valsartan diovan  (Novartis)

Journal: Biology Direct

Article Title: Nucleolin in the cell membrane promotes Ang II-mediated VSMC phenotypic switching by regulating the AT1R internalization function

doi: 10.1186/s13062-025-00615-0

Figure Lengend Snippet: Ang II stimulates NCL expression and activates PKC/MAPK to induce VSMC phenotype switching. A . Morphology of isolated VSMCs. Scale bar = 100 µM. B . IF assay for detecting α-SMA expression. Scale bar = 25 µM. C . RT-qPCR and WB analysis of NCL expression in VSMCs without and with Ang II treatment. D . WB analysis of AT1R, p-p38MAPK/p38MAPK, p-JNK/JNK, p-ERK/ERK, and p-PKCα/PKCα expression in VSMCs without and with Ang II treatment. * p < 0.05 vs. Control. E . WB analysis of α-SMA, SM22α, and OPN expression in VSMCs. F - G . IF assay for detecting α-SMA and OPN expression in VSMCs. VSMCs were treated with Ang II and valsartan, LY317615, SP600125 or SB203580, respectively. Scale bar = 25 µM. * p < 0.05 vs. Control, # p < 0.05 vs. Ang II. n = 3

Article Snippet: To investigate whether the AT1R and PKC/MAPK pathways mediate the effects of Ang II on VSMC, we constructed the following six groups: Control, Ang II, Ang II + Valsartan (VSMCs were pre-treated with 1 µM valsartan (AT1R inhibitor, HY-18204, MCE) for 1 h, and then treated with Ang II) [ ], Ang II + LY317615 (VSMCs were pre-treated with 10 µM LY317615 (PKC inhibitor, HY-10342, MCE) for 1 h, and then treated with Ang II), Ang II + SP600125 (VSMCs were pre-treated with 10 µM SP600125 (JNK inhibitor, HY-12041, MCE) for 1 h, and then treated with Ang II for 48 h), and Ang II + SB203580 (VSMCs were pre-treated with 10 µM SB203580 (p38 MAPK inhibitor, HY-10256, MCE) for 1 h, and then treated with Ang II) [ ].

Techniques: Expressing, Isolation, Quantitative RT-PCR, Control

Journal: Biology Direct

Article Title: Nucleolin in the cell membrane promotes Ang II-mediated VSMC phenotypic switching by regulating the AT1R internalization function

doi: 10.1186/s13062-025-00615-0

Figure Lengend Snippet: Ang II promotes VSMC phenotype switching through NCL. A . RT-qPCR and WB analysis of NCL expression in VSMCs transfected with sh-NC or sh-NCL. * p < 0.05 vs. sh-NC. B - C . RT-qPCR and WB analysis of NCL expression in VSMCs. D . CCK-8 assay for evaluating cell viability of VSMCs. E . EDU assay for detecting cell proliferation in VSMCs. Scale bar = 50 µM. F . Scratch assay for detecting cell migration in VSMCs. Scale bar = 100 µM. G . WB analysis of α-SMA, SM22α, and OPN expression. H . IF assay for detecting α-SMA and OPN expression in VSMCs. Scale bar = 25 µM. VSMCs were transfected with sh-NC or sh-NCL and then treated with Ang II. * p < 0.05 vs. Control, # p < 0.05 vs. Ang II + sh-NC. n = 3

Article Snippet: To investigate whether the AT1R and PKC/MAPK pathways mediate the effects of Ang II on VSMC, we constructed the following six groups: Control, Ang II, Ang II + Valsartan (VSMCs were pre-treated with 1 µM valsartan (AT1R inhibitor, HY-18204, MCE) for 1 h, and then treated with Ang II) [ ], Ang II + LY317615 (VSMCs were pre-treated with 10 µM LY317615 (PKC inhibitor, HY-10342, MCE) for 1 h, and then treated with Ang II), Ang II + SP600125 (VSMCs were pre-treated with 10 µM SP600125 (JNK inhibitor, HY-12041, MCE) for 1 h, and then treated with Ang II for 48 h), and Ang II + SB203580 (VSMCs were pre-treated with 10 µM SB203580 (p38 MAPK inhibitor, HY-10256, MCE) for 1 h, and then treated with Ang II) [ ].

Techniques: Quantitative RT-PCR, Expressing, Transfection, CCK-8 Assay, EdU Assay, Wound Healing Assay, Migration, Control

Journal: Biology Direct

Article Title: Nucleolin in the cell membrane promotes Ang II-mediated VSMC phenotypic switching by regulating the AT1R internalization function

doi: 10.1186/s13062-025-00615-0

Figure Lengend Snippet: Ang II stimulates NCL translocation to the cell membrane surface to bind to AT1R. A . WB analysis of NCL expression in the cell membrane, cytoplasm and nucleus of VSMCs. * p < 0.05 vs. Membrane, # p < 0.05 vs. Cytoplasm. B . WB analysis of NCL expression in the cell membrane, cytoplasm and nucleus of VSMCs without and with Ang II treatment. * p < 0.05 vs. Control. C . The diagram of the structure of NCL. D . Co-IP assay for validating the interaction of WT-NCL, NCLΔGAR, and NCLΔGARΔRBD with AT1R. n = 3

Article Snippet: To investigate whether the AT1R and PKC/MAPK pathways mediate the effects of Ang II on VSMC, we constructed the following six groups: Control, Ang II, Ang II + Valsartan (VSMCs were pre-treated with 1 µM valsartan (AT1R inhibitor, HY-18204, MCE) for 1 h, and then treated with Ang II) [ ], Ang II + LY317615 (VSMCs were pre-treated with 10 µM LY317615 (PKC inhibitor, HY-10342, MCE) for 1 h, and then treated with Ang II), Ang II + SP600125 (VSMCs were pre-treated with 10 µM SP600125 (JNK inhibitor, HY-12041, MCE) for 1 h, and then treated with Ang II for 48 h), and Ang II + SB203580 (VSMCs were pre-treated with 10 µM SB203580 (p38 MAPK inhibitor, HY-10256, MCE) for 1 h, and then treated with Ang II) [ ].

Techniques: Translocation Assay, Membrane, Expressing, Control, Co-Immunoprecipitation Assay

Journal: Biology Direct

Article Title: Nucleolin in the cell membrane promotes Ang II-mediated VSMC phenotypic switching by regulating the AT1R internalization function

doi: 10.1186/s13062-025-00615-0

Figure Lengend Snippet: NCL translocation to the cell membrane is regulated by glycosylation. A . WB analysis of the glycosylation changes in NCL protein extracted from VSMCs was treated with Ang II and PNGase F. B . WB analysis of α-SMA, SM22α, and OPN expression in VSMCs. VSMCs were treated with Ang II and PNGase F. * p < 0.05 vs. Ang II. n = 3

Article Snippet: To investigate whether the AT1R and PKC/MAPK pathways mediate the effects of Ang II on VSMC, we constructed the following six groups: Control, Ang II, Ang II + Valsartan (VSMCs were pre-treated with 1 µM valsartan (AT1R inhibitor, HY-18204, MCE) for 1 h, and then treated with Ang II) [ ], Ang II + LY317615 (VSMCs were pre-treated with 10 µM LY317615 (PKC inhibitor, HY-10342, MCE) for 1 h, and then treated with Ang II), Ang II + SP600125 (VSMCs were pre-treated with 10 µM SP600125 (JNK inhibitor, HY-12041, MCE) for 1 h, and then treated with Ang II for 48 h), and Ang II + SB203580 (VSMCs were pre-treated with 10 µM SB203580 (p38 MAPK inhibitor, HY-10256, MCE) for 1 h, and then treated with Ang II) [ ].

Techniques: Translocation Assay, Membrane, Expressing

Journal: Biology Direct

Article Title: Nucleolin in the cell membrane promotes Ang II-mediated VSMC phenotypic switching by regulating the AT1R internalization function

doi: 10.1186/s13062-025-00615-0

Figure Lengend Snippet: NCL delays Ang II-induced AT1R internalization and recruits Rab4 and Rab11 to promote recycling by inhibiting AT1R phosphorylation. A . RT-qPCR and WB analysis of NCL expression in VSMCs transfected with oe-NC or oe-NCL. * p < 0.05 vs. oe-NC. B . WB analysis of AT1R expression in the cell membrane and cytoplasm of VSMCs. C . WB analysis of β-arrestin2, Clathrin, AP-2, and Caveolae-1 expression in VSMCs. D . Detection of AT1R phosphorylation in VSMCs. Pulldown Westerns are indicated by pulldown (PD). E . Co-IP assay for validating the binding of AT1R to Rab4 and Rab11, respectively. F . WB analysis of Rab4 and Rab11expression in VSMCs. VSMCs were transfected with oe-NC or oe-NCL and then treated with Ang II. * p < 0.05 vs. Control, # p < 0.05 vs. Ang II + oe-NC. n = 3

Article Snippet: To investigate whether the AT1R and PKC/MAPK pathways mediate the effects of Ang II on VSMC, we constructed the following six groups: Control, Ang II, Ang II + Valsartan (VSMCs were pre-treated with 1 µM valsartan (AT1R inhibitor, HY-18204, MCE) for 1 h, and then treated with Ang II) [ ], Ang II + LY317615 (VSMCs were pre-treated with 10 µM LY317615 (PKC inhibitor, HY-10342, MCE) for 1 h, and then treated with Ang II), Ang II + SP600125 (VSMCs were pre-treated with 10 µM SP600125 (JNK inhibitor, HY-12041, MCE) for 1 h, and then treated with Ang II for 48 h), and Ang II + SB203580 (VSMCs were pre-treated with 10 µM SB203580 (p38 MAPK inhibitor, HY-10256, MCE) for 1 h, and then treated with Ang II) [ ].

Techniques: Quantitative RT-PCR, Expressing, Transfection, Membrane, Co-Immunoprecipitation Assay, Binding Assay, Control

Journal: Biology Direct

Article Title: Nucleolin in the cell membrane promotes Ang II-mediated VSMC phenotypic switching by regulating the AT1R internalization function

doi: 10.1186/s13062-025-00615-0

Figure Lengend Snippet: NCL induces VSMC phenotypic switching by reducing Ang II-induced AT1R internalization leading to sustained AT1R activation. VSMCs were transfected with oe-NC or oe-NCL and then treated with Ang II and 50 μm rasarfin. A . WB analysis of β-arrestin2, Clathrin, AP-2, and Caveolae-1 expression in VSMCs. B . Detection of AT1R phosphorylation in VSMCs. C . WB analysis of Rab4 and Rab11expression in VSMCs. D . EDU assay for detecting cell proliferation. Scale bar = 50 µM. E . Scratch assay for detecting cell migration. Scale bar = 100 µM. F . WB analysis of α-SMA, SM22α, and OPN expression. G . IF assay for detecting α-SMA and OPN expression. Scale bar = 25 µM. VSMCs were transfected with sh-NC or sh-NCL and then treated with Ang II and rasarfin. * p < 0.05 vs. Ang II + sh-NC, # p < 0.05 vs. Ang II + sh-NCL + DMSO. n = 3

Article Snippet: To investigate whether the AT1R and PKC/MAPK pathways mediate the effects of Ang II on VSMC, we constructed the following six groups: Control, Ang II, Ang II + Valsartan (VSMCs were pre-treated with 1 µM valsartan (AT1R inhibitor, HY-18204, MCE) for 1 h, and then treated with Ang II) [ ], Ang II + LY317615 (VSMCs were pre-treated with 10 µM LY317615 (PKC inhibitor, HY-10342, MCE) for 1 h, and then treated with Ang II), Ang II + SP600125 (VSMCs were pre-treated with 10 µM SP600125 (JNK inhibitor, HY-12041, MCE) for 1 h, and then treated with Ang II for 48 h), and Ang II + SB203580 (VSMCs were pre-treated with 10 µM SB203580 (p38 MAPK inhibitor, HY-10256, MCE) for 1 h, and then treated with Ang II) [ ].

Techniques: Activation Assay, Transfection, Expressing, EdU Assay, Wound Healing Assay, Migration

Journal: Biology Direct

Article Title: Nucleolin in the cell membrane promotes Ang II-mediated VSMC phenotypic switching by regulating the AT1R internalization function

doi: 10.1186/s13062-025-00615-0

Figure Lengend Snippet: NCL promotes VSMC phenotypic switching in mice. A . RT-qPCR and WB analysis of NCL expression in mice. B . Blood pressure monitoring in mice. C . H & E staining of thoracic aorta from mice. Scale bar = 100 and 25 µM. D. WB analysis of NCL expression. E . IF staining for detecting Ki67 expression. Scale bar = 25 µM. F . WB analysis of β-arrestin1, β-arrestin2, Clathrin, AP-2, and Caveolae-1 expression. G . WB analysis of Rab4 and Rab11expression. H . IF assay for detecting α-SMA and OPN expression. Scale bar = 25 µM. I. WB analysis of AT1R, p-p38MAPK/p38MAPK, p-JNK/JNK, p-ERK/ERK, and p-PKCα/PKCα expression. The mice were treated with Ang II and injected with sh-NC or sh-NCL lentiviruses in the tail vein. * p < 0.05 vs. sh-NC. * p < 0.05 vs. Sham, # p < 0.05 vs. Ang II + sh-NC. n = 5

Article Snippet: To investigate whether the AT1R and PKC/MAPK pathways mediate the effects of Ang II on VSMC, we constructed the following six groups: Control, Ang II, Ang II + Valsartan (VSMCs were pre-treated with 1 µM valsartan (AT1R inhibitor, HY-18204, MCE) for 1 h, and then treated with Ang II) [ ], Ang II + LY317615 (VSMCs were pre-treated with 10 µM LY317615 (PKC inhibitor, HY-10342, MCE) for 1 h, and then treated with Ang II), Ang II + SP600125 (VSMCs were pre-treated with 10 µM SP600125 (JNK inhibitor, HY-12041, MCE) for 1 h, and then treated with Ang II for 48 h), and Ang II + SB203580 (VSMCs were pre-treated with 10 µM SB203580 (p38 MAPK inhibitor, HY-10256, MCE) for 1 h, and then treated with Ang II) [ ].

Techniques: Quantitative RT-PCR, Expressing, Staining, Injection

Journal: Arthritis & Rheumatology (Hoboken, N.j.)

Article Title: Absence of Functional Autoantibodies Targeting Angiotensin II Receptor Type 1 and Endothelin‐1 Type A Receptor in Circulation and Purified IgG From Patients With Systemic Sclerosis

doi: 10.1002/art.43099

Figure Lengend Snippet: Pretreatment with SSc IgG does not alter AngII responses in CHO‐AT 1 cells. (A) Representative graph of baseline‐corrected normalized CI traces of CHO‐AT 1 cells stimulated with 10 −9.5 to 10 −7.5 M AngII without any IgG pretreatment. (B) Representative graphs of CHO‐AT 1 cells pretreated with 100 μg/mL of HD IgG or IgG derived from patients with SSc before stimulation with 10 −9.5 to 10 −7.5 M AngII. (C) Net AUC (mean ± SEM) of CHO‐AT 1 cells pretreated with 100 μg/mL of IgG before stimulation with AngII. Dots represent mean net AUC of two individual performed experiments with technical duplicates. Statistical analysis using the Mann‐Whitney U‐test with Dunn's correction for multiple testing. AngII, angiotensin II; AT 1 , angiotensin II receptor type 1; AUC, area under the curve; CHO, Chinese hamster ovary; CI, cell index; HD, healthy donor; ns, not specific; PBS, phosphate buffered saline; SSc, systemic sclerosis.

Article Snippet: Cells were serum‐starved for one hour before pretreatment with 2 μ M of valsartan (AT 1 antagonist, HY‐18204; MedChemExpress) and 2 μ M of BQ‐123 (ET A R antagonist, HY‐12378; MedChemExpress) or a vehicle (0.02% DMSO/phosphate buffered saline [PBS]) for one hour.

Techniques: Derivative Assay, MANN-WHITNEY, Saline

Journal: Arthritis & Rheumatology (Hoboken, N.j.)

Article Title: Absence of Functional Autoantibodies Targeting Angiotensin II Receptor Type 1 and Endothelin‐1 Type A Receptor in Circulation and Purified IgG From Patients With Systemic Sclerosis

doi: 10.1002/art.43099

Figure Lengend Snippet: Pretreatment with SSc IgG does not alter ET‐1 responses in CHO‐ET A R cells. (A) Representative graph of baseline‐corrected normalized CI traces of CHO‐ET A R cells stimulated with 10 −9 to 10 −7 M ET‐1 without any IgG pretreatment. (B) Representative graphs of CHO‐ET A R cells pretreated with 100 μg/mL of HD IgG or SSc IgG before stimulation with 10 −9 to 10 −7 M ET‐1. (C) Net AUC (mean ± SEM) of CHO‐ET A R cells pretreated with 100 μg/mL of IgG before stimulation with ET‐1. Dots represent mean net AUC of two individual performed experiments with technical duplicates. Statistical analysis using the Mann‐Whitney U‐test with Dunn's correction for multiple testing. AUC, area under the curve; CHO, Chinese hamster ovary; CI, cell index; ET‐1, endothelin‐1; ET A R, endothelin‐1 type A receptor; HD, healthy donor; ns, not specific; PBS, phosphate buffered saline; SSc, systemic sclerosis.

Article Snippet: Cells were serum‐starved for one hour before pretreatment with 2 μ M of valsartan (AT 1 antagonist, HY‐18204; MedChemExpress) and 2 μ M of BQ‐123 (ET A R antagonist, HY‐12378; MedChemExpress) or a vehicle (0.02% DMSO/phosphate buffered saline [PBS]) for one hour.

Techniques: MANN-WHITNEY, Saline