小陷胸汤加味含药血清对人脐静脉内皮细胞分泌NO/ET-1的调节作用

目的:探讨小陷胸汤加味中药方对血管内皮细胞的保护作用。方港:建立ox-LDL损伤人脐静脉内皮细胞株(ECV-304)模型,用小陷胸汤加味含药血清处理模型,并用放免和硝酸酶还原法在药物干预6h和24h后检测细胞上清液中ET-1和NO含量。结果:100 μg/ml的ox-LDL可损伤血管内皮细胞并导致其分泌NO和ET-1功能失调,小陷胸汤加味含药血清通过影响NO/ET-1的分泌而明显改善此失调状态。结论:小陷胸汤加味中药通过调节NO/ET-1水平显著拮抗ox-LDL对血管内皮细胞损害,具有防治AS的作用。     

Expression and function of vascular endothelial growth factor receptors (Flt-1 and Flk-1) in vascular adventitial fibroblasts

Vascular endothelial growth factor receptors (VEGFRs) are previously considered to exist exclusively in endothelial cells. However, little is known if the receptors are expressed in other non-endothelial cells. In this study, we measured activation of two VEGFRs, Flk-1 and Flt-1, and their biological functions in cultured adventitial fibroblasts and injured rat carotid injury arteries induced by balloon angioplasty. Our results indicated that Flt-1, but not Flk-1, existed in adventitial fibroblasts. Angiotensin II increased Flt-1 protein expression in a time- and concentration-dependent manner. Adventitial fibroblast migration stimulated by vascular endothelial growth factor (VEGF) and placental growth factor (PIGF) required Flt-1 expression. The Flt-1-induced adventitial fibroblast migration was blocked by anti-Flt-1 neutralizing antibody and soluble VEGFR1 protein (sFlt-1). However, Flt-1 activation did not enhance cell proliferation. In addition, Flt-1 expression was significantly increased in the neointima and adventitia in injured rat carotid arteries. We concluded that functional expression of Flt-1 in adventitial fibroblasts might be an important mediator in the pathogenesis of vascular remodeling after arterial injury.     

Cellular senescence determines endothelial cell damage induced by uremia

Renal dysfunction is closely associated with endothelial damage leading to cardiovascular disease. However, the extent to which endothelial damage induced by uremia is modulated by aging is poorly known. Aging can render endothelial cells more susceptible to apoptosis through an oxidative stress-dependent pathway. We examined whether senescence-associated to oxidative stress determines the injury induced by the uremia in endothelial cells.     

A large mobility of hydrophilic molecules at the outmost layer controls the protein adsorption and adhering behavior with the actin fiber orientation of human umbilical vein endothelial cells (HUVEC)

Adhesion behaviors of human umbilical vein endothelial cells (HUVECs) are interestingly affected by the mobility of hydrophilic chains on the material surfaces. Surfaces with different molecular mobilities were prepared using ABA-type block copolymers consisting polyrotaxane (PRX) or poly(ethylene glycol) (PEG) central block (A block), and amphiphilic anchoring B blocks of poly(2-methacryloyloxyethyl phosphorylcholine-co-n-butyl methacrylate) (PMB). Two different molecular mobilities of the PRX chains were designed by using normal α-cyclodextrin (α-CD) or α-CD whose hydroxyl groups were converted to methoxy groups in a given ratio to improve its molecular mobility (PRX–PMB and OMe-PRX–PMB). The surface mobility of these materials was assessed as the mobility factor (Mf), which is measured by quartz crystal microbalance with dissipation monitoring system. HUVECs adhered on OMe-PRX–PMB surface much more than PRX–PMB and PMB-block–PEG–block-PMB (PEG–PMB) surfaces. These different HUVEC adhesions were correlated with the density of cell-binding site of adsorbed fibronectin. In addition, the alignment of the actin cytoskeleton of adhered HUVECs was strongly suppressed on the PEG–PMB, PRX–PMB, and OMe-PRX–PMB in response to the increased Mf value. Remarkably, the HUVECs adhered on the OMe-PRX–PMB surface with much less actin organization. We concluded that not only the cell adhesion but also the cellular function are regulated by the molecular mobility of the outmost material surfaces.     

汉滩病毒感染诱导血管内皮细胞多糖包被损伤及其机制初步研究

目的 探讨汉滩病毒(hantaan virus,HTNV)感染血管内皮细胞致多糖包被(glycocalyx,GCX)损伤的分子机制.方法 利用HTNV感染人脐静脉血管内皮细胞(human umbilical vein endothelial cells,HUVECs),在感染不同时间段,ELISA检测细胞上清中GCX组...     

Discovery of a New Series of Naphthamides as Potent VEGFR-2 Kinase Inhibitors

相似文献   

Bisphosphonates affect migration ability and cell viability of HUVEC,fibroblasts and osteoblasts in vitro

Oral Diseases (2011) 17 , 194–199 Objectives: Bisphosphonate‐associated osteonecrosis of the jaw (BP‐ONJ) is a side effect in patients being treated with bisphosphonates. The bisphosphonates most often associated with BP‐ONJ are the highly potent nitrogen‐containing bisphosphonates, e.g. pamidronate or zoledronate. In terms of BP‐ONJ aetiology, several theories are being discussed: inhibition of bone remodelling, effect on soft tissues, and antiangiogenic effect of bisphosphonates. The aim of this in vitro study was to investigate the effect of different potent bisphosphonates on osteoblasts, fibroblasts and human umbilicord vein endothelial cells (HUVEC). Materials and methods: Three nitrogen‐containing bisphosphonates (ibandronate, pamidronate and zoledronate) and one non‐nitrogen‐containing bisphosphonate (clodronate) were compared concerning their potency on apoptosis induction (tunel), cell viability (calcein assay) and migration potency (boyden chamber) on osteoblasts, fibroblasts and HUVEC. Results: The nitrogen‐containing bisphosphonates, particularly pamidronate and zoledronate, affect cell viability, cell migration and the induction of apoptosis of osteoblasts, fibroblasts and HUVEC. Conclusions: These results support the theory that BP‐ONJ is a multifactorially caused disease because several cell lines of the oral cavity which are responsible for integrity and wound healing are negatively affected by nitrogen‐containing bisphosphonates. Perioperative interruption of bisphosphonate application during dental surgical procedures – if possible – might be feasible to promote better wound healing.     

腺苷对人静脉内皮细胞增殖的影响

目的探讨腺苷对人脐静脉内皮细胞（human umbilical vein endothelial cell，HUVEC）增殖的影响。方法MTT法观察腺苷的最佳作用浓度及最佳作用时问。结果4％FBS浓度下，腺苷具有明显的促HUVEC增殖作用，为最佳浓度。在10-^4 mol／L腺苷终浓度对细胞增殖有明显的促进作用，为最佳腺苷浓度。腺苷的促生艮作用在24h即出现，在48h已达到较高水平。结论在血供基本被阻断或血流基本正常的情况下，腺苷可能对细胞增殖尤影响；但在m流减少的情况下，腺苷的应用可以促进内皮细胞增殖，可能对血管新生有启动作用。     

Aldosterone and amiloride alter ENaC abundance in vascular endothelium

The amiloride-sensitive epithelial sodium channel (ENaC) is usually found in the apical membrane of epithelial cells but has also recently been described in vascular endothelium. Because little is known about the regulation and cell surface density of ENaC, we studied the influence of aldosterone, spironolactone, and amiloride on its abundance in the plasma membrane of human endothelial cells. Three different methods were applied, single ENaC molecule detection in the plasma membrane, quantification by Western blotting, and cell surface imaging using atomic force microscopy. We found that aldosterone increases the surface expression of ENaC molecules by 36% and the total cellular amount by 91%. The aldosterone receptor antagonist spironolactone prevents these effects completely. Acute application of amiloride to aldosterone-pretreated cells led to a decline of intracellular ENaC by 84%. We conclude that, in vascular endothelium, aldosterone induces ENaC expression and insertion into the plasma membrane. Upon functional blocking with amiloride, the channel disappears from the cell surface and from intracellular pools, indicating either rapid degradation and/or membrane pinch-off. This opens new perspectives in the regulation of ENaC expressed in the vascular endothelium.     

Comparative study of adhesion molecule expression in cultured human macro- and microvascular endothelial cells

Culture systems as models for disease are only valid as long as they are comparable to in vivo conditions. The phenotype of cultured endothelial cells (ECs) has only been sporadically compared to the corresponding phenotype in vivo. Thus, we compared by immunolocalization the endothelial expression of ICAM-1, VCAM, and E-selectin in vivo in stimulated/unstimulated human umbilical vein endothelial cells (HUVEC) as a model for macrovascular ECs and stimulated/unstimulated HPMEC (human pulmonary microvessel endothelial cells) as a model for pulmonary microvascular ECs with that in human lungs in vivo (normal and ARDS). Proinflammatory stimuli in vitro were used to stimulate conditions relevant for ARDS. ICAM-1 expression in stimulated HUVEC/HPMEC correlated well with in vivo expression (macro- and microvessels). For E-selectin, the staining pattern in macro/microvessels correlated moderately with unstimulated and well with stimulated HUVEC/HPMEC. For VCAM a good correlation was found for stimulated/unstimulated HUVEC and unstimulated HPMEC. The expression patterns in stimulated HUVEC corresponded well for all three molecules with those in vivo. Thus, the expression patterns in vitro are only partially transferable to in vivo conditions. The study suggests that E-selectin- and VCAM-coated beads could potentially serve in the isolation process of arteriolar and venular ECs.