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primary human vascular smooth muscle cells vsmcs  (ATCC)


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    ATCC primary human vascular smooth muscle cells vsmcs
    Primary Human Vascular Smooth Muscle Cells Vsmcs, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 840 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    F actin is reduced in diabetic CRMs: (A) F actin content in control and diabetic mouse coronary <t>VSMCs</t> obtained via staining with phalloidin. (B) G actin levels in control and <t>T2DM</t> mouse coronary VSMCs attained through staining with DNase. (C) F/G actin ratio of mouse normal and diabetic coronary VSMCs. (D) Representative images from Db/db (top) and db/db (bottom). Data are mean ± SEM. **p ≤ 0.005. n = 3 per group.
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    primary human vsmc  (ATCC)
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    F actin is reduced in diabetic CRMs: (A) F actin content in control and diabetic mouse coronary <t>VSMCs</t> obtained via staining with phalloidin. (B) G actin levels in control and <t>T2DM</t> mouse coronary VSMCs attained through staining with DNase. (C) F/G actin ratio of mouse normal and diabetic coronary VSMCs. (D) Representative images from Db/db (top) and db/db (bottom). Data are mean ± SEM. **p ≤ 0.005. n = 3 per group.
    Primary Human Vsmc, supplied by ATCC, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Identification of major aortic cell types and cell type–specific gene markers. A , Schematic diagram of the study design. Athero-prone areas of the aorta (ascending aorta, aortic arch, and thoracic aorta) were collected from female Ldlr −/− mice on normal laboratory (NL), high-cholesterol (HC), or HC+ trimethylamine- N -oxide (TMAO) diets (n=6/group), and 2 mouse samples from the same diet group were pooled together, with n=3 pools/group. B , Plasma TMAO levels (µM) in the NL-, HC-, and HC+TMAO-fed mice as measured by mass spectrometry (n=6/group). Statistical significance was determined by unpaired t test. C through E , Uniform Manifold Approximation and Projection (UMAP) representation of cell clusters in NL, HC, and HC+TMAO conditions, respectively. F , Cluster-specific expression of previously known cell type markers. G , Normalized expression values of top markers of vascular smooth muscle cells (vSMC) subtype clusters: vSMC 1: Acta2, vSMC 2: Atf3 , Rgs5 + vSMC: Rgs5, modulated vSMC: Spp1 . H , Proportions of identified cell types within total cells recovered for each diet condition in order of abundance. Statistical significance was determined by unpaired t test. False discovery rate (FDR) was calculated with Benjamini-Hochberg. DEG indicates differentially expressed genes; and Mod. vSMC, modulated vSMC.

    Journal: Arteriosclerosis, Thrombosis, and Vascular Biology

    Article Title: Trimethylamine- N -Oxide Affects Cell Type–Specific Pathways and Networks in Mouse Aorta to Promote Atherosclerotic Plaque Vulnerability

    doi: 10.1161/ATVBAHA.125.323047

    Figure Lengend Snippet: Identification of major aortic cell types and cell type–specific gene markers. A , Schematic diagram of the study design. Athero-prone areas of the aorta (ascending aorta, aortic arch, and thoracic aorta) were collected from female Ldlr −/− mice on normal laboratory (NL), high-cholesterol (HC), or HC+ trimethylamine- N -oxide (TMAO) diets (n=6/group), and 2 mouse samples from the same diet group were pooled together, with n=3 pools/group. B , Plasma TMAO levels (µM) in the NL-, HC-, and HC+TMAO-fed mice as measured by mass spectrometry (n=6/group). Statistical significance was determined by unpaired t test. C through E , Uniform Manifold Approximation and Projection (UMAP) representation of cell clusters in NL, HC, and HC+TMAO conditions, respectively. F , Cluster-specific expression of previously known cell type markers. G , Normalized expression values of top markers of vascular smooth muscle cells (vSMC) subtype clusters: vSMC 1: Acta2, vSMC 2: Atf3 , Rgs5 + vSMC: Rgs5, modulated vSMC: Spp1 . H , Proportions of identified cell types within total cells recovered for each diet condition in order of abundance. Statistical significance was determined by unpaired t test. False discovery rate (FDR) was calculated with Benjamini-Hochberg. DEG indicates differentially expressed genes; and Mod. vSMC, modulated vSMC.

    Article Snippet: Human immortalized coronary artery vSMCs (gift from Dr Clint Miller, University of Virginia, Charlottesville, VA) and human primary aortic vSMCs (PCS-100-012; ATCC) were cultured in vSMC growth medium with premixed supplements (catalog no. C-22062; PromoCell).

    Techniques: Clinical Proteomics, Mass Spectrometry, Expressing

    Identification of macrophage subtypes and differences in vascular smooth muscle cells (vSMC)–derived macrophages with trimethylamine- N -oxide (TMAO). A through C , Uniform Manifold Approximation and Projection (UMAP) of macrophage subclusters in normal laboratory (NL), high-cholesterol (HC), and HC+TMAO conditions, respectively. D , Subcluster-specific expression of previously known macrophage subtype markers. E , Proportions of macrophage subtypes within total macrophage number recovered for each diet condition in order of abundance. Statistical significance was determined by unpaired t test. false discovery rate (FDR) was calculated with Benjamini-Hochberg. F , Shared and cell type–specific differentially expressed genes (DEGs; FDR<0.05) induced by TMAO feeding in macrophage subtypes. DEGs unique to a cell type are highlighted in red in the upset plot and histogram, and shared DEGs are indicated in black. The histogram above each plot indicates the DEG counts for each category. DEG direction is indicated by the color of the gene name: red: upregulated, blue: downregulated. G , Top representative pathways from Reactome enriched for vSMC-derived macrophage DEGs (FDR<0.05). ECM indicates extracellular matrix; Max, maximum expression; Min, minimum expression; and Trem2 + , foamy Trem2 + macrophages.

    Journal: Arteriosclerosis, Thrombosis, and Vascular Biology

    Article Title: Trimethylamine- N -Oxide Affects Cell Type–Specific Pathways and Networks in Mouse Aorta to Promote Atherosclerotic Plaque Vulnerability

    doi: 10.1161/ATVBAHA.125.323047

    Figure Lengend Snippet: Identification of macrophage subtypes and differences in vascular smooth muscle cells (vSMC)–derived macrophages with trimethylamine- N -oxide (TMAO). A through C , Uniform Manifold Approximation and Projection (UMAP) of macrophage subclusters in normal laboratory (NL), high-cholesterol (HC), and HC+TMAO conditions, respectively. D , Subcluster-specific expression of previously known macrophage subtype markers. E , Proportions of macrophage subtypes within total macrophage number recovered for each diet condition in order of abundance. Statistical significance was determined by unpaired t test. false discovery rate (FDR) was calculated with Benjamini-Hochberg. F , Shared and cell type–specific differentially expressed genes (DEGs; FDR<0.05) induced by TMAO feeding in macrophage subtypes. DEGs unique to a cell type are highlighted in red in the upset plot and histogram, and shared DEGs are indicated in black. The histogram above each plot indicates the DEG counts for each category. DEG direction is indicated by the color of the gene name: red: upregulated, blue: downregulated. G , Top representative pathways from Reactome enriched for vSMC-derived macrophage DEGs (FDR<0.05). ECM indicates extracellular matrix; Max, maximum expression; Min, minimum expression; and Trem2 + , foamy Trem2 + macrophages.

    Article Snippet: Human immortalized coronary artery vSMCs (gift from Dr Clint Miller, University of Virginia, Charlottesville, VA) and human primary aortic vSMCs (PCS-100-012; ATCC) were cultured in vSMC growth medium with premixed supplements (catalog no. C-22062; PromoCell).

    Techniques: Derivative Assay, Expressing

    Trimethylamine-N-oxide (TMAO) alters cell-cell communications between major cell types involved in atherosclerosis progression. A , Predicted differential number of interactions between sender (rows) and receiver (columns) cell types comparing high-cholesterol (HC)+TMAO and HC by CellChat. In the heatmap, red represents increased signaling with TMAO feeding, and blue represents decreased signaling. B , Predicted differential number of interactions in the cell-cell communication network between HC+TMAO and HC by CellChat. The color of the network edges represents increased (red) or decreased (blue) signaling with TMAO feeding. C , Specific incoming and outgoing signaling pathways predicted to change in modulated vascular smooth muscle cells (vSMCs) between HC+TMAO and HC by CellChat. Signaling pathways increased and decreased as both incoming and outgoing signals are highlighted in red and blue, respectively. D , Top ligands predicted by NicheNet to target the modulated vSMC differentially expressed gene (DEGs) involved in apoptosis or ECM (extracellular matrix) organization. E , Top ligands predicted by NicheNet to target the vSMC-derived macrophage and Trem2 + macrophage DEGs. In D and E , DEG direction is indicated by red (upregulated with TMAO) or blue (downregulated with TMAO). Mac indicates macrophage; and Mod, vSMC, modulated vSMC.

    Journal: Arteriosclerosis, Thrombosis, and Vascular Biology

    Article Title: Trimethylamine- N -Oxide Affects Cell Type–Specific Pathways and Networks in Mouse Aorta to Promote Atherosclerotic Plaque Vulnerability

    doi: 10.1161/ATVBAHA.125.323047

    Figure Lengend Snippet: Trimethylamine-N-oxide (TMAO) alters cell-cell communications between major cell types involved in atherosclerosis progression. A , Predicted differential number of interactions between sender (rows) and receiver (columns) cell types comparing high-cholesterol (HC)+TMAO and HC by CellChat. In the heatmap, red represents increased signaling with TMAO feeding, and blue represents decreased signaling. B , Predicted differential number of interactions in the cell-cell communication network between HC+TMAO and HC by CellChat. The color of the network edges represents increased (red) or decreased (blue) signaling with TMAO feeding. C , Specific incoming and outgoing signaling pathways predicted to change in modulated vascular smooth muscle cells (vSMCs) between HC+TMAO and HC by CellChat. Signaling pathways increased and decreased as both incoming and outgoing signals are highlighted in red and blue, respectively. D , Top ligands predicted by NicheNet to target the modulated vSMC differentially expressed gene (DEGs) involved in apoptosis or ECM (extracellular matrix) organization. E , Top ligands predicted by NicheNet to target the vSMC-derived macrophage and Trem2 + macrophage DEGs. In D and E , DEG direction is indicated by red (upregulated with TMAO) or blue (downregulated with TMAO). Mac indicates macrophage; and Mod, vSMC, modulated vSMC.

    Article Snippet: Human immortalized coronary artery vSMCs (gift from Dr Clint Miller, University of Virginia, Charlottesville, VA) and human primary aortic vSMCs (PCS-100-012; ATCC) were cultured in vSMC growth medium with premixed supplements (catalog no. C-22062; PromoCell).

    Techniques: Protein-Protein interactions, Derivative Assay

    F actin is reduced in diabetic CRMs: (A) F actin content in control and diabetic mouse coronary VSMCs obtained via staining with phalloidin. (B) G actin levels in control and T2DM mouse coronary VSMCs attained through staining with DNase. (C) F/G actin ratio of mouse normal and diabetic coronary VSMCs. (D) Representative images from Db/db (top) and db/db (bottom). Data are mean ± SEM. **p ≤ 0.005. n = 3 per group.

    Journal: Frontiers in Physiology

    Article Title: Coronary cytoskeletal modulation of coronary blood flow in the presence and absence of type 2 diabetes: the role of cofilin

    doi: 10.3389/fphys.2025.1561867

    Figure Lengend Snippet: F actin is reduced in diabetic CRMs: (A) F actin content in control and diabetic mouse coronary VSMCs obtained via staining with phalloidin. (B) G actin levels in control and T2DM mouse coronary VSMCs attained through staining with DNase. (C) F/G actin ratio of mouse normal and diabetic coronary VSMCs. (D) Representative images from Db/db (top) and db/db (bottom). Data are mean ± SEM. **p ≤ 0.005. n = 3 per group.

    Article Snippet: Deidentified normal and T2DM human primary coronary VSMCs were obtained from both Lonza (Morristown, NJ) and ATCC (Manassas, VA).

    Techniques: Control, Staining

    Cofilin is increased in T2DM coronary microvessels: (A) Proteomics analysis of cofilin spectral hits in the normal CRMs db/db CRMs. (B) Cofilin protein expression obtained via western blot analysis in the coronary VSMCs of normal and diabetic human patients. Data are mean ± SEM. p-values are presented on the graph and *p < 0.05 and ****p ≤ 0.0001. n = 3-5 per group.

    Journal: Frontiers in Physiology

    Article Title: Coronary cytoskeletal modulation of coronary blood flow in the presence and absence of type 2 diabetes: the role of cofilin

    doi: 10.3389/fphys.2025.1561867

    Figure Lengend Snippet: Cofilin is increased in T2DM coronary microvessels: (A) Proteomics analysis of cofilin spectral hits in the normal CRMs db/db CRMs. (B) Cofilin protein expression obtained via western blot analysis in the coronary VSMCs of normal and diabetic human patients. Data are mean ± SEM. p-values are presented on the graph and *p < 0.05 and ****p ≤ 0.0001. n = 3-5 per group.

    Article Snippet: Deidentified normal and T2DM human primary coronary VSMCs were obtained from both Lonza (Morristown, NJ) and ATCC (Manassas, VA).

    Techniques: Expressing, Western Blot

    Cofilin knockdown causes altered F/G actin ratio and a significant increase in stiffness in human coronary VSMCs: (A) F/G actin ratio of normal and diabetic combined human coronary VSMCs treated with cofilin siRNA obtained via staining F actin (phalloidin) and G actin (DNase). (B) F/G actin ratio of cofilin siRNA treated normal coronary VSMCs. (C) F/G actin ratio of human diabetic coronary VSMCs treated with cofilin siRNA. (D) Elastic modulus (E inc ) of normal and diabetic combined human coronary VSMCs treated with cofilin siRNA acquired via atomic force microscopy. (E) Elastic modulus of cofilin siRNA treated human normal coronary VSMCs. (F) Elastic modulus of human diabetic coronary VSMCs treated with cofilin siRNA. Data are mean ± SEM. *p < 0.05. n = 4-8 per group.

    Journal: Frontiers in Physiology

    Article Title: Coronary cytoskeletal modulation of coronary blood flow in the presence and absence of type 2 diabetes: the role of cofilin

    doi: 10.3389/fphys.2025.1561867

    Figure Lengend Snippet: Cofilin knockdown causes altered F/G actin ratio and a significant increase in stiffness in human coronary VSMCs: (A) F/G actin ratio of normal and diabetic combined human coronary VSMCs treated with cofilin siRNA obtained via staining F actin (phalloidin) and G actin (DNase). (B) F/G actin ratio of cofilin siRNA treated normal coronary VSMCs. (C) F/G actin ratio of human diabetic coronary VSMCs treated with cofilin siRNA. (D) Elastic modulus (E inc ) of normal and diabetic combined human coronary VSMCs treated with cofilin siRNA acquired via atomic force microscopy. (E) Elastic modulus of cofilin siRNA treated human normal coronary VSMCs. (F) Elastic modulus of human diabetic coronary VSMCs treated with cofilin siRNA. Data are mean ± SEM. *p < 0.05. n = 4-8 per group.

    Article Snippet: Deidentified normal and T2DM human primary coronary VSMCs were obtained from both Lonza (Morristown, NJ) and ATCC (Manassas, VA).

    Techniques: Knockdown, Staining, Microscopy

    Cofilin siRNA disrupts the F/G actin ratio and increases stiffness in mouse coronary VMSCs: (A) F/G actin ratio of mouse normal and diabetic combined coronary VSMCs treated with cofilin siRNA obtained via staining F actin (phalloidin) and G actin (DNase). (B) Normal control mouse coronary VSMC F/G actin ratio after cofilin siRNA treatment. (C) F/G actin ratio of mouse diabetic coronary VSMCs treated with cofilin siRNA. (D) Normal and diabetic combined mouse coronary VSMCs treated with cofilin siRNA elastic modulus (E inc ) data obtained using atomic force microscopy. (E) Elastic modulus of cofilin siRNA treated normal control mouse coronary VSMCs. (F) Elastic modulus of mouse diabetic coronary VSMCs treated with cofilin siRNA. Data are mean ± SEM. **p < 0.005, ***p < 0.0005, and ****p < 0.0001 vs. respective scramble control. n = 2–10 per group.

    Journal: Frontiers in Physiology

    Article Title: Coronary cytoskeletal modulation of coronary blood flow in the presence and absence of type 2 diabetes: the role of cofilin

    doi: 10.3389/fphys.2025.1561867

    Figure Lengend Snippet: Cofilin siRNA disrupts the F/G actin ratio and increases stiffness in mouse coronary VMSCs: (A) F/G actin ratio of mouse normal and diabetic combined coronary VSMCs treated with cofilin siRNA obtained via staining F actin (phalloidin) and G actin (DNase). (B) Normal control mouse coronary VSMC F/G actin ratio after cofilin siRNA treatment. (C) F/G actin ratio of mouse diabetic coronary VSMCs treated with cofilin siRNA. (D) Normal and diabetic combined mouse coronary VSMCs treated with cofilin siRNA elastic modulus (E inc ) data obtained using atomic force microscopy. (E) Elastic modulus of cofilin siRNA treated normal control mouse coronary VSMCs. (F) Elastic modulus of mouse diabetic coronary VSMCs treated with cofilin siRNA. Data are mean ± SEM. **p < 0.005, ***p < 0.0005, and ****p < 0.0001 vs. respective scramble control. n = 2–10 per group.

    Article Snippet: Deidentified normal and T2DM human primary coronary VSMCs were obtained from both Lonza (Morristown, NJ) and ATCC (Manassas, VA).

    Techniques: Staining, Control, Microscopy

    Latrunculin B treatment of coronary VSMCs significantly reduces cellular stiffness: (A) Elastic modulus acquired via atomic force microscopy of LatB treated normal and diabetic human coronary VSMCs. (B) LatB treated mouse normal and diabetic coronary VSMC elastic modulus. Data are mean ± SEM. *p < 0.05, **p < 0.005, ***p < 0.0005, and ****p < 0.0001. n = 2-5 per group.

    Journal: Frontiers in Physiology

    Article Title: Coronary cytoskeletal modulation of coronary blood flow in the presence and absence of type 2 diabetes: the role of cofilin

    doi: 10.3389/fphys.2025.1561867

    Figure Lengend Snippet: Latrunculin B treatment of coronary VSMCs significantly reduces cellular stiffness: (A) Elastic modulus acquired via atomic force microscopy of LatB treated normal and diabetic human coronary VSMCs. (B) LatB treated mouse normal and diabetic coronary VSMC elastic modulus. Data are mean ± SEM. *p < 0.05, **p < 0.005, ***p < 0.0005, and ****p < 0.0001. n = 2-5 per group.

    Article Snippet: Deidentified normal and T2DM human primary coronary VSMCs were obtained from both Lonza (Morristown, NJ) and ATCC (Manassas, VA).

    Techniques: Microscopy

    Latrunculin B increases CBF: (A) Baseline CBF obtained from normal and T2DM hearts ex vivo on the Langendorff perfusion system. (B) Peak responses to ML-7 and ML-7 + LatB of ex vivo heart on Langendorff perfusion system. Data are mean ± SEM. *p < 0.05, **p < 0.005. n = 11 per group.

    Journal: Frontiers in Physiology

    Article Title: Coronary cytoskeletal modulation of coronary blood flow in the presence and absence of type 2 diabetes: the role of cofilin

    doi: 10.3389/fphys.2025.1561867

    Figure Lengend Snippet: Latrunculin B increases CBF: (A) Baseline CBF obtained from normal and T2DM hearts ex vivo on the Langendorff perfusion system. (B) Peak responses to ML-7 and ML-7 + LatB of ex vivo heart on Langendorff perfusion system. Data are mean ± SEM. *p < 0.05, **p < 0.005. n = 11 per group.

    Article Snippet: Deidentified normal and T2DM human primary coronary VSMCs were obtained from both Lonza (Morristown, NJ) and ATCC (Manassas, VA).

    Techniques: Ex Vivo