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(A) Concentration of growth factors (VEGF-A, PDGF-AA, GM-CSF, and M-CSF) produced by primary blood-derived MAIT cells following activation with anti-CD3/anti-CD28 and IL-12/IL-18 for 72 hours, compared with unstimulated controls. (B) Concentration of VEGF-A and GM-CSF in the supernatants of activated MAIT cells or conventional CD8⁺ and CD4⁺ T cell subsets. Conventional T cells were classified as naïve (CCR7⁺ CD45RA⁺), central memory (CCR7⁺ CD45RA⁻), effector memory (CCR7⁻ CD45RA⁻), or terminally differentiated effector memory (CCR7⁻ CD45RA⁺). (C) Concentration of VEGF-A <t>and</t> <t>VEGF-B</t> from a MAIT cell line stimulated with PHA and IL-2 for 24, 48, and 72 hours, and 6 days. (D-E) Peripheral blood mononuclear cells (PBMCs) were left unstimulated or stimulated for 72 hours with IL-12 (50 ng/mL) and IL-18 (50 ng/mL), 5-OP-RU (10 nM), or a combination of both stimuli. Intracellular flow cytometry staining was then performed to assess vimentin expression in MAIT cells identified as live CD3+ CD161+ Va7.2+ cells. (F-G) Vimentin expression in primary MAIT cells isolated from PBMCs and in a MAIT cell line was assessed by Western blot and quantified using ImageJ. Cells were left unstimulated or stimulated with anti-CD3/anti-CD28 and IL-12/IL-18 for 72 hours.
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(A) Concentration of growth factors (VEGF-A, PDGF-AA, GM-CSF, and M-CSF) produced by primary blood-derived MAIT cells following activation with anti-CD3/anti-CD28 and IL-12/IL-18 for 72 hours, compared with unstimulated controls. (B) Concentration of VEGF-A and GM-CSF in the supernatants of activated MAIT cells or conventional CD8⁺ and CD4⁺ T cell subsets. Conventional T cells were classified as naïve (CCR7⁺ CD45RA⁺), central memory (CCR7⁺ CD45RA⁻), effector memory (CCR7⁻ CD45RA⁻), or terminally differentiated effector memory (CCR7⁻ CD45RA⁺). (C) Concentration of VEGF-A <t>and</t> <t>VEGF-B</t> from a MAIT cell line stimulated with PHA and IL-2 for 24, 48, and 72 hours, and 6 days. (D-E) Peripheral blood mononuclear cells (PBMCs) were left unstimulated or stimulated for 72 hours with IL-12 (50 ng/mL) and IL-18 (50 ng/mL), 5-OP-RU (10 nM), or a combination of both stimuli. Intracellular flow cytometry staining was then performed to assess vimentin expression in MAIT cells identified as live CD3+ CD161+ Va7.2+ cells. (F-G) Vimentin expression in primary MAIT cells isolated from PBMCs and in a MAIT cell line was assessed by Western blot and quantified using ImageJ. Cells were left unstimulated or stimulated with anti-CD3/anti-CD28 and IL-12/IL-18 for 72 hours.
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VEGF-C <t>152s</t> treatment prior to ovariectomy limited the negative effects of subsequent E2 supplementation on lymphatic function and plaque burden in ldlr −/− mice. (A) Experimental design. 7 weeks old Ldlr −/− female mice received IP injections of VEGF-C 152s (e.g., VEGF-C) or vehicle. At 11 weeks, mice underwent either bilateral ovariectomy (OVX) or sham surgery, and switched on a high-fat diet (HFD). Estrogen (E2) supplementation began one week later. Lymphatic function was assessed in mice immediately prior to sacrifice at 20.5 weeks, after which organs were harvested. Green, orange and pink dashed lines represent VEGF-C 152s injections, HFD, and E2 implant durations, respectively. (B) Total body weight at the time of sacrifice and (C) over 21 weeks were reported. (D) Weight of visceral adipose tissue and (E) weight of the uterus, each expressed as percentage of total body weight. (F) Plasma total cholesterol and, (G) lipoprotein profile were assessed. (H) Contraction frequency of the popliteal collecting lymphatic vessels was measured by intravital microscopy. (I) Representative images of en face oil-red-O staining of the aorta and quantification of atherosclerotic plaque burden, expressed as percentage of total aortic area. Data points represent individual animals. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. HFD, high-fat diet; OVX, ovariectomy; VEGF-C, vascular endothelial growth factor C; CM, chylomicron; VLDL, very-low density lipoprotein; LDL, low-density lipoprotein; HDL, high-density lipoprotein.
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VEGF-C <t>152s</t> treatment prior to ovariectomy limited the negative effects of subsequent E2 supplementation on lymphatic function and plaque burden in ldlr −/− mice. (A) Experimental design. 7 weeks old Ldlr −/− female mice received IP injections of VEGF-C 152s (e.g., VEGF-C) or vehicle. At 11 weeks, mice underwent either bilateral ovariectomy (OVX) or sham surgery, and switched on a high-fat diet (HFD). Estrogen (E2) supplementation began one week later. Lymphatic function was assessed in mice immediately prior to sacrifice at 20.5 weeks, after which organs were harvested. Green, orange and pink dashed lines represent VEGF-C 152s injections, HFD, and E2 implant durations, respectively. (B) Total body weight at the time of sacrifice and (C) over 21 weeks were reported. (D) Weight of visceral adipose tissue and (E) weight of the uterus, each expressed as percentage of total body weight. (F) Plasma total cholesterol and, (G) lipoprotein profile were assessed. (H) Contraction frequency of the popliteal collecting lymphatic vessels was measured by intravital microscopy. (I) Representative images of en face oil-red-O staining of the aorta and quantification of atherosclerotic plaque burden, expressed as percentage of total aortic area. Data points represent individual animals. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. HFD, high-fat diet; OVX, ovariectomy; VEGF-C, vascular endothelial growth factor C; CM, chylomicron; VLDL, very-low density lipoprotein; LDL, low-density lipoprotein; HDL, high-density lipoprotein.
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VEGF-C <t>152s</t> treatment prior to ovariectomy limited the negative effects of subsequent E2 supplementation on lymphatic function and plaque burden in ldlr −/− mice. (A) Experimental design. 7 weeks old Ldlr −/− female mice received IP injections of VEGF-C 152s (e.g., VEGF-C) or vehicle. At 11 weeks, mice underwent either bilateral ovariectomy (OVX) or sham surgery, and switched on a high-fat diet (HFD). Estrogen (E2) supplementation began one week later. Lymphatic function was assessed in mice immediately prior to sacrifice at 20.5 weeks, after which organs were harvested. Green, orange and pink dashed lines represent VEGF-C 152s injections, HFD, and E2 implant durations, respectively. (B) Total body weight at the time of sacrifice and (C) over 21 weeks were reported. (D) Weight of visceral adipose tissue and (E) weight of the uterus, each expressed as percentage of total body weight. (F) Plasma total cholesterol and, (G) lipoprotein profile were assessed. (H) Contraction frequency of the popliteal collecting lymphatic vessels was measured by intravital microscopy. (I) Representative images of en face oil-red-O staining of the aorta and quantification of atherosclerotic plaque burden, expressed as percentage of total aortic area. Data points represent individual animals. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. HFD, high-fat diet; OVX, ovariectomy; VEGF-C, vascular endothelial growth factor C; CM, chylomicron; VLDL, very-low density lipoprotein; LDL, low-density lipoprotein; HDL, high-density lipoprotein.
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VEGF-C <t>152s</t> treatment prior to ovariectomy limited the negative effects of subsequent E2 supplementation on lymphatic function and plaque burden in ldlr −/− mice. (A) Experimental design. 7 weeks old Ldlr −/− female mice received IP injections of VEGF-C 152s (e.g., VEGF-C) or vehicle. At 11 weeks, mice underwent either bilateral ovariectomy (OVX) or sham surgery, and switched on a high-fat diet (HFD). Estrogen (E2) supplementation began one week later. Lymphatic function was assessed in mice immediately prior to sacrifice at 20.5 weeks, after which organs were harvested. Green, orange and pink dashed lines represent VEGF-C 152s injections, HFD, and E2 implant durations, respectively. (B) Total body weight at the time of sacrifice and (C) over 21 weeks were reported. (D) Weight of visceral adipose tissue and (E) weight of the uterus, each expressed as percentage of total body weight. (F) Plasma total cholesterol and, (G) lipoprotein profile were assessed. (H) Contraction frequency of the popliteal collecting lymphatic vessels was measured by intravital microscopy. (I) Representative images of en face oil-red-O staining of the aorta and quantification of atherosclerotic plaque burden, expressed as percentage of total aortic area. Data points represent individual animals. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. HFD, high-fat diet; OVX, ovariectomy; VEGF-C, vascular endothelial growth factor C; CM, chylomicron; VLDL, very-low density lipoprotein; LDL, low-density lipoprotein; HDL, high-density lipoprotein.
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VEGF-C <t>152s</t> treatment prior to ovariectomy limited the negative effects of subsequent E2 supplementation on lymphatic function and plaque burden in ldlr −/− mice. (A) Experimental design. 7 weeks old Ldlr −/− female mice received IP injections of VEGF-C 152s (e.g., VEGF-C) or vehicle. At 11 weeks, mice underwent either bilateral ovariectomy (OVX) or sham surgery, and switched on a high-fat diet (HFD). Estrogen (E2) supplementation began one week later. Lymphatic function was assessed in mice immediately prior to sacrifice at 20.5 weeks, after which organs were harvested. Green, orange and pink dashed lines represent VEGF-C 152s injections, HFD, and E2 implant durations, respectively. (B) Total body weight at the time of sacrifice and (C) over 21 weeks were reported. (D) Weight of visceral adipose tissue and (E) weight of the uterus, each expressed as percentage of total body weight. (F) Plasma total cholesterol and, (G) lipoprotein profile were assessed. (H) Contraction frequency of the popliteal collecting lymphatic vessels was measured by intravital microscopy. (I) Representative images of en face oil-red-O staining of the aorta and quantification of atherosclerotic plaque burden, expressed as percentage of total aortic area. Data points represent individual animals. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. HFD, high-fat diet; OVX, ovariectomy; VEGF-C, vascular endothelial growth factor C; CM, chylomicron; VLDL, very-low density lipoprotein; LDL, low-density lipoprotein; HDL, high-density lipoprotein.
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Image Search Results


(A) Concentration of growth factors (VEGF-A, PDGF-AA, GM-CSF, and M-CSF) produced by primary blood-derived MAIT cells following activation with anti-CD3/anti-CD28 and IL-12/IL-18 for 72 hours, compared with unstimulated controls. (B) Concentration of VEGF-A and GM-CSF in the supernatants of activated MAIT cells or conventional CD8⁺ and CD4⁺ T cell subsets. Conventional T cells were classified as naïve (CCR7⁺ CD45RA⁺), central memory (CCR7⁺ CD45RA⁻), effector memory (CCR7⁻ CD45RA⁻), or terminally differentiated effector memory (CCR7⁻ CD45RA⁺). (C) Concentration of VEGF-A and VEGF-B from a MAIT cell line stimulated with PHA and IL-2 for 24, 48, and 72 hours, and 6 days. (D-E) Peripheral blood mononuclear cells (PBMCs) were left unstimulated or stimulated for 72 hours with IL-12 (50 ng/mL) and IL-18 (50 ng/mL), 5-OP-RU (10 nM), or a combination of both stimuli. Intracellular flow cytometry staining was then performed to assess vimentin expression in MAIT cells identified as live CD3+ CD161+ Va7.2+ cells. (F-G) Vimentin expression in primary MAIT cells isolated from PBMCs and in a MAIT cell line was assessed by Western blot and quantified using ImageJ. Cells were left unstimulated or stimulated with anti-CD3/anti-CD28 and IL-12/IL-18 for 72 hours.

Journal: bioRxiv

Article Title: MAIT cells derived ligands signal via VEGFR2 to promote tissue repair and liver regeneration

doi: 10.64898/2026.03.23.713159

Figure Lengend Snippet: (A) Concentration of growth factors (VEGF-A, PDGF-AA, GM-CSF, and M-CSF) produced by primary blood-derived MAIT cells following activation with anti-CD3/anti-CD28 and IL-12/IL-18 for 72 hours, compared with unstimulated controls. (B) Concentration of VEGF-A and GM-CSF in the supernatants of activated MAIT cells or conventional CD8⁺ and CD4⁺ T cell subsets. Conventional T cells were classified as naïve (CCR7⁺ CD45RA⁺), central memory (CCR7⁺ CD45RA⁻), effector memory (CCR7⁻ CD45RA⁻), or terminally differentiated effector memory (CCR7⁻ CD45RA⁺). (C) Concentration of VEGF-A and VEGF-B from a MAIT cell line stimulated with PHA and IL-2 for 24, 48, and 72 hours, and 6 days. (D-E) Peripheral blood mononuclear cells (PBMCs) were left unstimulated or stimulated for 72 hours with IL-12 (50 ng/mL) and IL-18 (50 ng/mL), 5-OP-RU (10 nM), or a combination of both stimuli. Intracellular flow cytometry staining was then performed to assess vimentin expression in MAIT cells identified as live CD3+ CD161+ Va7.2+ cells. (F-G) Vimentin expression in primary MAIT cells isolated from PBMCs and in a MAIT cell line was assessed by Western blot and quantified using ImageJ. Cells were left unstimulated or stimulated with anti-CD3/anti-CD28 and IL-12/IL-18 for 72 hours.

Article Snippet: Supernatants were analysed for growth factor expression using a LEGENDplexTM Human Growth Factor Panel (BioLegend) and Human VEGF-A and VEGF-B ELISA kits (LSBio), following the manufacturers’ instructions.

Techniques: Concentration Assay, Produced, Derivative Assay, Activation Assay, Flow Cytometry, Staining, Expressing, Isolation, Western Blot

VEGF-C 152s treatment prior to ovariectomy limited the negative effects of subsequent E2 supplementation on lymphatic function and plaque burden in ldlr −/− mice. (A) Experimental design. 7 weeks old Ldlr −/− female mice received IP injections of VEGF-C 152s (e.g., VEGF-C) or vehicle. At 11 weeks, mice underwent either bilateral ovariectomy (OVX) or sham surgery, and switched on a high-fat diet (HFD). Estrogen (E2) supplementation began one week later. Lymphatic function was assessed in mice immediately prior to sacrifice at 20.5 weeks, after which organs were harvested. Green, orange and pink dashed lines represent VEGF-C 152s injections, HFD, and E2 implant durations, respectively. (B) Total body weight at the time of sacrifice and (C) over 21 weeks were reported. (D) Weight of visceral adipose tissue and (E) weight of the uterus, each expressed as percentage of total body weight. (F) Plasma total cholesterol and, (G) lipoprotein profile were assessed. (H) Contraction frequency of the popliteal collecting lymphatic vessels was measured by intravital microscopy. (I) Representative images of en face oil-red-O staining of the aorta and quantification of atherosclerotic plaque burden, expressed as percentage of total aortic area. Data points represent individual animals. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. HFD, high-fat diet; OVX, ovariectomy; VEGF-C, vascular endothelial growth factor C; CM, chylomicron; VLDL, very-low density lipoprotein; LDL, low-density lipoprotein; HDL, high-density lipoprotein.

Journal: Frontiers in Cardiovascular Medicine

Article Title: Sex-specific lymphatic responses to estrogen shape atherosclerosis in high-risk mice

doi: 10.3389/fcvm.2026.1699372

Figure Lengend Snippet: VEGF-C 152s treatment prior to ovariectomy limited the negative effects of subsequent E2 supplementation on lymphatic function and plaque burden in ldlr −/− mice. (A) Experimental design. 7 weeks old Ldlr −/− female mice received IP injections of VEGF-C 152s (e.g., VEGF-C) or vehicle. At 11 weeks, mice underwent either bilateral ovariectomy (OVX) or sham surgery, and switched on a high-fat diet (HFD). Estrogen (E2) supplementation began one week later. Lymphatic function was assessed in mice immediately prior to sacrifice at 20.5 weeks, after which organs were harvested. Green, orange and pink dashed lines represent VEGF-C 152s injections, HFD, and E2 implant durations, respectively. (B) Total body weight at the time of sacrifice and (C) over 21 weeks were reported. (D) Weight of visceral adipose tissue and (E) weight of the uterus, each expressed as percentage of total body weight. (F) Plasma total cholesterol and, (G) lipoprotein profile were assessed. (H) Contraction frequency of the popliteal collecting lymphatic vessels was measured by intravital microscopy. (I) Representative images of en face oil-red-O staining of the aorta and quantification of atherosclerotic plaque burden, expressed as percentage of total aortic area. Data points represent individual animals. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. HFD, high-fat diet; OVX, ovariectomy; VEGF-C, vascular endothelial growth factor C; CM, chylomicron; VLDL, very-low density lipoprotein; LDL, low-density lipoprotein; HDL, high-density lipoprotein.

Article Snippet: Mice received intraperitoneal (IP) injections of VEGF-C (152s) at a dose of 50 ng per 25 g of body weight [purified recombinant rat VEGF-C protein (152s), Fitzgerald, catalog no. 30R-AV006-22] or vehicle control (phosphate-buffered saline, PBS), administered three times per week for four consecutive weeks.

Techniques: Clinical Proteomics, Intravital Microscopy, Staining