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Cell Applications Inc
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ScienCell
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Lonza
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ScienCell
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ScienCell
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KU Leuven
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Lonza
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InSCREENeX gmbh
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Primary Human Umbilical Endothelial Cells isolated from the arteries of the umbilical cord. Primary Human Umbilical Artery Endothelial Cells (HUAEC) are isolated from the arteries of the umbilical cord and are often used for in
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Image Search Results
Journal: British Journal of Pharmacology
Article Title: Enhanced serelaxin signalling in co‐cultures of human primary endothelial and smooth muscle cells
doi: 10.1111/bph.13371
Figure Lengend Snippet: cGMP accumulation in co‐cultures of human primary vascular smooth muscle cells following addition of serelaxin to endothelium. HUAEC , HUVEC or HCAEC were co‐cultured with (A) HUASMC or (B) HUVSMC (all n = 5), and the ECs were treated with serelaxin for 30 min. Serelaxin addition to HUAEC did not cause cGMP accumulation in HUAEC (▲) (C) HUASMC (□) or (D) HUVSMC (◯) co‐cultured with HUAEC, whereas direct stimulation of either (C) HUASMC (n = 5) or (D) HUVSMC with serelaxin caused a concentration‐dependent increase in cGMP accumulation (dashed lines). In contrast, serelaxin addition to HUVEC concentration‐dependently increased cGMP accumulation not only in HUVEC (■) but also in (E) HUASMC (□) or (F) HUVSMC (◯) co‐cultured with HUVEC with the responses in smooth muscle cells being greater or in the case of HUVSMC much greater than cGMP responses to direct stimulation of (E) HUASMC or (F) HUVSMC (dashed lines). A similar pattern of cGMP accumulation was observed with (G, H) HCAEC (●) and (G) HUASMC (□) or (H) HUVSMC (◯) co‐cultured with HCAEC.
Article Snippet: Primary cultures of human
Techniques: Cell Culture, Concentration Assay
Journal: British Journal of Pharmacology
Article Title: Enhanced serelaxin signalling in co‐cultures of human primary endothelial and smooth muscle cells
doi: 10.1111/bph.13371
Figure Lengend Snippet: cAMP accumulation in co‐cultures of human primary vascular smooth muscle cells following addition of serelaxin to endothelium (all n = 5). HUAEC, HUVEC or HCAEC were co‐cultured with (A) HUASMC or (B) HUVSMC, and the endothelial cells were treated with serelaxin for 30 min. Serelaxin added to HUAEC did not cause cAMP accumulation either in (C, D) HUAEC (▲), (C) HUASMC (□) or (D) HUVSMC (◯), whereas direct stimulation of (C) HUASMC or (D) HUVSMC with serelaxin caused a concentration‐dependent increase in cAMP accumulation (dashed lines). Although direct addition of serelaxin to HUVEC concentration‐dependently increased cAMP accumulation in (E, F) HUVEC (■), there was no significant effect on cAMP accumulation in (E) HUASMC (□) or (F) HUVSMC (◯). Direct addition of serelaxin to (E) HUASMC or (F) HUVSMC stimulated cAMP accumulation (dashed lines). Serelaxin concentration‐dependently increased cAMP accumulation in (G, H) HCAEC (●) but also caused a robust concentration‐dependent increase in cAMP accumulation in both (G) HUASMC (□) and (H) HUVSMC (◯).
Article Snippet: Primary cultures of human
Techniques: Cell Culture, Concentration Assay
Journal: Experimental and Therapeutic Medicine
Article Title: Pterostilbene reduces endothelial cell injury in vascular arterial walls by regulating the Nrf2-mediated AMPK/STAT3 pathway in an atherosclerosis rat model
doi: 10.3892/etm.2019.8211
Figure Lengend Snippet: Pts decreases H 2 O 2 -induced cytotoxicity in endothelial cells. (A) Effect of Pts on cell viability in H 2 O 2 -induced endothelial cell cytotoxicity. (B) Oxidative stress injury induces ROS production and NO generation in endothelial cells treated with Pts and PBS. (C) Expression levels of antioxidant proteins SOD, CAT and HO-1 in endothelial cells. (D) Apoptosis of endothelial cells in Pts and control groups. *P<0.05 and **P<0.01 vs. control. CAT, catalase; H 2 O 2 , hydrogen peroxide; HO-1, heme oxygenase-1; NO, nitric oxide; Pts, pterostilbene; ROS, reactive oxygen species; SOD, superoxide dismutase.
Article Snippet:
Techniques: Expressing, Control
Journal: Experimental and Therapeutic Medicine
Article Title: Pterostilbene reduces endothelial cell injury in vascular arterial walls by regulating the Nrf2-mediated AMPK/STAT3 pathway in an atherosclerosis rat model
doi: 10.3892/etm.2019.8211
Figure Lengend Snippet: Pts inhibits the Nrf2-mediated AMPK/STAT3 pathway in endothelial cells. (A) Effect of Pts on Nrf2, AMPK, pAMPK, STAT3 and pSTAT3 levels in endothelial cells. (B) Effects of Nrf2 knockdown on Pts-regulated AMPK, pAMPK, STAT3 and pSTAT3 levels in endothelial cells. **P<0.01. AMPK, 5′ adenosine monophosphate-activated protein kinase; Nrf2, nuclear factor erythroid 2-related factor 2; p, phosphorylated; Pts, pterostilbene; STAT3, signal transducer and activator of transcription 3; ns, not significant; NC, negative control; si, small interfering RNA.
Article Snippet:
Techniques: Knockdown, Negative Control, Small Interfering RNA
Journal: Experimental and Therapeutic Medicine
Article Title: Pterostilbene reduces endothelial cell injury in vascular arterial walls by regulating the Nrf2-mediated AMPK/STAT3 pathway in an atherosclerosis rat model
doi: 10.3892/etm.2019.8211
Figure Lengend Snippet: Effect of si-Nrf2 and Pts on oxidative stress injury and apoptosis in endothelial cells. (A) Effects of Nrf2 knockdown on Pts-regulated SOD, CAT and HO-1 protein expression in endothelial cells. (B) Effects of Nrf2 knockdown on apoptosis in endothelial cells. **P<0.01. CAT, catalase; HO-1, heme oxygenase-1; Nrf2, nuclear factor erythroid 2-related factor 2; Pts, pterostilbene; si, small interfering RNA; SOD, superoxide dismutase; NC, negative control; ns, not significant.
Article Snippet:
Techniques: Knockdown, Expressing, Small Interfering RNA, Negative Control