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Effect of Tet2 deficiency on Ccl2 <t>and</t> <t>Ccl8</t> mRNA stability and IL-6 neutralization on liver fibrosis progression. (A) The frequency of Ccr2 + and Ccr3 + pMDMs in Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 4 for each group). (B) Expression of Ccr2 and Ccr3 on monocytes, Tet2 +/+ pMDMs, and Tet2 −/− pMDMs ( n = 4 for each group). (C) The infiltration difference of other Ccr2 or Ccr3 expressing cell types in Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 4 for each group). (D) GAPDH mRNA decay curve in Tet2 +/+ pMDMs and Tet2 −/− pMDMs ( n = 6 for each group). (E) Transcriptional level of Elavl1, Znf36, and Ybx1 in Tet2 +/+ pMDMs and Tet2 −/− pMDMs ( n = 4 for each group). (F–I) Serum levels of (F) IL-1α, (G) IL-2, (H) <t>TNFα,</t> and (I) IL-1β in livers of Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 5 for each group). (J) Serum IL-6 levels in scramble, WT-MT, and KO-MT mice ( n = 4 for each group). (K) Il-6 levels in CD45.2 + pMDMs isolated from livers of WT-MT and KO-MT mice ( n = 4). (L) mRNA levels of Acta2 and Col1a1 in Tet2 +/+ and Tet2 −/− HSCs ( n = 4 for each group). (M and N) Effect of anti–IL-6 Abs treatment on mRNA levels of Col1a1 (M) and Acta2 (N) in Tet2 +/+ and Tet2 −/− HSCs co-cultured with Tet2 +/+ or Tet2 −/− MDMs detected by RT-PCR in vitro ( n = 3 for each group). (O) Effect on recombinant Ccl2 and Ccl8 on Il-6 expression in Tet2 +/+ pMDMs and Tet2 −/− pMDMs ( n = 3 for each group). (P) Detection of MDMs in livers by flow cytometry after Bindarit or IL-6 Abs treatment for 2 wk ( n = 5 for each group). (Q) H&E staining of liver tissues treated with PBS, Bindarit, IL-6 Abs, or Bindarit plus IL-6 Abs in Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 4 for each group). Data are representative of at least two independent experiments with similar results (A–P). All data are shown as mean ± SD and were analyzed by two-tailed, unpaired Student’s t test (A, C, D, E, K, L, and O) or one-way ANOVA with Tukey’s multiple comparison test (B and J) or two-way ANOVA with Sidak’s multiple comparison test (F–I, M, and N). ****P < 0.0001; ***P < 0.001; **P < 0.01; *P < 0.05; P > 0.05 not significant (ns).
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Effect of Tet2 deficiency on Ccl2 <t>and</t> <t>Ccl8</t> mRNA stability and IL-6 neutralization on liver fibrosis progression. (A) The frequency of Ccr2 + and Ccr3 + pMDMs in Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 4 for each group). (B) Expression of Ccr2 and Ccr3 on monocytes, Tet2 +/+ pMDMs, and Tet2 −/− pMDMs ( n = 4 for each group). (C) The infiltration difference of other Ccr2 or Ccr3 expressing cell types in Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 4 for each group). (D) GAPDH mRNA decay curve in Tet2 +/+ pMDMs and Tet2 −/− pMDMs ( n = 6 for each group). (E) Transcriptional level of Elavl1, Znf36, and Ybx1 in Tet2 +/+ pMDMs and Tet2 −/− pMDMs ( n = 4 for each group). (F–I) Serum levels of (F) IL-1α, (G) IL-2, (H) <t>TNFα,</t> and (I) IL-1β in livers of Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 5 for each group). (J) Serum IL-6 levels in scramble, WT-MT, and KO-MT mice ( n = 4 for each group). (K) Il-6 levels in CD45.2 + pMDMs isolated from livers of WT-MT and KO-MT mice ( n = 4). (L) mRNA levels of Acta2 and Col1a1 in Tet2 +/+ and Tet2 −/− HSCs ( n = 4 for each group). (M and N) Effect of anti–IL-6 Abs treatment on mRNA levels of Col1a1 (M) and Acta2 (N) in Tet2 +/+ and Tet2 −/− HSCs co-cultured with Tet2 +/+ or Tet2 −/− MDMs detected by RT-PCR in vitro ( n = 3 for each group). (O) Effect on recombinant Ccl2 and Ccl8 on Il-6 expression in Tet2 +/+ pMDMs and Tet2 −/− pMDMs ( n = 3 for each group). (P) Detection of MDMs in livers by flow cytometry after Bindarit or IL-6 Abs treatment for 2 wk ( n = 5 for each group). (Q) H&E staining of liver tissues treated with PBS, Bindarit, IL-6 Abs, or Bindarit plus IL-6 Abs in Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 4 for each group). Data are representative of at least two independent experiments with similar results (A–P). All data are shown as mean ± SD and were analyzed by two-tailed, unpaired Student’s t test (A, C, D, E, K, L, and O) or one-way ANOVA with Tukey’s multiple comparison test (B and J) or two-way ANOVA with Sidak’s multiple comparison test (F–I, M, and N). ****P < 0.0001; ***P < 0.001; **P < 0.01; *P < 0.05; P > 0.05 not significant (ns).
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Effect of Tet2 deficiency on Ccl2 <t>and</t> <t>Ccl8</t> mRNA stability and IL-6 neutralization on liver fibrosis progression. (A) The frequency of Ccr2 + and Ccr3 + pMDMs in Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 4 for each group). (B) Expression of Ccr2 and Ccr3 on monocytes, Tet2 +/+ pMDMs, and Tet2 −/− pMDMs ( n = 4 for each group). (C) The infiltration difference of other Ccr2 or Ccr3 expressing cell types in Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 4 for each group). (D) GAPDH mRNA decay curve in Tet2 +/+ pMDMs and Tet2 −/− pMDMs ( n = 6 for each group). (E) Transcriptional level of Elavl1, Znf36, and Ybx1 in Tet2 +/+ pMDMs and Tet2 −/− pMDMs ( n = 4 for each group). (F–I) Serum levels of (F) IL-1α, (G) IL-2, (H) <t>TNFα,</t> and (I) IL-1β in livers of Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 5 for each group). (J) Serum IL-6 levels in scramble, WT-MT, and KO-MT mice ( n = 4 for each group). (K) Il-6 levels in CD45.2 + pMDMs isolated from livers of WT-MT and KO-MT mice ( n = 4). (L) mRNA levels of Acta2 and Col1a1 in Tet2 +/+ and Tet2 −/− HSCs ( n = 4 for each group). (M and N) Effect of anti–IL-6 Abs treatment on mRNA levels of Col1a1 (M) and Acta2 (N) in Tet2 +/+ and Tet2 −/− HSCs co-cultured with Tet2 +/+ or Tet2 −/− MDMs detected by RT-PCR in vitro ( n = 3 for each group). (O) Effect on recombinant Ccl2 and Ccl8 on Il-6 expression in Tet2 +/+ pMDMs and Tet2 −/− pMDMs ( n = 3 for each group). (P) Detection of MDMs in livers by flow cytometry after Bindarit or IL-6 Abs treatment for 2 wk ( n = 5 for each group). (Q) H&E staining of liver tissues treated with PBS, Bindarit, IL-6 Abs, or Bindarit plus IL-6 Abs in Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 4 for each group). Data are representative of at least two independent experiments with similar results (A–P). All data are shown as mean ± SD and were analyzed by two-tailed, unpaired Student’s t test (A, C, D, E, K, L, and O) or one-way ANOVA with Tukey’s multiple comparison test (B and J) or two-way ANOVA with Sidak’s multiple comparison test (F–I, M, and N). ****P < 0.0001; ***P < 0.001; **P < 0.01; *P < 0.05; P > 0.05 not significant (ns).
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Effect of Tet2 deficiency on Ccl2 <t>and</t> <t>Ccl8</t> mRNA stability and IL-6 neutralization on liver fibrosis progression. (A) The frequency of Ccr2 + and Ccr3 + pMDMs in Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 4 for each group). (B) Expression of Ccr2 and Ccr3 on monocytes, Tet2 +/+ pMDMs, and Tet2 −/− pMDMs ( n = 4 for each group). (C) The infiltration difference of other Ccr2 or Ccr3 expressing cell types in Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 4 for each group). (D) GAPDH mRNA decay curve in Tet2 +/+ pMDMs and Tet2 −/− pMDMs ( n = 6 for each group). (E) Transcriptional level of Elavl1, Znf36, and Ybx1 in Tet2 +/+ pMDMs and Tet2 −/− pMDMs ( n = 4 for each group). (F–I) Serum levels of (F) IL-1α, (G) IL-2, (H) <t>TNFα,</t> and (I) IL-1β in livers of Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 5 for each group). (J) Serum IL-6 levels in scramble, WT-MT, and KO-MT mice ( n = 4 for each group). (K) Il-6 levels in CD45.2 + pMDMs isolated from livers of WT-MT and KO-MT mice ( n = 4). (L) mRNA levels of Acta2 and Col1a1 in Tet2 +/+ and Tet2 −/− HSCs ( n = 4 for each group). (M and N) Effect of anti–IL-6 Abs treatment on mRNA levels of Col1a1 (M) and Acta2 (N) in Tet2 +/+ and Tet2 −/− HSCs co-cultured with Tet2 +/+ or Tet2 −/− MDMs detected by RT-PCR in vitro ( n = 3 for each group). (O) Effect on recombinant Ccl2 and Ccl8 on Il-6 expression in Tet2 +/+ pMDMs and Tet2 −/− pMDMs ( n = 3 for each group). (P) Detection of MDMs in livers by flow cytometry after Bindarit or IL-6 Abs treatment for 2 wk ( n = 5 for each group). (Q) H&E staining of liver tissues treated with PBS, Bindarit, IL-6 Abs, or Bindarit plus IL-6 Abs in Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 4 for each group). Data are representative of at least two independent experiments with similar results (A–P). All data are shown as mean ± SD and were analyzed by two-tailed, unpaired Student’s t test (A, C, D, E, K, L, and O) or one-way ANOVA with Tukey’s multiple comparison test (B and J) or two-way ANOVA with Sidak’s multiple comparison test (F–I, M, and N). ****P < 0.0001; ***P < 0.001; **P < 0.01; *P < 0.05; P > 0.05 not significant (ns).
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NSC Sox2 transplantation decreases the expression of proinflammatory factors and increases the expression of anti-inflammatory factors and neurotrophic factors in hippocampus. (A, B) <t>ELISA</t> results of TNF-α (A) and IL-1β (B) in hippocampus. (C) Typical western blot bands of TNF-α, IL-6, IL-10, BDNF, and NGF. (D) Statistical analysis of proteins. All data are presented as the mean ± SD ( n = 5). ** P < 0.01, *** P < 0.001, vs . Sham group (one-way analysis of variance followed by post hoc Tukey’s honestly significant difference test). BDNF: Brain-derived growth factor; ELISA: enzyme-linked <t>immunosorbent</t> assay; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IL: interleukin; IVH: intraventricular hemorrhage; NGF: nerve growth factor; NSC: neural stem cell; PBS: phosphate-buffered saline; SD: standard deviation; Sox2: sex-determining region Y-box 2; TNF-α: tumor necrosis factor-alpha.
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Effects of si-PVT1 transfection on CoCl 2 –induced angiogenesis and inflammatory levels in HUVECs. A. Changes in vascular endothelial growth factor (VEGF) expression in HUVECs following CoCl 2 induction and si-PVT1 transfection. B. Effects of CoCl 2 induction and LncRNA PVT1 inhibition on fibroblast growth factor-2 (FGF-2) expression in HUVECs. Effects of different transfection treatments on inflammatory cytokine <t>expression:</t> <t>TNF-α</t> (C) and IL-6 (D) . * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001
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Effect of Tet2 deficiency on Ccl2 and Ccl8 mRNA stability and IL-6 neutralization on liver fibrosis progression. (A) The frequency of Ccr2 + and Ccr3 + pMDMs in Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 4 for each group). (B) Expression of Ccr2 and Ccr3 on monocytes, Tet2 +/+ pMDMs, and Tet2 −/− pMDMs ( n = 4 for each group). (C) The infiltration difference of other Ccr2 or Ccr3 expressing cell types in Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 4 for each group). (D) GAPDH mRNA decay curve in Tet2 +/+ pMDMs and Tet2 −/− pMDMs ( n = 6 for each group). (E) Transcriptional level of Elavl1, Znf36, and Ybx1 in Tet2 +/+ pMDMs and Tet2 −/− pMDMs ( n = 4 for each group). (F–I) Serum levels of (F) IL-1α, (G) IL-2, (H) TNFα, and (I) IL-1β in livers of Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 5 for each group). (J) Serum IL-6 levels in scramble, WT-MT, and KO-MT mice ( n = 4 for each group). (K) Il-6 levels in CD45.2 + pMDMs isolated from livers of WT-MT and KO-MT mice ( n = 4). (L) mRNA levels of Acta2 and Col1a1 in Tet2 +/+ and Tet2 −/− HSCs ( n = 4 for each group). (M and N) Effect of anti–IL-6 Abs treatment on mRNA levels of Col1a1 (M) and Acta2 (N) in Tet2 +/+ and Tet2 −/− HSCs co-cultured with Tet2 +/+ or Tet2 −/− MDMs detected by RT-PCR in vitro ( n = 3 for each group). (O) Effect on recombinant Ccl2 and Ccl8 on Il-6 expression in Tet2 +/+ pMDMs and Tet2 −/− pMDMs ( n = 3 for each group). (P) Detection of MDMs in livers by flow cytometry after Bindarit or IL-6 Abs treatment for 2 wk ( n = 5 for each group). (Q) H&E staining of liver tissues treated with PBS, Bindarit, IL-6 Abs, or Bindarit plus IL-6 Abs in Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 4 for each group). Data are representative of at least two independent experiments with similar results (A–P). All data are shown as mean ± SD and were analyzed by two-tailed, unpaired Student’s t test (A, C, D, E, K, L, and O) or one-way ANOVA with Tukey’s multiple comparison test (B and J) or two-way ANOVA with Sidak’s multiple comparison test (F–I, M, and N). ****P < 0.0001; ***P < 0.001; **P < 0.01; *P < 0.05; P > 0.05 not significant (ns).

Journal: The Journal of Experimental Medicine

Article Title: Tet2 deficiency–induced expansion of monocyte-derived macrophages promotes liver fibrosis

doi: 10.1084/jem.20251114

Figure Lengend Snippet: Effect of Tet2 deficiency on Ccl2 and Ccl8 mRNA stability and IL-6 neutralization on liver fibrosis progression. (A) The frequency of Ccr2 + and Ccr3 + pMDMs in Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 4 for each group). (B) Expression of Ccr2 and Ccr3 on monocytes, Tet2 +/+ pMDMs, and Tet2 −/− pMDMs ( n = 4 for each group). (C) The infiltration difference of other Ccr2 or Ccr3 expressing cell types in Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 4 for each group). (D) GAPDH mRNA decay curve in Tet2 +/+ pMDMs and Tet2 −/− pMDMs ( n = 6 for each group). (E) Transcriptional level of Elavl1, Znf36, and Ybx1 in Tet2 +/+ pMDMs and Tet2 −/− pMDMs ( n = 4 for each group). (F–I) Serum levels of (F) IL-1α, (G) IL-2, (H) TNFα, and (I) IL-1β in livers of Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 5 for each group). (J) Serum IL-6 levels in scramble, WT-MT, and KO-MT mice ( n = 4 for each group). (K) Il-6 levels in CD45.2 + pMDMs isolated from livers of WT-MT and KO-MT mice ( n = 4). (L) mRNA levels of Acta2 and Col1a1 in Tet2 +/+ and Tet2 −/− HSCs ( n = 4 for each group). (M and N) Effect of anti–IL-6 Abs treatment on mRNA levels of Col1a1 (M) and Acta2 (N) in Tet2 +/+ and Tet2 −/− HSCs co-cultured with Tet2 +/+ or Tet2 −/− MDMs detected by RT-PCR in vitro ( n = 3 for each group). (O) Effect on recombinant Ccl2 and Ccl8 on Il-6 expression in Tet2 +/+ pMDMs and Tet2 −/− pMDMs ( n = 3 for each group). (P) Detection of MDMs in livers by flow cytometry after Bindarit or IL-6 Abs treatment for 2 wk ( n = 5 for each group). (Q) H&E staining of liver tissues treated with PBS, Bindarit, IL-6 Abs, or Bindarit plus IL-6 Abs in Tet2 WT -CCl 4 and Tet2 ΔMye -CCl 4 mice ( n = 4 for each group). Data are representative of at least two independent experiments with similar results (A–P). All data are shown as mean ± SD and were analyzed by two-tailed, unpaired Student’s t test (A, C, D, E, K, L, and O) or one-way ANOVA with Tukey’s multiple comparison test (B and J) or two-way ANOVA with Sidak’s multiple comparison test (F–I, M, and N). ****P < 0.0001; ***P < 0.001; **P < 0.01; *P < 0.05; P > 0.05 not significant (ns).

Article Snippet: ELISA was used to detect the levels of Col IV (#20024; Ruixin Biotechnology), HA (#20067; Ruixin Biotechnology), Ccl8 (#RX27820; Ruixin Biotechnology), Ccl2 (MG9180; Fantia), TNFα (#KE10002; Proteintech), IL-2 (#BGM4904; Bangjing), IL-1α (KE10098; Proteintech), IL-1β (KE10003; Proteintech), and IL-6 (#KE10091; Proteintech) in serum and liver tissue grinding fluid.

Techniques: Neutralization, Expressing, Isolation, Cell Culture, Reverse Transcription Polymerase Chain Reaction, In Vitro, Recombinant, Flow Cytometry, Staining, Two Tailed Test, Comparison

NSC Sox2 transplantation decreases the expression of proinflammatory factors and increases the expression of anti-inflammatory factors and neurotrophic factors in hippocampus. (A, B) ELISA results of TNF-α (A) and IL-1β (B) in hippocampus. (C) Typical western blot bands of TNF-α, IL-6, IL-10, BDNF, and NGF. (D) Statistical analysis of proteins. All data are presented as the mean ± SD ( n = 5). ** P < 0.01, *** P < 0.001, vs . Sham group (one-way analysis of variance followed by post hoc Tukey’s honestly significant difference test). BDNF: Brain-derived growth factor; ELISA: enzyme-linked immunosorbent assay; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IL: interleukin; IVH: intraventricular hemorrhage; NGF: nerve growth factor; NSC: neural stem cell; PBS: phosphate-buffered saline; SD: standard deviation; Sox2: sex-determining region Y-box 2; TNF-α: tumor necrosis factor-alpha.

Journal: Neural Regeneration Research

Article Title: Sox2-overexpressing neural stem cells alleviate ventricular enlargement and neurological dysfunction in posthemorrhagic hydrocephalus

doi: 10.4103/NRR.NRR-D-24-01491

Figure Lengend Snippet: NSC Sox2 transplantation decreases the expression of proinflammatory factors and increases the expression of anti-inflammatory factors and neurotrophic factors in hippocampus. (A, B) ELISA results of TNF-α (A) and IL-1β (B) in hippocampus. (C) Typical western blot bands of TNF-α, IL-6, IL-10, BDNF, and NGF. (D) Statistical analysis of proteins. All data are presented as the mean ± SD ( n = 5). ** P < 0.01, *** P < 0.001, vs . Sham group (one-way analysis of variance followed by post hoc Tukey’s honestly significant difference test). BDNF: Brain-derived growth factor; ELISA: enzyme-linked immunosorbent assay; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IL: interleukin; IVH: intraventricular hemorrhage; NGF: nerve growth factor; NSC: neural stem cell; PBS: phosphate-buffered saline; SD: standard deviation; Sox2: sex-determining region Y-box 2; TNF-α: tumor necrosis factor-alpha.

Article Snippet: The supernatant was collected for the assay using enzyme-linked immunosorbent assay (ELISA) kits (EK0527, EK0394, Boster Bio, Anaheim, CA, USA).

Techniques: Transplantation Assay, Expressing, Enzyme-linked Immunosorbent Assay, Western Blot, Derivative Assay, Saline, Standard Deviation

Effects of si-PVT1 transfection on CoCl 2 –induced angiogenesis and inflammatory levels in HUVECs. A. Changes in vascular endothelial growth factor (VEGF) expression in HUVECs following CoCl 2 induction and si-PVT1 transfection. B. Effects of CoCl 2 induction and LncRNA PVT1 inhibition on fibroblast growth factor-2 (FGF-2) expression in HUVECs. Effects of different transfection treatments on inflammatory cytokine expression: TNF-α (C) and IL-6 (D) . * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

Journal: Annals of Hematology

Article Title: LncRNA PVT1 targets miR-143-3p to modulate endothelial cell function and thereby participate in deep vein thrombosis (DVT) of the lower limbs

doi: 10.1007/s00277-026-06833-4

Figure Lengend Snippet: Effects of si-PVT1 transfection on CoCl 2 –induced angiogenesis and inflammatory levels in HUVECs. A. Changes in vascular endothelial growth factor (VEGF) expression in HUVECs following CoCl 2 induction and si-PVT1 transfection. B. Effects of CoCl 2 induction and LncRNA PVT1 inhibition on fibroblast growth factor-2 (FGF-2) expression in HUVECs. Effects of different transfection treatments on inflammatory cytokine expression: TNF-α (C) and IL-6 (D) . * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

Article Snippet: We used the following kits to assess the effects of different transfection treatments on endothelial cell angiogenesis and inflammatory levels: the Human VEGF ELISA Kit (97053ES, YENSEN, Shanghai), Human Fibroblast Growth Factor 2 (FGF2) ELISA Detection Kit (JL14546, JONLNBIO, Shanghai), Human TNF-α ELISA Kit (EK182, MULTI SCIENCES, Shanghai), and Human IL-6 ELISA Kit (EK106, MULTI SCIENCES, Shanghai).

Techniques: Transfection, Expressing, Inhibition

Effects of miR-143-3p inhibitor on HUVEC function and inflammatory levels. Expression of LncRNA PVT1 (A) and miR-143-3p (B) in HUVECs following miR inhibitor transfection. C. Effect of miR inhibitor on viability of damaged HUVECs. D. Apoptotic changes in damaged HUVECs after miR inhibitor transfection. E. Effect of miR inhibitor on apoptosis-related gene expression in damaged HUVECs. F. Changes in VEGF and FG-2 expression in damaged HUVECs following miR inhibitor transfection. G. Effect of miR inhibitor on expression of inflammatory cytokines TNF-α and IL-6 in damaged HUVECs. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

Journal: Annals of Hematology

Article Title: LncRNA PVT1 targets miR-143-3p to modulate endothelial cell function and thereby participate in deep vein thrombosis (DVT) of the lower limbs

doi: 10.1007/s00277-026-06833-4

Figure Lengend Snippet: Effects of miR-143-3p inhibitor on HUVEC function and inflammatory levels. Expression of LncRNA PVT1 (A) and miR-143-3p (B) in HUVECs following miR inhibitor transfection. C. Effect of miR inhibitor on viability of damaged HUVECs. D. Apoptotic changes in damaged HUVECs after miR inhibitor transfection. E. Effect of miR inhibitor on apoptosis-related gene expression in damaged HUVECs. F. Changes in VEGF and FG-2 expression in damaged HUVECs following miR inhibitor transfection. G. Effect of miR inhibitor on expression of inflammatory cytokines TNF-α and IL-6 in damaged HUVECs. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

Article Snippet: We used the following kits to assess the effects of different transfection treatments on endothelial cell angiogenesis and inflammatory levels: the Human VEGF ELISA Kit (97053ES, YENSEN, Shanghai), Human Fibroblast Growth Factor 2 (FGF2) ELISA Detection Kit (JL14546, JONLNBIO, Shanghai), Human TNF-α ELISA Kit (EK182, MULTI SCIENCES, Shanghai), and Human IL-6 ELISA Kit (EK106, MULTI SCIENCES, Shanghai).

Techniques: Expressing, Transfection, Gene Expression