar, 100 mm.
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Figure 6. MIF represses adipogenesis and activates ERK1/2 in vitro (A) Representative images of SVF cells and the corresponding culture dishes with oil red O staining. The SVF cells were induced to differentiate into Adi in the absence (control) or presence of MIF, CXCL11, or <t>CXCL12.</t> Scale bar, 100 mm.
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Figure 6. MIF represses adipogenesis and activates ERK1/2 in vitro (A) Representative images of SVF cells and the corresponding culture dishes with oil red O staining. The SVF cells were induced to differentiate into Adi in the absence (control) or presence of MIF, CXCL11, or <t>CXCL12.</t> Scale bar, 100 mm.
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(A–C) Immunofluorescence staining of proliferative vessels (CD31+/BrdU+) in the peri-infarct region on day 7 after MCAO. CD31: green, BrdU: red. Images are shown at 200× magnification; scale bar=50 μm. (D) Quantification showed that crenolanib treatment on days 1–3 significantly decreased the number of proliferative vessels in the peri-infarct area on day 7 after stroke. *p<0.05 vs. MCAO+vehicle group; n=8/group. (E) ELISA analysis of ischemic border on day 7 after MCAO showed that crenolanib treatment on days 1–3 decreased the average level of VEGF in MCAO mice, but the change was not statistically significant. n=8/group. (F–G) Immunofluorescence staining of <t>SDF-1</t> and MCP-1 in the peri-infarct region on day 7 after MCAO. The white lines show the brain boundaries. Images are shown at 100× magnification; scale bar=25 μm. (H–I) ELISA analysis of SDF-1 and MCP-1 on day 7 after MCAO showed that levels of SDF-1 and MCP-1 in the ischemic border were lower in MCAO mice treated with crenolanib (on days 1–3) than in MCAO mice treated with vehicle. *p<0.05 vs. MCAO+vehicle group; n=8/group.
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The effect of TTT on VEGFA and <t>CXCL12</t> expression (A) ELISA for serum levels of VEGFA and CXCL12. (B) qPCR for skin tissue expression of VEGFA and CXCL12. *, p < 0.05, **, p < 0.01, ***, p < 0.001 compared to the sham group or unilateral TTT group.
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The effect of TTT on VEGFA and <t>CXCL12</t> expression (A) ELISA for serum levels of VEGFA and CXCL12. (B) qPCR for skin tissue expression of VEGFA and CXCL12. *, p < 0.05, **, p < 0.01, ***, p < 0.001 compared to the sham group or unilateral TTT group.
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Image Search Results


Figure 6. MIF represses adipogenesis and activates ERK1/2 in vitro (A) Representative images of SVF cells and the corresponding culture dishes with oil red O staining. The SVF cells were induced to differentiate into Adi in the absence (control) or presence of MIF, CXCL11, or CXCL12. Scale bar, 100 mm.

Journal: Cell metabolism

Article Title: MIF-ACKR3 causes irreversible fat loss by impairing adipogenesis in cancer cachexia.

doi: 10.1016/j.cmet.2025.01.018

Figure Lengend Snippet: Figure 6. MIF represses adipogenesis and activates ERK1/2 in vitro (A) Representative images of SVF cells and the corresponding culture dishes with oil red O staining. The SVF cells were induced to differentiate into Adi in the absence (control) or presence of MIF, CXCL11, or CXCL12. Scale bar, 100 mm.

Article Snippet: When the cells reached confluence, differentiation was induced by changing the medium to Induction Medium (DMEM/F-12 containing 10% FBS, 1% P/S, 10 mg/mL insulin, 0.5 mM 3-isobutyl-1methylxantine, 1 mM dexamethasone, 2.5 mM rosiglitazone) and incubated for 2 d. Then the cells were switched to Maintenance Medium (DMEM/F-12 containing 10% FBS, 1%P/S, 10 mg/mL insulin) for 2 d, followed by replacement with fresh MaintenanceMedium and incubated for another 2 d. For the chronic treatment, 5 mg/mL MIF (MedChemExpress, HY-P7388), 1 ng/mL CXCL11 (MedChemExpress, HY-P700169AF), or 0.2 ng/mL CXCL12 (MedChemExpress, HY-P72782) was added into the Induction Medium andMaintenanceMedium throughout the differentiation process.

Techniques: In Vitro, Staining, Control

(A–C) Immunofluorescence staining of proliferative vessels (CD31+/BrdU+) in the peri-infarct region on day 7 after MCAO. CD31: green, BrdU: red. Images are shown at 200× magnification; scale bar=50 μm. (D) Quantification showed that crenolanib treatment on days 1–3 significantly decreased the number of proliferative vessels in the peri-infarct area on day 7 after stroke. *p<0.05 vs. MCAO+vehicle group; n=8/group. (E) ELISA analysis of ischemic border on day 7 after MCAO showed that crenolanib treatment on days 1–3 decreased the average level of VEGF in MCAO mice, but the change was not statistically significant. n=8/group. (F–G) Immunofluorescence staining of SDF-1 and MCP-1 in the peri-infarct region on day 7 after MCAO. The white lines show the brain boundaries. Images are shown at 100× magnification; scale bar=25 μm. (H–I) ELISA analysis of SDF-1 and MCP-1 on day 7 after MCAO showed that levels of SDF-1 and MCP-1 in the ischemic border were lower in MCAO mice treated with crenolanib (on days 1–3) than in MCAO mice treated with vehicle. *p<0.05 vs. MCAO+vehicle group; n=8/group.

Journal: Neuroscience

Article Title: Effects of crenolanib, a non-selective inhibitor of PDGFR, in a mouse model of transient middle cerebral artery occlusion

doi: 10.1016/j.neuroscience.2017.09.025

Figure Lengend Snippet: (A–C) Immunofluorescence staining of proliferative vessels (CD31+/BrdU+) in the peri-infarct region on day 7 after MCAO. CD31: green, BrdU: red. Images are shown at 200× magnification; scale bar=50 μm. (D) Quantification showed that crenolanib treatment on days 1–3 significantly decreased the number of proliferative vessels in the peri-infarct area on day 7 after stroke. *p<0.05 vs. MCAO+vehicle group; n=8/group. (E) ELISA analysis of ischemic border on day 7 after MCAO showed that crenolanib treatment on days 1–3 decreased the average level of VEGF in MCAO mice, but the change was not statistically significant. n=8/group. (F–G) Immunofluorescence staining of SDF-1 and MCP-1 in the peri-infarct region on day 7 after MCAO. The white lines show the brain boundaries. Images are shown at 100× magnification; scale bar=25 μm. (H–I) ELISA analysis of SDF-1 and MCP-1 on day 7 after MCAO showed that levels of SDF-1 and MCP-1 in the ischemic border were lower in MCAO mice treated with crenolanib (on days 1–3) than in MCAO mice treated with vehicle. *p<0.05 vs. MCAO+vehicle group; n=8/group.

Article Snippet: Based on our established protocol ( Zhao et al., 2015 , Han et al., 2016 , Wang et al., 2017 ), brain sections (20 μm) were processed with Nissl staining to quantify infarct volume or stained with antibodies against PDGFRβ (1:300, Abcam, Cambridge, MA, USA), GFAP (1:300, Santa Cruz Biotechnology, Dallas, TX, USA), doublecortin (DCX; 1:250, Santa Cruz Biotechnology), cleaved-caspase 3 (cCasp3; 1:500, Millipore, Billerica, MA, USA), CD31 (1:100, Abcam), BrdU (1:250, Abcam), Lectin fluorescein lycopersicon esculentum (tomato) (Lectin, 1:1000; Vector Laboratories, Burlingame, CA), SDF-1 (1:50, Proteintech, Sanying Biotechnology, Wuhan, China), MCP-1 (Proteintech), CD68 (1:500, Santa Cruz Biotechnology), occludin (1:250, Proteintech), and albumin (1:500, Santa Cruz Biotechnology).

Techniques: Immunofluorescence, Staining, Enzyme-linked Immunosorbent Assay

The effect of TTT on VEGFA and CXCL12 expression (A) ELISA for serum levels of VEGFA and CXCL12. (B) qPCR for skin tissue expression of VEGFA and CXCL12. *, p < 0.05, **, p < 0.01, ***, p < 0.001 compared to the sham group or unilateral TTT group.

Journal: Annals of Medicine

Article Title: Tibial transverse transport promotes wound healing in diabetic foot ulcers by stimulating endothelial progenitor cell mobilization and homing mediated neovascularization

doi: 10.1080/07853890.2024.2404186

Figure Lengend Snippet: The effect of TTT on VEGFA and CXCL12 expression (A) ELISA for serum levels of VEGFA and CXCL12. (B) qPCR for skin tissue expression of VEGFA and CXCL12. *, p < 0.05, **, p < 0.01, ***, p < 0.001 compared to the sham group or unilateral TTT group.

Article Snippet: Specifically, rabbit VEGFA ELISA kit (kl-deim-00300, Ke Lei Biological Technology Co., Ltd., Shanghai, China) and CXCL12 ELISA kit (CSB-E12656Rb, Cusabio, Wuhan, China) were assayed.

Techniques: Expressing, Enzyme-linked Immunosorbent Assay

Mechanism diagram of TTT promoting wound healing in DFUs (by figdraw). TTT induces wound fibroblasts to release VEGFA and CXCL12, thereby mediating EPC mobilization and homing, promoting angiogenesis and wound healing.

Journal: Annals of Medicine

Article Title: Tibial transverse transport promotes wound healing in diabetic foot ulcers by stimulating endothelial progenitor cell mobilization and homing mediated neovascularization

doi: 10.1080/07853890.2024.2404186

Figure Lengend Snippet: Mechanism diagram of TTT promoting wound healing in DFUs (by figdraw). TTT induces wound fibroblasts to release VEGFA and CXCL12, thereby mediating EPC mobilization and homing, promoting angiogenesis and wound healing.

Article Snippet: Specifically, rabbit VEGFA ELISA kit (kl-deim-00300, Ke Lei Biological Technology Co., Ltd., Shanghai, China) and CXCL12 ELISA kit (CSB-E12656Rb, Cusabio, Wuhan, China) were assayed.

Techniques: