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SLC7A5 is upregulated during vascular remodeling. (A) Volcano plot of the GSE220512 dataset showing that Slc7a5 is significantly upregulated in neointimal tissue from mouse carotid arteries at Day 7 after wire injury compared with Day 0 controls. (B) Quantitative PCR analysis of SLC7A5 mRNA expression at indicated time points. (C) Representative Western blot and quantitative analysis showing SLC7A5 protein expression at 0, 7, and 14 days after vascular injury (n = 6). (D) Immunohistochemical staining of SLC7A5 in vascular tissues from sham, 7-day, and 14-day groups, showing increased expression in the medial layer during remodeling. bar = 50 μm. (E) Western blot and quantification of SLC7A5 expression in endothelial cells (ECs), macrophages, and vascular smooth muscle cells (VSMCs) (n = 3). (F) Immunofluorescence staining showing increased SLC7A5 expression in VSMCs <t>following</t> <t>PDGF-BB</t> stimulation compared with control. bar = 50 μm. Data are presented as mean ± SEM. Statistical significance is indicated as shown.

Pdgf Bb, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pdgf+bb/pmc13407181-35-13-15?v=MedChemExpress
Average 94 stars, based on 3 article reviews

pdgf bb - by Bioz Stars, 2026-08

94/100 stars

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1) Product Images from "SLC7A5 promotes vascular remodeling in the rat carotid artery following balloon injury through PI3K/Akt signaling pathway"

Article Title: SLC7A5 promotes vascular remodeling in the rat carotid artery following balloon injury through PI3K/Akt signaling pathway

Journal: Frontiers in Pharmacology

doi: 10.3389/fphar.2026.1857850

Figure Legend Snippet: SLC7A5 is upregulated during vascular remodeling. (A) Volcano plot of the GSE220512 dataset showing that Slc7a5 is significantly upregulated in neointimal tissue from mouse carotid arteries at Day 7 after wire injury compared with Day 0 controls. (B) Quantitative PCR analysis of SLC7A5 mRNA expression at indicated time points. (C) Representative Western blot and quantitative analysis showing SLC7A5 protein expression at 0, 7, and 14 days after vascular injury (n = 6). (D) Immunohistochemical staining of SLC7A5 in vascular tissues from sham, 7-day, and 14-day groups, showing increased expression in the medial layer during remodeling. bar = 50 μm. (E) Western blot and quantification of SLC7A5 expression in endothelial cells (ECs), macrophages, and vascular smooth muscle cells (VSMCs) (n = 3). (F) Immunofluorescence staining showing increased SLC7A5 expression in VSMCs following PDGF-BB stimulation compared with control. bar = 50 μm. Data are presented as mean ± SEM. Statistical significance is indicated as shown.

Techniques Used: Real-time Polymerase Chain Reaction, Expressing, Western Blot, Immunohistochemical staining, Staining, Immunofluorescence, Control

Knockdown of SLC7A5 inhibits PDGF-BB–induced VSMC proliferation, migration, and phenotypic switching. (A) Western blot analysis and quantification of PCNA expression in VSMCs under different treatments (n = 4). (B) Representative images of EdU staining and quantification of EdU-positive cells (n = 4) bar = 50 μm. (C) Western blot analysis and quantification of MMP2 expression (n = 4). (D) Representative images of wound healing assays at indicated time points and quantitative analysis of migration rate (n = 4) bar = 50 μm. (E) Western blot analysis and quantification of α-SMA expression (n = 4). (F) Representative immunofluorescence staining of α-SMA (green) and DAPI (blue), along with quantitative analysis of fluorescence intensity (n = 4) bar = 100 μm. PDGF-BB was used to induce VSMC activation. siSLC7A5 was used to silence SLC7A5 expression, and siNC served as a negative control. Data were presented as mean ± SEM from at four independent experiments. Statistical significance was determined using one-way ANOVA followed by appropriate post hoc tests.

Figure Legend Snippet: Knockdown of SLC7A5 inhibits PDGF-BB–induced VSMC proliferation, migration, and phenotypic switching. (A) Western blot analysis and quantification of PCNA expression in VSMCs under different treatments (n = 4). (B) Representative images of EdU staining and quantification of EdU-positive cells (n = 4) bar = 50 μm. (C) Western blot analysis and quantification of MMP2 expression (n = 4). (D) Representative images of wound healing assays at indicated time points and quantitative analysis of migration rate (n = 4) bar = 50 μm. (E) Western blot analysis and quantification of α-SMA expression (n = 4). (F) Representative immunofluorescence staining of α-SMA (green) and DAPI (blue), along with quantitative analysis of fluorescence intensity (n = 4) bar = 100 μm. PDGF-BB was used to induce VSMC activation. siSLC7A5 was used to silence SLC7A5 expression, and siNC served as a negative control. Data were presented as mean ± SEM from at four independent experiments. Statistical significance was determined using one-way ANOVA followed by appropriate post hoc tests.

Techniques Used: Knockdown, Migration, Western Blot, Expressing, Staining, Immunofluorescence, Fluorescence, Activation Assay, Negative Control

SLC7A5 knockdown attenuates the activation of the PI3K/Akt signaling pathway induced by PDGF-BB. (A–C) Western blot analysis of PI3K/Akt signaling pathway–related proteins, including phosphorylated PI3K (p-PI3K), total PI3K, phosphorylated Akt (p-Akt), and total Akt.

Figure Legend Snippet: SLC7A5 knockdown attenuates the activation of the PI3K/Akt signaling pathway induced by PDGF-BB. (A–C) Western blot analysis of PI3K/Akt signaling pathway–related proteins, including phosphorylated PI3K (p-PI3K), total PI3K, phosphorylated Akt (p-Akt), and total Akt.

Techniques Used: Knockdown, Activation Assay, Western Blot

Inhibition of SLC7A5 suppresses PDGF-BB–induced VSMC activation and PI3K/Akt signaling in vitro . (A) Western blot analysis and quantification of PCNA expression (n = 4). (B) Representative images of EdU staining and quantification of proliferating cells. bar = 100 μm. (C) Western blot analysis and quantification of MMP2 expression (n=4). (D) Representative images of wound healing assays at 0 h and 24 h, and quantitative analysis of migration rate. bar=100 μm. (E) Western blot analysis and quantification of α-SMA expression (n=4). (F) Representative immunofluorescence staining of α-SMA (green) and DAPI (blue). bar=100 μm. (G) Western blot analysis of PI3K/Akt signaling pathway–related proteins, including phosphorylated PI3K (p-PI3K), total PI3K, phosphorylated Akt (p-Akt), and total Akt (n=4). Data are presented as mean ± SEM from at four independent experiments. Statistical significance was determined by one-way ANOVAfollowed by appropriate post hoc tests. bar=100 μm.

Figure Legend Snippet: Inhibition of SLC7A5 suppresses PDGF-BB–induced VSMC activation and PI3K/Akt signaling in vitro . (A) Western blot analysis and quantification of PCNA expression (n = 4). (B) Representative images of EdU staining and quantification of proliferating cells. bar = 100 μm. (C) Western blot analysis and quantification of MMP2 expression (n=4). (D) Representative images of wound healing assays at 0 h and 24 h, and quantitative analysis of migration rate. bar=100 μm. (E) Western blot analysis and quantification of α-SMA expression (n=4). (F) Representative immunofluorescence staining of α-SMA (green) and DAPI (blue). bar=100 μm. (G) Western blot analysis of PI3K/Akt signaling pathway–related proteins, including phosphorylated PI3K (p-PI3K), total PI3K, phosphorylated Akt (p-Akt), and total Akt (n=4). Data are presented as mean ± SEM from at four independent experiments. Statistical significance was determined by one-way ANOVAfollowed by appropriate post hoc tests. bar=100 μm.

Techniques Used: Inhibition, Activation Assay, In Vitro, Western Blot, Expressing, Staining, Migration, Immunofluorescence

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Journal: Frontiers in Pharmacology

Article Title: SLC7A5 promotes vascular remodeling in the rat carotid artery following balloon injury through PI3K/Akt signaling pathway

doi: 10.3389/fphar.2026.1857850

Figure Lengend Snippet: SLC7A5 is upregulated during vascular remodeling. (A) Volcano plot of the GSE220512 dataset showing that Slc7a5 is significantly upregulated in neointimal tissue from mouse carotid arteries at Day 7 after wire injury compared with Day 0 controls. (B) Quantitative PCR analysis of SLC7A5 mRNA expression at indicated time points. (C) Representative Western blot and quantitative analysis showing SLC7A5 protein expression at 0, 7, and 14 days after vascular injury (n = 6). (D) Immunohistochemical staining of SLC7A5 in vascular tissues from sham, 7-day, and 14-day groups, showing increased expression in the medial layer during remodeling. bar = 50 μm. (E) Western blot and quantification of SLC7A5 expression in endothelial cells (ECs), macrophages, and vascular smooth muscle cells (VSMCs) (n = 3). (F) Immunofluorescence staining showing increased SLC7A5 expression in VSMCs following PDGF-BB stimulation compared with control. bar = 50 μm. Data are presented as mean ± SEM. Statistical significance is indicated as shown.

Article Snippet: JPH203 (KYT-0353) provided by Targetmol was dissolved in DMSO to prepare stock solution,and PDGF-BB from MCE (HY-P7278) was reconstituted in sterile normal saline according to the manufacturer’s instructions.

Techniques: Real-time Polymerase Chain Reaction, Expressing, Western Blot, Immunohistochemical staining, Staining, Immunofluorescence, Control

Journal: Frontiers in Pharmacology

Article Title: SLC7A5 promotes vascular remodeling in the rat carotid artery following balloon injury through PI3K/Akt signaling pathway

doi: 10.3389/fphar.2026.1857850

Figure Lengend Snippet: Knockdown of SLC7A5 inhibits PDGF-BB–induced VSMC proliferation, migration, and phenotypic switching. (A) Western blot analysis and quantification of PCNA expression in VSMCs under different treatments (n = 4). (B) Representative images of EdU staining and quantification of EdU-positive cells (n = 4) bar = 50 μm. (C) Western blot analysis and quantification of MMP2 expression (n = 4). (D) Representative images of wound healing assays at indicated time points and quantitative analysis of migration rate (n = 4) bar = 50 μm. (E) Western blot analysis and quantification of α-SMA expression (n = 4). (F) Representative immunofluorescence staining of α-SMA (green) and DAPI (blue), along with quantitative analysis of fluorescence intensity (n = 4) bar = 100 μm. PDGF-BB was used to induce VSMC activation. siSLC7A5 was used to silence SLC7A5 expression, and siNC served as a negative control. Data were presented as mean ± SEM from at four independent experiments. Statistical significance was determined using one-way ANOVA followed by appropriate post hoc tests.

Techniques: Knockdown, Migration, Western Blot, Expressing, Staining, Immunofluorescence, Fluorescence, Activation Assay, Negative Control

Journal: Frontiers in Pharmacology

Article Title: SLC7A5 promotes vascular remodeling in the rat carotid artery following balloon injury through PI3K/Akt signaling pathway

doi: 10.3389/fphar.2026.1857850

Figure Lengend Snippet: SLC7A5 knockdown attenuates the activation of the PI3K/Akt signaling pathway induced by PDGF-BB. (A–C) Western blot analysis of PI3K/Akt signaling pathway–related proteins, including phosphorylated PI3K (p-PI3K), total PI3K, phosphorylated Akt (p-Akt), and total Akt.

Techniques: Knockdown, Activation Assay, Western Blot

Journal: Frontiers in Pharmacology

Article Title: SLC7A5 promotes vascular remodeling in the rat carotid artery following balloon injury through PI3K/Akt signaling pathway

doi: 10.3389/fphar.2026.1857850

Figure Lengend Snippet: Inhibition of SLC7A5 suppresses PDGF-BB–induced VSMC activation and PI3K/Akt signaling in vitro . (A) Western blot analysis and quantification of PCNA expression (n = 4). (B) Representative images of EdU staining and quantification of proliferating cells. bar = 100 μm. (C) Western blot analysis and quantification of MMP2 expression (n=4). (D) Representative images of wound healing assays at 0 h and 24 h, and quantitative analysis of migration rate. bar=100 μm. (E) Western blot analysis and quantification of α-SMA expression (n=4). (F) Representative immunofluorescence staining of α-SMA (green) and DAPI (blue). bar=100 μm. (G) Western blot analysis of PI3K/Akt signaling pathway–related proteins, including phosphorylated PI3K (p-PI3K), total PI3K, phosphorylated Akt (p-Akt), and total Akt (n=4). Data are presented as mean ± SEM from at four independent experiments. Statistical significance was determined by one-way ANOVAfollowed by appropriate post hoc tests. bar=100 μm.

Techniques: Inhibition, Activation Assay, In Vitro, Western Blot, Expressing, Staining, Migration, Immunofluorescence

Continuous intraosseous administration of SCS prevents glucocorticoid-induced bone degeneration. ( A ) Schematic illustration of the glucocorticoid (GC; MPS)-induced bone deterioration and intraosseous SCS treatment. ( B-D ) Representative H&E staining images of the femur at 6 weeks (B). Magnified views of the cortical bone and trabecular bone in the marrow cavity are shown on the right. Solid arrows indicate normal osteocytes, while hollow arrows indicate empty osteocyte lacunae. Quantification of empty lacunae ratios in cortical bone (C) and trabecular bone (D). n = 6 biological replicates. (Scale bars, 500 μm and 25 μm) ( E-H ) Representative immunofluorescence staining of OPN + mature osteoblasts, osteolectin + osteoprogenitors, and VE-cadherin + endothelial cells (ECs) in femur at 6 weeks (E), and corresponding quantifications (F–H). n = 6 biological replicates. (Scale bars, 100 μm and 20 μm) ( I and J ) Representative flow cytometry plots of capillary subtypes in the femur (I), with quantification of CD45 − Ter119 − CD31 hi Emcn hi ECs (J). n = 6 biological replicates. ( K and L ) Flow cytometry plots showing Sca-1 hi CD31 hi arteriolar ECs (K), and corresponding quantification (L). n = 6 biological replicates. ( M and N ) Representative micro-CT 3D images of the femur (M). Quantitative analysis of percent bone volume (BV/TV) (N). n = 6 biological replicates. (Scale bars, 1.5 mm, 600 μm and 545 μm) ( O and P ) ELISA analysis of VEGF (O) and PDGF-BB (P) levels in bone marrow supernatant and peripheral serum from PBS- and SCS-treated groups at week 6. n = 6 biological replicates. ( Q ) ELISA quantification of the osteogenic factor osteocalcin in peripheral serum at week 6. n = 6 biological replicates. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; ns, not significant. Statistical significance was determined using one-way ANOVA with Tukey's post hoc test ( C, D, F, G, H, J, L, N, O, P and Q ).

Journal: Bioactive Materials

Article Title: Sulfated polysaccharide prevents senescent adipocyte-driven osteonecrosis by stem cell fate reprogramming

doi: 10.1016/j.bioactmat.2025.11.039

Figure Lengend Snippet: Continuous intraosseous administration of SCS prevents glucocorticoid-induced bone degeneration. ( A ) Schematic illustration of the glucocorticoid (GC; MPS)-induced bone deterioration and intraosseous SCS treatment. ( B-D ) Representative H&E staining images of the femur at 6 weeks (B). Magnified views of the cortical bone and trabecular bone in the marrow cavity are shown on the right. Solid arrows indicate normal osteocytes, while hollow arrows indicate empty osteocyte lacunae. Quantification of empty lacunae ratios in cortical bone (C) and trabecular bone (D). n = 6 biological replicates. (Scale bars, 500 μm and 25 μm) ( E-H ) Representative immunofluorescence staining of OPN + mature osteoblasts, osteolectin + osteoprogenitors, and VE-cadherin + endothelial cells (ECs) in femur at 6 weeks (E), and corresponding quantifications (F–H). n = 6 biological replicates. (Scale bars, 100 μm and 20 μm) ( I and J ) Representative flow cytometry plots of capillary subtypes in the femur (I), with quantification of CD45 − Ter119 − CD31 hi Emcn hi ECs (J). n = 6 biological replicates. ( K and L ) Flow cytometry plots showing Sca-1 hi CD31 hi arteriolar ECs (K), and corresponding quantification (L). n = 6 biological replicates. ( M and N ) Representative micro-CT 3D images of the femur (M). Quantitative analysis of percent bone volume (BV/TV) (N). n = 6 biological replicates. (Scale bars, 1.5 mm, 600 μm and 545 μm) ( O and P ) ELISA analysis of VEGF (O) and PDGF-BB (P) levels in bone marrow supernatant and peripheral serum from PBS- and SCS-treated groups at week 6. n = 6 biological replicates. ( Q ) ELISA quantification of the osteogenic factor osteocalcin in peripheral serum at week 6. n = 6 biological replicates. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; ns, not significant. Statistical significance was determined using one-way ANOVA with Tukey's post hoc test ( C, D, F, G, H, J, L, N, O, P and Q ).

Article Snippet: Levels of angiogenesis-associated factors, including VEGF (Neobioscience, EMC103.96) and PDGF-BB (R&D Systems, MBB00), were quantified in both bone marrow supernatants and serum using ELISA kits according to the manufacturer's instructions.

Techniques: Staining, Immunofluorescence, Flow Cytometry, Micro-CT, Enzyme-linked Immunosorbent Assay

SCS targets downstream senescent lineage commitment of bone marrow MSCs to mitigate GC-induced bone deterioration. ( A ) Schematic diagram illustrating the experimental design: CD45 − Ter119 − CD31 − LepR + MSCs isolated from mice co-treated with SCS and MPS for 7 days were subjected to in vitro lineage-competitive differentiation, followed by DEX-induced senescence in lineage-mixed cells. These cells were then adoptively transplanted into healthy bone marrow cavity to assess bone deterioration development. ( B ) Representative H&E-stained images of the femur 12 weeks after adoptive transfer. PBS-DEX group: LepR + MSCs from PBS and MPS co-treated mice subjected to in vitro lineage differentiation and DEX-induced senescence, followed by transplantation. SCS-DEX group: LepR + MSCs from SCS and MPS co-treated mice processed similarly. PBS group: solvent control without cell transplantation. Solid arrows indicate intact osteocytes; hollow arrows indicate empty lacunae. (Scale bars, 250 μm and 25 μm) ( C – E ) Quantitative analysis of marrow hypertrophic adipocyte diameter (C), proportion of empty osteocyte lacunae in trabecular bone (D), and adipocyte number (E) in the metaphysis 12 weeks post-transplantation. n = 19 biological replicates (C), n = 6 biological replicates (D), n = 8 biological replicates (E). ( F ) Quantification of empty lacunae in epiphysis at 12 weeks post-transplantation. n = 6 biological replicates. ( G – I ) Representative flow cytometry plots of capillary ECs subtypes in the femur at 12 weeks (G), with quantification of CD45 − Ter119 − CD31 hi Emcn hi ECs (H) and CD45 − Ter119 − CD31 lo Emcn lo ECs (I). n = 6 biological replicates. ( J and K ) Representative flow cytometry plots (J) and corresponding quantification (K) of CD45 − Ter119 − Sca-1 hi CD31 hi arteriolar ECs in the femur at 12 weeks post-transplantation. n = 6 biological replicates. ( L ) Representative micro-CT images of the femur at 12 weeks post-transplantation across different treatment groups. (Scale bars, 1.5 mm and 500 μm) ( M – P ) Quantitative analysis of bone parameters in the metaphysis: bone mineral density (BMD) (M), percent bone volume (BV/TV) (N), trabecular separation (Tb.Sp) (O), and trabecular number (Tb.N) (P). n = 6 biological replicates. ( Q ) Serum ELISA analysis of the osteogenic marker osteocalcin at 12 weeks post-transplantation. n = 6 biological replicates. ( R and S ) ELISA analysis of PDGF-BB (R) and VEGF (S) in both bone marrow supernatant and peripheral serum at 12 weeks post-transplantation. n = 6 biological replicates. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; ns, not significant. Statistical significance was determined using one-way ANOVA with Tukey's post hoc test ( C, D, E, F, H, I, K, M, N, O, P, Q, R and S ).

Journal: Bioactive Materials

Article Title: Sulfated polysaccharide prevents senescent adipocyte-driven osteonecrosis by stem cell fate reprogramming

doi: 10.1016/j.bioactmat.2025.11.039

Figure Lengend Snippet: SCS targets downstream senescent lineage commitment of bone marrow MSCs to mitigate GC-induced bone deterioration. ( A ) Schematic diagram illustrating the experimental design: CD45 − Ter119 − CD31 − LepR + MSCs isolated from mice co-treated with SCS and MPS for 7 days were subjected to in vitro lineage-competitive differentiation, followed by DEX-induced senescence in lineage-mixed cells. These cells were then adoptively transplanted into healthy bone marrow cavity to assess bone deterioration development. ( B ) Representative H&E-stained images of the femur 12 weeks after adoptive transfer. PBS-DEX group: LepR + MSCs from PBS and MPS co-treated mice subjected to in vitro lineage differentiation and DEX-induced senescence, followed by transplantation. SCS-DEX group: LepR + MSCs from SCS and MPS co-treated mice processed similarly. PBS group: solvent control without cell transplantation. Solid arrows indicate intact osteocytes; hollow arrows indicate empty lacunae. (Scale bars, 250 μm and 25 μm) ( C – E ) Quantitative analysis of marrow hypertrophic adipocyte diameter (C), proportion of empty osteocyte lacunae in trabecular bone (D), and adipocyte number (E) in the metaphysis 12 weeks post-transplantation. n = 19 biological replicates (C), n = 6 biological replicates (D), n = 8 biological replicates (E). ( F ) Quantification of empty lacunae in epiphysis at 12 weeks post-transplantation. n = 6 biological replicates. ( G – I ) Representative flow cytometry plots of capillary ECs subtypes in the femur at 12 weeks (G), with quantification of CD45 − Ter119 − CD31 hi Emcn hi ECs (H) and CD45 − Ter119 − CD31 lo Emcn lo ECs (I). n = 6 biological replicates. ( J and K ) Representative flow cytometry plots (J) and corresponding quantification (K) of CD45 − Ter119 − Sca-1 hi CD31 hi arteriolar ECs in the femur at 12 weeks post-transplantation. n = 6 biological replicates. ( L ) Representative micro-CT images of the femur at 12 weeks post-transplantation across different treatment groups. (Scale bars, 1.5 mm and 500 μm) ( M – P ) Quantitative analysis of bone parameters in the metaphysis: bone mineral density (BMD) (M), percent bone volume (BV/TV) (N), trabecular separation (Tb.Sp) (O), and trabecular number (Tb.N) (P). n = 6 biological replicates. ( Q ) Serum ELISA analysis of the osteogenic marker osteocalcin at 12 weeks post-transplantation. n = 6 biological replicates. ( R and S ) ELISA analysis of PDGF-BB (R) and VEGF (S) in both bone marrow supernatant and peripheral serum at 12 weeks post-transplantation. n = 6 biological replicates. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; ns, not significant. Statistical significance was determined using one-way ANOVA with Tukey's post hoc test ( C, D, E, F, H, I, K, M, N, O, P, Q, R and S ).

Techniques: Isolation, In Vitro, Staining, Adoptive Transfer Assay, Transplantation Assay, Solvent, Control, Flow Cytometry, Micro-CT, Enzyme-linked Immunosorbent Assay, Marker

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1) Product Images from "SLC7A5 promotes vascular remodeling in the rat carotid artery following balloon injury through PI3K/Akt signaling pathway"

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