ang ii valsartan  (MedChemExpress)

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