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Cusabio mouse hmgb2 elisa kit

Figure 2. <t>Hmgb2</t> deletion attenuates neointimal hyperplasia in injured femoral arteries of mice, whereas perivascular high-mobility group box (HMGB) 2 administration aggravates this pathology. A, Representative images of H&E staining of sham and wire-injured femoral artery sections from C57Bl/6 and Hmgb2–/– mice. Quantification of neointimal growth index (B) and intima-to-media (I/M) ratio (C) was performed in sham or injured arteries of C57Bl/6 and Hmgb2–/– mice. *P<0.05 vs injured arteries of C57Bl/6 mice; n=12. D, Immuno- fluorescent staining of α-smooth muscle actin (α-SMA) was performed in sections of injured arteries from C57Bl/6 and Hmgb2–/– mice. *P<0.05 vs injured arteries of C57Bl/6 mice; n=7. E, Expression of Col1a1, MMP2, and MMP9 in sham and injured arteries of C57Bl/6 and Hmgb2–/– mice. Data are quantified in Figure VI in the online-only Data Supplement. F, The mRNA levels of Col1a1, Col3a1, MMP2, and MMP9 in sham and injured arteries of C57Bl/6 and Hmgb2–/– mice as determined by reverse transcriptase polymerase chain reaction (RT- PCR). *P<0.05 vs injured arteries of C57Bl/6 mice; #P<0.05 vs sham arteries of C57Bl/6 or Hmgb2–/– mice; n=4. G, Representative images of H&E staining of sections of wire-injured arteries of PBS- or HMGB2-treated mice. H and I, Quantification of neointimal growth index (H) and intima-to-media (I/M) ratio (I) of wire-injured arteries of PBS- or HMGB2-treated mice. *P<0.05 vs PBS-treated group; n=10. J, Rep- resentative images of immunofluorescent staining for α-SMA performed in wire-injured arteries of PBS- or HMGB2-administrated mice (left). Staining was also quantified (right). *P<0.05 vs PBS-treated group; n=6 to 7. Masson’s trichrome staining of injury-induced femoral artery from C57Bl/6 and Hmgb2–/– mice (K) and PBS- or HMGB2-treated mice (L). Scale bar: 50 μm.

Mouse Hmgb2 Elisa Kit, supplied by Cusabio, used in various techniques. Bioz Stars score: 93/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Association of Serum HMGB2 Levels With In-Stent Restenosis: HMGB2 Promotes Neointimal Hyperplasia in Mice With Femoral Artery Injury and Proliferation and Migration of VSMCs."

Article Title: Association of Serum HMGB2 Levels With In-Stent Restenosis: HMGB2 Promotes Neointimal Hyperplasia in Mice With Femoral Artery Injury and Proliferation and Migration of VSMCs.

Journal: Arteriosclerosis, thrombosis, and vascular biology

doi: 10.1161/ATVBAHA.116.308210

Figure 2. Hmgb2 deletion attenuates neointimal hyperplasia in injured femoral arteries of mice, whereas perivascular high-mobility group box (HMGB) 2 administration aggravates this pathology. A, Representative images of H&E staining of sham and wire-injured femoral artery sections from C57Bl/6 and Hmgb2–/– mice. Quantification of neointimal growth index (B) and intima-to-media (I/M) ratio (C) was performed in sham or injured arteries of C57Bl/6 and Hmgb2–/– mice. *P<0.05 vs injured arteries of C57Bl/6 mice; n=12. D, Immuno- fluorescent staining of α-smooth muscle actin (α-SMA) was performed in sections of injured arteries from C57Bl/6 and Hmgb2–/– mice. *P<0.05 vs injured arteries of C57Bl/6 mice; n=7. E, Expression of Col1a1, MMP2, and MMP9 in sham and injured arteries of C57Bl/6 and Hmgb2–/– mice. Data are quantified in Figure VI in the online-only Data Supplement. F, The mRNA levels of Col1a1, Col3a1, MMP2, and MMP9 in sham and injured arteries of C57Bl/6 and Hmgb2–/– mice as determined by reverse transcriptase polymerase chain reaction (RT- PCR). *P<0.05 vs injured arteries of C57Bl/6 mice; #P<0.05 vs sham arteries of C57Bl/6 or Hmgb2–/– mice; n=4. G, Representative images of H&E staining of sections of wire-injured arteries of PBS- or HMGB2-treated mice. H and I, Quantification of neointimal growth index (H) and intima-to-media (I/M) ratio (I) of wire-injured arteries of PBS- or HMGB2-treated mice. *P<0.05 vs PBS-treated group; n=10. J, Rep- resentative images of immunofluorescent staining for α-SMA performed in wire-injured arteries of PBS- or HMGB2-administrated mice (left). Staining was also quantified (right). *P<0.05 vs PBS-treated group; n=6 to 7. Masson’s trichrome staining of injury-induced femoral artery from C57Bl/6 and Hmgb2–/– mice (K) and PBS- or HMGB2-treated mice (L). Scale bar: 50 μm.

Figure Legend Snippet: Figure 2. Hmgb2 deletion attenuates neointimal hyperplasia in injured femoral arteries of mice, whereas perivascular high-mobility group box (HMGB) 2 administration aggravates this pathology. A, Representative images of H&E staining of sham and wire-injured femoral artery sections from C57Bl/6 and Hmgb2–/– mice. Quantification of neointimal growth index (B) and intima-to-media (I/M) ratio (C) was performed in sham or injured arteries of C57Bl/6 and Hmgb2–/– mice. *P<0.05 vs injured arteries of C57Bl/6 mice; n=12. D, Immuno- fluorescent staining of α-smooth muscle actin (α-SMA) was performed in sections of injured arteries from C57Bl/6 and Hmgb2–/– mice. *P<0.05 vs injured arteries of C57Bl/6 mice; n=7. E, Expression of Col1a1, MMP2, and MMP9 in sham and injured arteries of C57Bl/6 and Hmgb2–/– mice. Data are quantified in Figure VI in the online-only Data Supplement. F, The mRNA levels of Col1a1, Col3a1, MMP2, and MMP9 in sham and injured arteries of C57Bl/6 and Hmgb2–/– mice as determined by reverse transcriptase polymerase chain reaction (RT- PCR). *P<0.05 vs injured arteries of C57Bl/6 mice; #P<0.05 vs sham arteries of C57Bl/6 or Hmgb2–/– mice; n=4. G, Representative images of H&E staining of sections of wire-injured arteries of PBS- or HMGB2-treated mice. H and I, Quantification of neointimal growth index (H) and intima-to-media (I/M) ratio (I) of wire-injured arteries of PBS- or HMGB2-treated mice. *P<0.05 vs PBS-treated group; n=10. J, Rep- resentative images of immunofluorescent staining for α-SMA performed in wire-injured arteries of PBS- or HMGB2-administrated mice (left). Staining was also quantified (right). *P<0.05 vs PBS-treated group; n=6 to 7. Masson’s trichrome staining of injury-induced femoral artery from C57Bl/6 and Hmgb2–/– mice (K) and PBS- or HMGB2-treated mice (L). Scale bar: 50 μm.

Techniques Used: Staining, Expressing, Reverse Transcription, Polymerase Chain Reaction, Reverse Transcription Polymerase Chain Reaction

Figure 4. Reactive oxygen species (ROS) mediates high-mobility group box (HMGB) 2–promoted neointimal hyperplasia in mice. A, Rep- resentative images of dihydroethidium (DHE) staining in femoral arteries of C57Bl/6 or Hmgb2–/– mice with femoral artery wire injury or sham. B, Quantitative analysis of the DHE fluorescence intensity in arteries. #P<0.05 vs sham; *P<0.05 vs injured artery of C57Bl/6 mice; n=6. C, PF-127 gel containing PBS or HMGB2 was delivered around the femoral artery. Apocynin (APO) or vehicle was given in drinking water at a concentration of 1.5 mmol/L for 4 weeks. The sections of wire-injured arteries were stained with H&E, representative images are shown. Quantification of neointimal growth index (D) and intima-to-media (I/M) ratio (E). *P<0.05 vs PBS administration; #P<0.05 vs HMGB2 administration; n=10 to 11. F, Representative images of dihydroethidium (DHE) staining in wire-injured femoral arteries of C57Bl/6 mice with perivascular administration of HMGB2 or PBS, in the presence or absence of APO. G,: Quantitative analysis of the DHE fluores- cent intensity in arteries. *P<0.05 vs sham; #P<0.05 vs injured artery of C57Bl/6 mice; n=5. Scale bar: 50 μm.

Figure Legend Snippet: Figure 4. Reactive oxygen species (ROS) mediates high-mobility group box (HMGB) 2–promoted neointimal hyperplasia in mice. A, Rep- resentative images of dihydroethidium (DHE) staining in femoral arteries of C57Bl/6 or Hmgb2–/– mice with femoral artery wire injury or sham. B, Quantitative analysis of the DHE fluorescence intensity in arteries. #P<0.05 vs sham; *P<0.05 vs injured artery of C57Bl/6 mice; n=6. C, PF-127 gel containing PBS or HMGB2 was delivered around the femoral artery. Apocynin (APO) or vehicle was given in drinking water at a concentration of 1.5 mmol/L for 4 weeks. The sections of wire-injured arteries were stained with H&E, representative images are shown. Quantification of neointimal growth index (D) and intima-to-media (I/M) ratio (E). *P<0.05 vs PBS administration; #P<0.05 vs HMGB2 administration; n=10 to 11. F, Representative images of dihydroethidium (DHE) staining in wire-injured femoral arteries of C57Bl/6 mice with perivascular administration of HMGB2 or PBS, in the presence or absence of APO. G,: Quantitative analysis of the DHE fluores- cent intensity in arteries. *P<0.05 vs sham; #P<0.05 vs injured artery of C57Bl/6 mice; n=5. Scale bar: 50 μm.

Techniques Used: Staining, Fluorescence, Concentration Assay

Figure 5. P47phox phosphorylation–dependent reactive oxygen species (ROS) activation mediates high-mobility group box (HMGB) 2–induced effects in vivo and in vitro. A, Western blot analysis of phospho–p47phox levels in injured femoral arteries of C57Bl/6 and Hmgb2–/– mice and in sham arteries. B, Quantification of phospho–p47phox levels in A. #P<0.05 vs sham; *P<0.05 vs injured arteries of C57Bl/6; n=3. C, Immunofluorescent staining of phospho–p47phox (red) and α-smooth muscle actin (α-SMA; green) in sections of sham or wire injury fem- oral artery in C57Bl/6 and Hmgb2–/– mice. Representative images are shown. D, Quantification of phospho–p47phox levels in femoral arter- ies of C. #P<0.05 vs sham; *P<0.05 vs injured artery of C57Bl/6; n=5. E, Human aortic smooth muscle cells (hASMCs) were stimulated with HMGB2 for various times (0, 15, 30, and 60 minutes). Phospho–p47phox and total p47phox levels were determined using Western blot analy- sis, with quantification as given in Figure XIF in the online-only Data Supplement. F, H, I, and K, In hASMCs transfected with scramble-small interfering RNA (siRNA) or p47phox-siRNA for 24 h and then stimulated by HMGB2 or PBS in experiments, ROS, proliferation assay, Boyden chamber assay, and Wound-healing assay were performed, and respectively, quantified in G, J, and L. *P<0.05 vs scramble-siRNA with PBS stimulation; #P<0.05 vs scramble-siRNA with HMGB2 stimulation; n=3 to 6. Scale bar: 50 μm. DCF indicates 2′,7′-dichlorodihydrofluorescein.

Figure Legend Snippet: Figure 5. P47phox phosphorylation–dependent reactive oxygen species (ROS) activation mediates high-mobility group box (HMGB) 2–induced effects in vivo and in vitro. A, Western blot analysis of phospho–p47phox levels in injured femoral arteries of C57Bl/6 and Hmgb2–/– mice and in sham arteries. B, Quantification of phospho–p47phox levels in A. #P<0.05 vs sham; *P<0.05 vs injured arteries of C57Bl/6; n=3. C, Immunofluorescent staining of phospho–p47phox (red) and α-smooth muscle actin (α-SMA; green) in sections of sham or wire injury fem- oral artery in C57Bl/6 and Hmgb2–/– mice. Representative images are shown. D, Quantification of phospho–p47phox levels in femoral arter- ies of C. #P<0.05 vs sham; *P<0.05 vs injured artery of C57Bl/6; n=5. E, Human aortic smooth muscle cells (hASMCs) were stimulated with HMGB2 for various times (0, 15, 30, and 60 minutes). Phospho–p47phox and total p47phox levels were determined using Western blot analy- sis, with quantification as given in Figure XIF in the online-only Data Supplement. F, H, I, and K, In hASMCs transfected with scramble-small interfering RNA (siRNA) or p47phox-siRNA for 24 h and then stimulated by HMGB2 or PBS in experiments, ROS, proliferation assay, Boyden chamber assay, and Wound-healing assay were performed, and respectively, quantified in G, J, and L. *P<0.05 vs scramble-siRNA with PBS stimulation; #P<0.05 vs scramble-siRNA with HMGB2 stimulation; n=3 to 6. Scale bar: 50 μm. DCF indicates 2′,7′-dichlorodihydrofluorescein.

Techniques Used: Phospho-proteomics, Activation Assay, In Vivo, In Vitro, Western Blot, Staining, Transfection, Small Interfering RNA, Proliferation Assay, Boyden Chamber Assay, Wound Healing Assay

Figure 6. High-mobility group box (HMGB) 2 promotes p47phox phosphorylation and migration and proliferation of vascular smooth muscle cells (VSMCs) via receptor of advanced glycation end products (RAGE) but not NOX4. A, Human aortic smooth muscle cells (HASMCs) were transfected with scramble-small interfering RNA (siRNA), Toll-like receptor (TLR) 2-siRNA, TLR4-siRNA, or RAGE-siRNA for 24 h, followed by stimulation with PBS or HMGB2. The levels of phospho–p47phox and p47phox were determined by Western blot analysis. Quantification can be found in Figure XIII in the online-only Data Supplement. B and C, VSMCs derived from Rage–/– and Tlr4–/– mice were treated with PBS or HMGB2. The levels of phospho–p47phox and p47phox were determined by Western blot analysis. Quanti- fication can be found in Figure XIII in the online-only Data Supplement. D, F, and H, VSMCs derived from C57Bl/6 and Rage–/– mice were treated with PBS or HMGB2 in experiments. Reactive oxygen species (ROS), Boyden chamber, and proliferation assay were performed, and respectively, quantified in E and G. *P<0.05 vs C57Bl/6 mouse-derived VSMCs; #P<0.05 vs C57Bl/6 mouse-derived VSMCs with HMGB2 stimulation; n=3 to 5. I, Immunofluorescence confocal microscopy showed increased expression of HMGB2 and RAGE and colo- calization of these 2 proteins in neointima after vascular injury. n=4. Scale bar: 50 μm.

Figure Legend Snippet: Figure 6. High-mobility group box (HMGB) 2 promotes p47phox phosphorylation and migration and proliferation of vascular smooth muscle cells (VSMCs) via receptor of advanced glycation end products (RAGE) but not NOX4. A, Human aortic smooth muscle cells (HASMCs) were transfected with scramble-small interfering RNA (siRNA), Toll-like receptor (TLR) 2-siRNA, TLR4-siRNA, or RAGE-siRNA for 24 h, followed by stimulation with PBS or HMGB2. The levels of phospho–p47phox and p47phox were determined by Western blot analysis. Quantification can be found in Figure XIII in the online-only Data Supplement. B and C, VSMCs derived from Rage–/– and Tlr4–/– mice were treated with PBS or HMGB2. The levels of phospho–p47phox and p47phox were determined by Western blot analysis. Quanti- fication can be found in Figure XIII in the online-only Data Supplement. D, F, and H, VSMCs derived from C57Bl/6 and Rage–/– mice were treated with PBS or HMGB2 in experiments. Reactive oxygen species (ROS), Boyden chamber, and proliferation assay were performed, and respectively, quantified in E and G. *P<0.05 vs C57Bl/6 mouse-derived VSMCs; #P<0.05 vs C57Bl/6 mouse-derived VSMCs with HMGB2 stimulation; n=3 to 5. I, Immunofluorescence confocal microscopy showed increased expression of HMGB2 and RAGE and colo- calization of these 2 proteins in neointima after vascular injury. n=4. Scale bar: 50 μm.

Techniques Used: Phospho-proteomics, Migration, Transfection, Small Interfering RNA, Western Blot, Derivative Assay, Proliferation Assay, Immunofluorescence, Confocal Microscopy, Expressing

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Journal: Arteriosclerosis, thrombosis, and vascular biology

Article Title: Association of Serum HMGB2 Levels With In-Stent Restenosis: HMGB2 Promotes Neointimal Hyperplasia in Mice With Femoral Artery Injury and Proliferation and Migration of VSMCs.

doi: 10.1161/ATVBAHA.116.308210

Figure Lengend Snippet: Figure 2. Hmgb2 deletion attenuates neointimal hyperplasia in injured femoral arteries of mice, whereas perivascular high-mobility group box (HMGB) 2 administration aggravates this pathology. A, Representative images of H&E staining of sham and wire-injured femoral artery sections from C57Bl/6 and Hmgb2–/– mice. Quantification of neointimal growth index (B) and intima-to-media (I/M) ratio (C) was performed in sham or injured arteries of C57Bl/6 and Hmgb2–/– mice. *P<0.05 vs injured arteries of C57Bl/6 mice; n=12. D, Immuno- fluorescent staining of α-smooth muscle actin (α-SMA) was performed in sections of injured arteries from C57Bl/6 and Hmgb2–/– mice. *P<0.05 vs injured arteries of C57Bl/6 mice; n=7. E, Expression of Col1a1, MMP2, and MMP9 in sham and injured arteries of C57Bl/6 and Hmgb2–/– mice. Data are quantified in Figure VI in the online-only Data Supplement. F, The mRNA levels of Col1a1, Col3a1, MMP2, and MMP9 in sham and injured arteries of C57Bl/6 and Hmgb2–/– mice as determined by reverse transcriptase polymerase chain reaction (RT- PCR). *P<0.05 vs injured arteries of C57Bl/6 mice; #P<0.05 vs sham arteries of C57Bl/6 or Hmgb2–/– mice; n=4. G, Representative images of H&E staining of sections of wire-injured arteries of PBS- or HMGB2-treated mice. H and I, Quantification of neointimal growth index (H) and intima-to-media (I/M) ratio (I) of wire-injured arteries of PBS- or HMGB2-treated mice. *P<0.05 vs PBS-treated group; n=10. J, Rep- resentative images of immunofluorescent staining for α-SMA performed in wire-injured arteries of PBS- or HMGB2-administrated mice (left). Staining was also quantified (right). *P<0.05 vs PBS-treated group; n=6 to 7. Masson’s trichrome staining of injury-induced femoral artery from C57Bl/6 and Hmgb2–/– mice (K) and PBS- or HMGB2-treated mice (L). Scale bar: 50 μm.

Article Snippet: The mice serum HMGB2 concentration was measured using a mouse HMGB2 ELISA kit (CSB-EL010560MO, CUSABIO Life Science) according to the manufacturer’s guidelines.

Techniques: Staining, Expressing, Reverse Transcription, Polymerase Chain Reaction, Reverse Transcription Polymerase Chain Reaction

Journal: Arteriosclerosis, thrombosis, and vascular biology

Article Title: Association of Serum HMGB2 Levels With In-Stent Restenosis: HMGB2 Promotes Neointimal Hyperplasia in Mice With Femoral Artery Injury and Proliferation and Migration of VSMCs.

doi: 10.1161/ATVBAHA.116.308210

Figure Lengend Snippet: Figure 4. Reactive oxygen species (ROS) mediates high-mobility group box (HMGB) 2–promoted neointimal hyperplasia in mice. A, Rep- resentative images of dihydroethidium (DHE) staining in femoral arteries of C57Bl/6 or Hmgb2–/– mice with femoral artery wire injury or sham. B, Quantitative analysis of the DHE fluorescence intensity in arteries. #P<0.05 vs sham; *P<0.05 vs injured artery of C57Bl/6 mice; n=6. C, PF-127 gel containing PBS or HMGB2 was delivered around the femoral artery. Apocynin (APO) or vehicle was given in drinking water at a concentration of 1.5 mmol/L for 4 weeks. The sections of wire-injured arteries were stained with H&E, representative images are shown. Quantification of neointimal growth index (D) and intima-to-media (I/M) ratio (E). *P<0.05 vs PBS administration; #P<0.05 vs HMGB2 administration; n=10 to 11. F, Representative images of dihydroethidium (DHE) staining in wire-injured femoral arteries of C57Bl/6 mice with perivascular administration of HMGB2 or PBS, in the presence or absence of APO. G,: Quantitative analysis of the DHE fluores- cent intensity in arteries. *P<0.05 vs sham; #P<0.05 vs injured artery of C57Bl/6 mice; n=5. Scale bar: 50 μm.

Article Snippet: The mice serum HMGB2 concentration was measured using a mouse HMGB2 ELISA kit (CSB-EL010560MO, CUSABIO Life Science) according to the manufacturer’s guidelines.

Techniques: Staining, Fluorescence, Concentration Assay

Journal: Arteriosclerosis, thrombosis, and vascular biology

Article Title: Association of Serum HMGB2 Levels With In-Stent Restenosis: HMGB2 Promotes Neointimal Hyperplasia in Mice With Femoral Artery Injury and Proliferation and Migration of VSMCs.

doi: 10.1161/ATVBAHA.116.308210

Figure Lengend Snippet: Figure 5. P47phox phosphorylation–dependent reactive oxygen species (ROS) activation mediates high-mobility group box (HMGB) 2–induced effects in vivo and in vitro. A, Western blot analysis of phospho–p47phox levels in injured femoral arteries of C57Bl/6 and Hmgb2–/– mice and in sham arteries. B, Quantification of phospho–p47phox levels in A. #P<0.05 vs sham; *P<0.05 vs injured arteries of C57Bl/6; n=3. C, Immunofluorescent staining of phospho–p47phox (red) and α-smooth muscle actin (α-SMA; green) in sections of sham or wire injury fem- oral artery in C57Bl/6 and Hmgb2–/– mice. Representative images are shown. D, Quantification of phospho–p47phox levels in femoral arter- ies of C. #P<0.05 vs sham; *P<0.05 vs injured artery of C57Bl/6; n=5. E, Human aortic smooth muscle cells (hASMCs) were stimulated with HMGB2 for various times (0, 15, 30, and 60 minutes). Phospho–p47phox and total p47phox levels were determined using Western blot analy- sis, with quantification as given in Figure XIF in the online-only Data Supplement. F, H, I, and K, In hASMCs transfected with scramble-small interfering RNA (siRNA) or p47phox-siRNA for 24 h and then stimulated by HMGB2 or PBS in experiments, ROS, proliferation assay, Boyden chamber assay, and Wound-healing assay were performed, and respectively, quantified in G, J, and L. *P<0.05 vs scramble-siRNA with PBS stimulation; #P<0.05 vs scramble-siRNA with HMGB2 stimulation; n=3 to 6. Scale bar: 50 μm. DCF indicates 2′,7′-dichlorodihydrofluorescein.

Article Snippet: The mice serum HMGB2 concentration was measured using a mouse HMGB2 ELISA kit (CSB-EL010560MO, CUSABIO Life Science) according to the manufacturer’s guidelines.

Techniques: Phospho-proteomics, Activation Assay, In Vivo, In Vitro, Western Blot, Staining, Transfection, Small Interfering RNA, Proliferation Assay, Boyden Chamber Assay, Wound Healing Assay

Journal: Arteriosclerosis, thrombosis, and vascular biology

Article Title: Association of Serum HMGB2 Levels With In-Stent Restenosis: HMGB2 Promotes Neointimal Hyperplasia in Mice With Femoral Artery Injury and Proliferation and Migration of VSMCs.

doi: 10.1161/ATVBAHA.116.308210

Figure Lengend Snippet: Figure 6. High-mobility group box (HMGB) 2 promotes p47phox phosphorylation and migration and proliferation of vascular smooth muscle cells (VSMCs) via receptor of advanced glycation end products (RAGE) but not NOX4. A, Human aortic smooth muscle cells (HASMCs) were transfected with scramble-small interfering RNA (siRNA), Toll-like receptor (TLR) 2-siRNA, TLR4-siRNA, or RAGE-siRNA for 24 h, followed by stimulation with PBS or HMGB2. The levels of phospho–p47phox and p47phox were determined by Western blot analysis. Quantification can be found in Figure XIII in the online-only Data Supplement. B and C, VSMCs derived from Rage–/– and Tlr4–/– mice were treated with PBS or HMGB2. The levels of phospho–p47phox and p47phox were determined by Western blot analysis. Quanti- fication can be found in Figure XIII in the online-only Data Supplement. D, F, and H, VSMCs derived from C57Bl/6 and Rage–/– mice were treated with PBS or HMGB2 in experiments. Reactive oxygen species (ROS), Boyden chamber, and proliferation assay were performed, and respectively, quantified in E and G. *P<0.05 vs C57Bl/6 mouse-derived VSMCs; #P<0.05 vs C57Bl/6 mouse-derived VSMCs with HMGB2 stimulation; n=3 to 5. I, Immunofluorescence confocal microscopy showed increased expression of HMGB2 and RAGE and colo- calization of these 2 proteins in neointima after vascular injury. n=4. Scale bar: 50 μm.

Article Snippet: The mice serum HMGB2 concentration was measured using a mouse HMGB2 ELISA kit (CSB-EL010560MO, CUSABIO Life Science) according to the manufacturer’s guidelines.

Techniques: Phospho-proteomics, Migration, Transfection, Small Interfering RNA, Western Blot, Derivative Assay, Proliferation Assay, Immunofluorescence, Confocal Microscopy, Expressing

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