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MedChemExpress ang ii at1 receptor candesartan
ULK1 expression is elevated in hypertrophic cardiac tissues and cardiomyocytes. (A) C57BL/6J mice at 8-weeks-old were subjected to sham or TAC surgery. Representative whole heart images (scale bar, 0.5 cm), M-mode echocardiography, H&E staining (scale bar, 100 µm) and WGA staining (scale bar, 50 µm) of heart tissue. Assessment of (B) HW/BW, (C) LVW/BW and (D) HW/TL (n=6). Statistical graphs for (E) LVEF (%), (F) FS (%), (G) IVS, d (mm) and (H) LVPW, d (mm) (n=6). (I) Cardiomyocyte cross-sectional area acquired from WGA staining. Cells were measured from different microscopic fields of 6 samples in each group. The mRNA levels of (J) BNP and (K) β-MHC in the hearts from sham or TAC-surgery mice (n=6). The mRNA levels of (L) BNP and (M) β-MHC in HL-1 cells treated with <t>Ang</t> <t>II</t> (n=3). (N) Stained cells and (O) quantification of cell surface area of HL-1 cells treated with Ang II. Scale bar, 50 µm (n=3). Western blot analysis and summarized data demonstrating (P) Beclin1 and (Q) VPS34 protein expression in HL-1 cells treated with Ang II (n=3). (R) Western blot analysis and summarized data demonstrating ULK1 protein levels in the hearts obtained after sham or TAC surgery (n=6). (S) Western blot analysis and summarized data demonstrating ULK1 protein levels in the cardiomyocytes stimulated with Ang II (n=6). All data are presented as mean ± SEM. *P < 0.05 and **P<0.01 vs. sham or control group. ULK1, serine/threonine protein kinase ULK1; TAC, transverse aortic constriction; HW, heart weight; BW, body weight; LVW, left ventricular weight; TL, tibia length; LVEF, left ventricular ejection fraction; FS, fractional shortening; d, diastole; IVS, interventricular septal thickness; LVPW, left ventricular posterior wall thickness; CSA, cross-sectional area; BNP , brain natriuretic peptide; β-MHC , β-myosin heavy chain; α-SMA, α smooth muscle actin; Ang II, angiotensin II; VPS34, PI3K catalytic subunit type 3; WGA, wheat germ agglutinin.
Ang Ii At1 Receptor Candesartan, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Thermo Fisher ang ii angiotensin ii ar adrenergic receptor at1r ang ii type 1 receptor cam calmodulin cryo em cryo electron microscopy dag
ULK1 expression is elevated in hypertrophic cardiac tissues and cardiomyocytes. (A) C57BL/6J mice at 8-weeks-old were subjected to sham or TAC surgery. Representative whole heart images (scale bar, 0.5 cm), M-mode echocardiography, H&E staining (scale bar, 100 µm) and WGA staining (scale bar, 50 µm) of heart tissue. Assessment of (B) HW/BW, (C) LVW/BW and (D) HW/TL (n=6). Statistical graphs for (E) LVEF (%), (F) FS (%), (G) IVS, d (mm) and (H) LVPW, d (mm) (n=6). (I) Cardiomyocyte cross-sectional area acquired from WGA staining. Cells were measured from different microscopic fields of 6 samples in each group. The mRNA levels of (J) BNP and (K) β-MHC in the hearts from sham or TAC-surgery mice (n=6). The mRNA levels of (L) BNP and (M) β-MHC in HL-1 cells treated with <t>Ang</t> <t>II</t> (n=3). (N) Stained cells and (O) quantification of cell surface area of HL-1 cells treated with Ang II. Scale bar, 50 µm (n=3). Western blot analysis and summarized data demonstrating (P) Beclin1 and (Q) VPS34 protein expression in HL-1 cells treated with Ang II (n=3). (R) Western blot analysis and summarized data demonstrating ULK1 protein levels in the hearts obtained after sham or TAC surgery (n=6). (S) Western blot analysis and summarized data demonstrating ULK1 protein levels in the cardiomyocytes stimulated with Ang II (n=6). All data are presented as mean ± SEM. *P < 0.05 and **P<0.01 vs. sham or control group. ULK1, serine/threonine protein kinase ULK1; TAC, transverse aortic constriction; HW, heart weight; BW, body weight; LVW, left ventricular weight; TL, tibia length; LVEF, left ventricular ejection fraction; FS, fractional shortening; d, diastole; IVS, interventricular septal thickness; LVPW, left ventricular posterior wall thickness; CSA, cross-sectional area; BNP , brain natriuretic peptide; β-MHC , β-myosin heavy chain; α-SMA, α smooth muscle actin; Ang II, angiotensin II; VPS34, PI3K catalytic subunit type 3; WGA, wheat germ agglutinin.
Ang Ii Angiotensin Ii Ar Adrenergic Receptor At1r Ang Ii Type 1 Receptor Cam Calmodulin Cryo Em Cryo Electron Microscopy Dag, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/ang ii angiotensin ii ar adrenergic receptor at1r ang ii type 1 receptor cam calmodulin cryo em cryo electron microscopy dag/product/Thermo Fisher
Average 95 stars, based on 1 article reviews
ang ii angiotensin ii ar adrenergic receptor at1r ang ii type 1 receptor cam calmodulin cryo em cryo electron microscopy dag - by Bioz Stars, 2026-03
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96
MedChemExpress ang ii
ULK1 expression is elevated in hypertrophic cardiac tissues and cardiomyocytes. (A) C57BL/6J mice at 8-weeks-old were subjected to sham or TAC surgery. Representative whole heart images (scale bar, 0.5 cm), M-mode echocardiography, H&E staining (scale bar, 100 µm) and WGA staining (scale bar, 50 µm) of heart tissue. Assessment of (B) HW/BW, (C) LVW/BW and (D) HW/TL (n=6). Statistical graphs for (E) LVEF (%), (F) FS (%), (G) IVS, d (mm) and (H) LVPW, d (mm) (n=6). (I) Cardiomyocyte cross-sectional area acquired from WGA staining. Cells were measured from different microscopic fields of 6 samples in each group. The mRNA levels of (J) BNP and (K) β-MHC in the hearts from sham or TAC-surgery mice (n=6). The mRNA levels of (L) BNP and (M) β-MHC in HL-1 cells treated with <t>Ang</t> <t>II</t> (n=3). (N) Stained cells and (O) quantification of cell surface area of HL-1 cells treated with Ang II. Scale bar, 50 µm (n=3). Western blot analysis and summarized data demonstrating (P) Beclin1 and (Q) VPS34 protein expression in HL-1 cells treated with Ang II (n=3). (R) Western blot analysis and summarized data demonstrating ULK1 protein levels in the hearts obtained after sham or TAC surgery (n=6). (S) Western blot analysis and summarized data demonstrating ULK1 protein levels in the cardiomyocytes stimulated with Ang II (n=6). All data are presented as mean ± SEM. *P < 0.05 and **P<0.01 vs. sham or control group. ULK1, serine/threonine protein kinase ULK1; TAC, transverse aortic constriction; HW, heart weight; BW, body weight; LVW, left ventricular weight; TL, tibia length; LVEF, left ventricular ejection fraction; FS, fractional shortening; d, diastole; IVS, interventricular septal thickness; LVPW, left ventricular posterior wall thickness; CSA, cross-sectional area; BNP , brain natriuretic peptide; β-MHC , β-myosin heavy chain; α-SMA, α smooth muscle actin; Ang II, angiotensin II; VPS34, PI3K catalytic subunit type 3; WGA, wheat germ agglutinin.
Ang Ii, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress human angiotensin ang ii
Macrophage migration inhibitory factor (MIF) promotes inflammatory cell migration and infiltration through C – C motif chemokine receptor 2 (CCR2) and C-X-C motif chemokine receptor (CXCR) 4 and promotes splenic monocyte mobilization via interaction with <t>angiotensin</t> Ⅱ type 1 receptor (AT-1R) after myocardial infarction (MI). A, peripheral blood mononuclear cells (PBMCs) chemotaxis in response to homogenized sham or infarct heart tissue from wild type (WT) mice at day 3 post-MI, or MI homogenate together with inhibition of C–C motif chemokine receptor 2 (CCR2), C-X-C motif chemokine receptor (CXCR) 2 and CXCR4, respectively. Cells/HPF, cells/high power field. PBMCs harvested from WT mice at 3 days post-MI. CCR2i, CCR2 inhibition. CXCR2i, CXCR2 inhibition. CXCR4i, CXCR4 inhibition. n = 4–8 per group. *** P < 0.001 vs. sham . B, PBMCs chemotaxis in response to recombinant human MIF (rMIF) or rMIF with inhibition of CCR2, CXCR2 and CXCR4, respectively. PBMCs harvested from WT mice at 3 days post-MI. n = 4–8 per group. *** P < 0.001 vs. control . C, Representative immunoblotting images for monocyte chemoattractant protein-1 (MCP-1), CXCR4 and internal reference protein (heat shock protein 60, HSP-60) in hearts from WT and global MIF deficient (MIFKO) mice with sham-operation or 72 h MI. D-E, Quantitative analysis of MCP-1 and CXCR4 expression. n = 6–9 per group. ** P < 0.01 vs. sham in the same genotype. *** P < 0.001 vs. sham in the same genotype. F, Splenic monocyte (from normal WT mice) chemotaxis in response to plasma from normal mice or mice with 1.5 h MI, or MI plasma together with losartan. Lor, losartan, AT-1R inhibitor. n = 6–8 per group. *** P < 0.001 vs. normal. G, Splenic monocytes (from normal WT mice) chemotaxis in response to rMIF and <t>angiotensin</t> <t>II</t> (Ang II), or together with losartan addition, respectively. n = 6–8 per group. ** P < 0.01 vs. Control. *** P < 0.001 vs. Control. H, Representative immunoblotting images for AT-1R and internal reference protein (HSP-60) in spleens from WT and global MIF deficient (MIFKO) mice with sham-operation and 1.5 h MI. I, Quantitative analysis of AT-1R expression. n = 8 per group. *** P < 0.001 vs. sham in the same genotype . J. Co-immunoprecipitation (Co-IP) assay using an anti-AT-1R antibody or IgG demonstrated the interaction between AT-1R and MIF, as well as between AT-1R and CD74 in splenic monocytes and spleen tissue. Input, input sample. IgG, negative control sample. IP, Co-IP sample.
Human Angiotensin Ang Ii, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress angiotensin ii ang ii
Macrophage migration inhibitory factor (MIF) promotes inflammatory cell migration and infiltration through C – C motif chemokine receptor 2 (CCR2) and C-X-C motif chemokine receptor (CXCR) 4 and promotes splenic monocyte mobilization via interaction with <t>angiotensin</t> Ⅱ type 1 receptor (AT-1R) after myocardial infarction (MI). A, peripheral blood mononuclear cells (PBMCs) chemotaxis in response to homogenized sham or infarct heart tissue from wild type (WT) mice at day 3 post-MI, or MI homogenate together with inhibition of C–C motif chemokine receptor 2 (CCR2), C-X-C motif chemokine receptor (CXCR) 2 and CXCR4, respectively. Cells/HPF, cells/high power field. PBMCs harvested from WT mice at 3 days post-MI. CCR2i, CCR2 inhibition. CXCR2i, CXCR2 inhibition. CXCR4i, CXCR4 inhibition. n = 4–8 per group. *** P < 0.001 vs. sham . B, PBMCs chemotaxis in response to recombinant human MIF (rMIF) or rMIF with inhibition of CCR2, CXCR2 and CXCR4, respectively. PBMCs harvested from WT mice at 3 days post-MI. n = 4–8 per group. *** P < 0.001 vs. control . C, Representative immunoblotting images for monocyte chemoattractant protein-1 (MCP-1), CXCR4 and internal reference protein (heat shock protein 60, HSP-60) in hearts from WT and global MIF deficient (MIFKO) mice with sham-operation or 72 h MI. D-E, Quantitative analysis of MCP-1 and CXCR4 expression. n = 6–9 per group. ** P < 0.01 vs. sham in the same genotype. *** P < 0.001 vs. sham in the same genotype. F, Splenic monocyte (from normal WT mice) chemotaxis in response to plasma from normal mice or mice with 1.5 h MI, or MI plasma together with losartan. Lor, losartan, AT-1R inhibitor. n = 6–8 per group. *** P < 0.001 vs. normal. G, Splenic monocytes (from normal WT mice) chemotaxis in response to rMIF and <t>angiotensin</t> <t>II</t> (Ang II), or together with losartan addition, respectively. n = 6–8 per group. ** P < 0.01 vs. Control. *** P < 0.001 vs. Control. H, Representative immunoblotting images for AT-1R and internal reference protein (HSP-60) in spleens from WT and global MIF deficient (MIFKO) mice with sham-operation and 1.5 h MI. I, Quantitative analysis of AT-1R expression. n = 8 per group. *** P < 0.001 vs. sham in the same genotype . J. Co-immunoprecipitation (Co-IP) assay using an anti-AT-1R antibody or IgG demonstrated the interaction between AT-1R and MIF, as well as between AT-1R and CD74 in splenic monocytes and spleen tissue. Input, input sample. IgG, negative control sample. IP, Co-IP sample.
Angiotensin Ii Ang Ii, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ULK1 expression is elevated in hypertrophic cardiac tissues and cardiomyocytes. (A) C57BL/6J mice at 8-weeks-old were subjected to sham or TAC surgery. Representative whole heart images (scale bar, 0.5 cm), M-mode echocardiography, H&E staining (scale bar, 100 µm) and WGA staining (scale bar, 50 µm) of heart tissue. Assessment of (B) HW/BW, (C) LVW/BW and (D) HW/TL (n=6). Statistical graphs for (E) LVEF (%), (F) FS (%), (G) IVS, d (mm) and (H) LVPW, d (mm) (n=6). (I) Cardiomyocyte cross-sectional area acquired from WGA staining. Cells were measured from different microscopic fields of 6 samples in each group. The mRNA levels of (J) BNP and (K) β-MHC in the hearts from sham or TAC-surgery mice (n=6). The mRNA levels of (L) BNP and (M) β-MHC in HL-1 cells treated with Ang II (n=3). (N) Stained cells and (O) quantification of cell surface area of HL-1 cells treated with Ang II. Scale bar, 50 µm (n=3). Western blot analysis and summarized data demonstrating (P) Beclin1 and (Q) VPS34 protein expression in HL-1 cells treated with Ang II (n=3). (R) Western blot analysis and summarized data demonstrating ULK1 protein levels in the hearts obtained after sham or TAC surgery (n=6). (S) Western blot analysis and summarized data demonstrating ULK1 protein levels in the cardiomyocytes stimulated with Ang II (n=6). All data are presented as mean ± SEM. *P < 0.05 and **P<0.01 vs. sham or control group. ULK1, serine/threonine protein kinase ULK1; TAC, transverse aortic constriction; HW, heart weight; BW, body weight; LVW, left ventricular weight; TL, tibia length; LVEF, left ventricular ejection fraction; FS, fractional shortening; d, diastole; IVS, interventricular septal thickness; LVPW, left ventricular posterior wall thickness; CSA, cross-sectional area; BNP , brain natriuretic peptide; β-MHC , β-myosin heavy chain; α-SMA, α smooth muscle actin; Ang II, angiotensin II; VPS34, PI3K catalytic subunit type 3; WGA, wheat germ agglutinin.

Journal: Molecular Medicine Reports

Article Title: ULK1 activates NCOA4-mediated ferritinophagy via the Beclin1/VPS34 complex in cardiomyocyte hypertrophy

doi: 10.3892/mmr.2026.13826

Figure Lengend Snippet: ULK1 expression is elevated in hypertrophic cardiac tissues and cardiomyocytes. (A) C57BL/6J mice at 8-weeks-old were subjected to sham or TAC surgery. Representative whole heart images (scale bar, 0.5 cm), M-mode echocardiography, H&E staining (scale bar, 100 µm) and WGA staining (scale bar, 50 µm) of heart tissue. Assessment of (B) HW/BW, (C) LVW/BW and (D) HW/TL (n=6). Statistical graphs for (E) LVEF (%), (F) FS (%), (G) IVS, d (mm) and (H) LVPW, d (mm) (n=6). (I) Cardiomyocyte cross-sectional area acquired from WGA staining. Cells were measured from different microscopic fields of 6 samples in each group. The mRNA levels of (J) BNP and (K) β-MHC in the hearts from sham or TAC-surgery mice (n=6). The mRNA levels of (L) BNP and (M) β-MHC in HL-1 cells treated with Ang II (n=3). (N) Stained cells and (O) quantification of cell surface area of HL-1 cells treated with Ang II. Scale bar, 50 µm (n=3). Western blot analysis and summarized data demonstrating (P) Beclin1 and (Q) VPS34 protein expression in HL-1 cells treated with Ang II (n=3). (R) Western blot analysis and summarized data demonstrating ULK1 protein levels in the hearts obtained after sham or TAC surgery (n=6). (S) Western blot analysis and summarized data demonstrating ULK1 protein levels in the cardiomyocytes stimulated with Ang II (n=6). All data are presented as mean ± SEM. *P < 0.05 and **P<0.01 vs. sham or control group. ULK1, serine/threonine protein kinase ULK1; TAC, transverse aortic constriction; HW, heart weight; BW, body weight; LVW, left ventricular weight; TL, tibia length; LVEF, left ventricular ejection fraction; FS, fractional shortening; d, diastole; IVS, interventricular septal thickness; LVPW, left ventricular posterior wall thickness; CSA, cross-sectional area; BNP , brain natriuretic peptide; β-MHC , β-myosin heavy chain; α-SMA, α smooth muscle actin; Ang II, angiotensin II; VPS34, PI3K catalytic subunit type 3; WGA, wheat germ agglutinin.

Article Snippet: The Ang II AT1-receptor candesartan (CS; cat. no. HY-B0205) was purchased from MedChemExpress.

Techniques: Expressing, Staining, Western Blot, Control

Mechanisms of ULK1 activating NCOA4-mediated ferritinophagy via Beclin1/VPS34 complex in cardiomyocyte hypertrophy. This figure was created using Figdraw ( www.figdraw.com ). ULK1, serine/threonine protein kinase ULK1; NCOA4, nuclear receptor coactivator 4; VPS34, PI3K catalytic subunit type 3; LC3, microtubule-associated protein 1 light chain 3; TAC, transverse aortic constriction; Ang II, angiotensin II; ROS, reactive oxygen species.

Journal: Molecular Medicine Reports

Article Title: ULK1 activates NCOA4-mediated ferritinophagy via the Beclin1/VPS34 complex in cardiomyocyte hypertrophy

doi: 10.3892/mmr.2026.13826

Figure Lengend Snippet: Mechanisms of ULK1 activating NCOA4-mediated ferritinophagy via Beclin1/VPS34 complex in cardiomyocyte hypertrophy. This figure was created using Figdraw ( www.figdraw.com ). ULK1, serine/threonine protein kinase ULK1; NCOA4, nuclear receptor coactivator 4; VPS34, PI3K catalytic subunit type 3; LC3, microtubule-associated protein 1 light chain 3; TAC, transverse aortic constriction; Ang II, angiotensin II; ROS, reactive oxygen species.

Article Snippet: The Ang II AT1-receptor candesartan (CS; cat. no. HY-B0205) was purchased from MedChemExpress.

Techniques:

Macrophage migration inhibitory factor (MIF) promotes inflammatory cell migration and infiltration through C – C motif chemokine receptor 2 (CCR2) and C-X-C motif chemokine receptor (CXCR) 4 and promotes splenic monocyte mobilization via interaction with angiotensin Ⅱ type 1 receptor (AT-1R) after myocardial infarction (MI). A, peripheral blood mononuclear cells (PBMCs) chemotaxis in response to homogenized sham or infarct heart tissue from wild type (WT) mice at day 3 post-MI, or MI homogenate together with inhibition of C–C motif chemokine receptor 2 (CCR2), C-X-C motif chemokine receptor (CXCR) 2 and CXCR4, respectively. Cells/HPF, cells/high power field. PBMCs harvested from WT mice at 3 days post-MI. CCR2i, CCR2 inhibition. CXCR2i, CXCR2 inhibition. CXCR4i, CXCR4 inhibition. n = 4–8 per group. *** P < 0.001 vs. sham . B, PBMCs chemotaxis in response to recombinant human MIF (rMIF) or rMIF with inhibition of CCR2, CXCR2 and CXCR4, respectively. PBMCs harvested from WT mice at 3 days post-MI. n = 4–8 per group. *** P < 0.001 vs. control . C, Representative immunoblotting images for monocyte chemoattractant protein-1 (MCP-1), CXCR4 and internal reference protein (heat shock protein 60, HSP-60) in hearts from WT and global MIF deficient (MIFKO) mice with sham-operation or 72 h MI. D-E, Quantitative analysis of MCP-1 and CXCR4 expression. n = 6–9 per group. ** P < 0.01 vs. sham in the same genotype. *** P < 0.001 vs. sham in the same genotype. F, Splenic monocyte (from normal WT mice) chemotaxis in response to plasma from normal mice or mice with 1.5 h MI, or MI plasma together with losartan. Lor, losartan, AT-1R inhibitor. n = 6–8 per group. *** P < 0.001 vs. normal. G, Splenic monocytes (from normal WT mice) chemotaxis in response to rMIF and angiotensin II (Ang II), or together with losartan addition, respectively. n = 6–8 per group. ** P < 0.01 vs. Control. *** P < 0.001 vs. Control. H, Representative immunoblotting images for AT-1R and internal reference protein (HSP-60) in spleens from WT and global MIF deficient (MIFKO) mice with sham-operation and 1.5 h MI. I, Quantitative analysis of AT-1R expression. n = 8 per group. *** P < 0.001 vs. sham in the same genotype . J. Co-immunoprecipitation (Co-IP) assay using an anti-AT-1R antibody or IgG demonstrated the interaction between AT-1R and MIF, as well as between AT-1R and CD74 in splenic monocytes and spleen tissue. Input, input sample. IgG, negative control sample. IP, Co-IP sample.

Journal: Journal of Advanced Research

Article Title: Novel function of macrophage migration inhibitory factor in regulating post-infarct inflammation and the therapeutic significance

doi: 10.1016/j.jare.2025.05.030

Figure Lengend Snippet: Macrophage migration inhibitory factor (MIF) promotes inflammatory cell migration and infiltration through C – C motif chemokine receptor 2 (CCR2) and C-X-C motif chemokine receptor (CXCR) 4 and promotes splenic monocyte mobilization via interaction with angiotensin Ⅱ type 1 receptor (AT-1R) after myocardial infarction (MI). A, peripheral blood mononuclear cells (PBMCs) chemotaxis in response to homogenized sham or infarct heart tissue from wild type (WT) mice at day 3 post-MI, or MI homogenate together with inhibition of C–C motif chemokine receptor 2 (CCR2), C-X-C motif chemokine receptor (CXCR) 2 and CXCR4, respectively. Cells/HPF, cells/high power field. PBMCs harvested from WT mice at 3 days post-MI. CCR2i, CCR2 inhibition. CXCR2i, CXCR2 inhibition. CXCR4i, CXCR4 inhibition. n = 4–8 per group. *** P < 0.001 vs. sham . B, PBMCs chemotaxis in response to recombinant human MIF (rMIF) or rMIF with inhibition of CCR2, CXCR2 and CXCR4, respectively. PBMCs harvested from WT mice at 3 days post-MI. n = 4–8 per group. *** P < 0.001 vs. control . C, Representative immunoblotting images for monocyte chemoattractant protein-1 (MCP-1), CXCR4 and internal reference protein (heat shock protein 60, HSP-60) in hearts from WT and global MIF deficient (MIFKO) mice with sham-operation or 72 h MI. D-E, Quantitative analysis of MCP-1 and CXCR4 expression. n = 6–9 per group. ** P < 0.01 vs. sham in the same genotype. *** P < 0.001 vs. sham in the same genotype. F, Splenic monocyte (from normal WT mice) chemotaxis in response to plasma from normal mice or mice with 1.5 h MI, or MI plasma together with losartan. Lor, losartan, AT-1R inhibitor. n = 6–8 per group. *** P < 0.001 vs. normal. G, Splenic monocytes (from normal WT mice) chemotaxis in response to rMIF and angiotensin II (Ang II), or together with losartan addition, respectively. n = 6–8 per group. ** P < 0.01 vs. Control. *** P < 0.001 vs. Control. H, Representative immunoblotting images for AT-1R and internal reference protein (HSP-60) in spleens from WT and global MIF deficient (MIFKO) mice with sham-operation and 1.5 h MI. I, Quantitative analysis of AT-1R expression. n = 8 per group. *** P < 0.001 vs. sham in the same genotype . J. Co-immunoprecipitation (Co-IP) assay using an anti-AT-1R antibody or IgG demonstrated the interaction between AT-1R and MIF, as well as between AT-1R and CD74 in splenic monocytes and spleen tissue. Input, input sample. IgG, negative control sample. IP, Co-IP sample.

Article Snippet: For group 3, 500 μl DMEM with or without human angiotensin (Ang) II (10 μM, MedChemExpress) was added to the lower chamber.

Techniques: Migration, Chemotaxis Assay, Inhibition, Recombinant, Control, Western Blot, Expressing, Clinical Proteomics, Co-Immunoprecipitation Assay, Negative Control