hy b0317 losartan medchemexpress  (MedChemExpress)

Journal: bioRxiv

Article Title: sPRR Signaling in Macrophages via the AT1R/Yap/Taz Axis to Induce Renal Fibrosis

doi: 10.64898/2026.04.03.716436

Figure Lengend Snippet: (A) Western blot analyses showing abundance of Yap/Taz in BMDMs treated with 10 nM sPRR-His for 24 hours. Numbers (1-3) indicate individual sample within the same group. (B) Representative immunofluorescent staining images showing nuclear localization of Yap/Taz in BMDMs stimulated with sPRR-His or sPRR-His plus losartan. Scale bar = 20 μm. (C) Western blot analyses showing verteporfin inhibited sPRR-His-stimulated fibrosis in BMDMs. (D) Western blot analyses showing verteporfin inhibited sPRR-His-promoted macrophage alternative activation. (E) Real-time qRT-PCR analysis showing that verteporfin inhibited sPRR-His-stimulated macrophage alternative activation. BMDMs were pretreated with 10 nM verteporfin for 1 hour and then 10 nM sPRR-His for 24 hours. * p < 0.05 versus BMDMs treated with vehicle alone, n=6; # P <0.05 versus BMDMs treated with sPRR-His, n = 6.

Article Snippet: The BMDMs were treated with losartan (10 μM, cat: HY-17512; Medchem express), verteporfin (10 nM, cat: SML0534; Sigma-Aldrich), or PF-429242 (10 μM, cat: HY-13447A, Medchem Express) for 1 hour to block AT1, Yap, and S1P, respectively.

Techniques: Western Blot, Staining, Activation Assay, Quantitative RT-PCR

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 all groups, splenic monocytes were pre-treated for 1 h using DMEM with or without AT-1R inhibitor (losartan, 10 μM, MedChemExpress) and 2 × 10 5 cells in 500 μl were added to the top chamber insert and then were processed following the same protocol as outlined for the PBMCs.

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