Dehydroepiandrosterone inhibits the proliferation of human umbilical vein endothelial cells by enhancing the expression of p53 and p21, restricting the phosphorylation of retinoblastoma protein, and is androgen‐ and estrogen‐receptor independent

Zapata, Estrella; Ventura, Josep L.; Cruz, Karina De la; Rodríguez, Enrique; Damian, Pablo Fernando Barbosa; Massó, Felipe; Montaño, Luis F.; López‐Marure, Rebeca

doi:10.1111/j.1742-4658.2005.04563.x

Cited by 43 publications

(32 citation statements)

References 54 publications

(67 reference statements)

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“…Id1 has been reported to inhibit the tumor-suppressor protein p53, 22 which is regulated by ox-LDL, 31 and p53 inhibits cell proliferation. 28 We therefore examined whether p53 accumulated in the nucleus after treatment with ox-LDL. Nuclear localization of p53 was markedly up-regulated at 24 h after exposure to 40 and 100 lg mL 21 ox-LDL (Figs.…”

Section: Ox-ldl Enhances P53 Protein Nuclear Localization In Human Ecmentioning

confidence: 99%

Coordination of Id1 and p53 Activation by Oxidized LDL Regulates Endothelial Cell Proliferation and Migration

et al. 2011

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Considering that oxidized low-density lipoprotein (ox-LDL) may inhibit endothelial cell (EC) migration and proliferation during endothelialization, we hypothesize that the Id1 protein promotes endothelialization exposed to ox-LDL. Cell proliferation was evaluated by cell counts, and cell migration was evaluated by wound closure assay. The role of Id1 in the cell migration and proliferation was appraised through building Id1 overexpression and silencing ECs. Here, we report that Id1 in human umbilical vascular ECs (HUVECs) was up-regulated by ox-LDL in a dose- and time-dependent manner. Low concentrations of ox-LDL increased the proliferation and migration of EC. High concentrations of ox-LDL suppressed HUVECs proliferation and migration, whose inhibitory effects were abolished by Id1 over-expression. Attenuated proliferation and migration of ECs exposed to high concentrations of ox-LDL may be correlated with the nuclear localization of p53, which was obviously weakened by over-expression of Id1 and strengthened by silencing Id1. Collectively, changes in EC, comprising proliferation and migration, upon exposure to various concentrations of ox-LDL are, at least in part, attributed to the modulatory effect of the Id1 protein, which suggests that manipulating Id1 protein activity may offer therapeutic opportunities to promote re-endothelialization under high concentrations of ox-LDL.

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Section: Ox-ldl Enhances P53 Protein Nuclear Localization In Human Ecmentioning

confidence: 99%

Coordination of Id1 and p53 Activation by Oxidized LDL Regulates Endothelial Cell Proliferation and Migration

et al. 2011

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“…HUVEC were derived from primary human endothelial cells by proteolytic dissociation of the umbilical cord veins from normal deliveries, by treatment with collagenase type II (0.2 mg/ml), and cultured on gelatin-coated culture dishes in medium M199 supplemented with 10% fetal bovine serum (FBS), glutamine (2 mM), heparin (1 mg/ml), and endothelial mitogen (20 μg/ml), as previously described (Zapata et al, 2005). Cells were used for experiments on their second passage.…”

Section: Culture Of Endothelial Cellsmentioning

confidence: 99%

PM_2.5and PM₁₀Induce the Expression of Adhesion Molecules and the Adhesion of Monocytic Cells to Human Umbilical Vein Endothelial Cells

Montiel-Dávalos

Alfaro-Moreno

López‐Marure

2007

Inhalation Toxicology

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Exposure to airborne particles has been associated with an increase in cardiopulmonary events. Endothelial cells could be playing an important role in the response to airborne particles due their involvement in proinflammatory events, and there is some evidence of particle translocation from lung into circulation. One of the initiating events of inflammation is endothelial activation. We determined the concentration-response effect of a particulate matter with different aerodynamic sizes (PM2.5 [particulate matter with aerodynamic diameter of 2.5 microm and less] and PM10 [particulate matter with aerodynamic diameter of 10 microm and less]) obtained from Mexico City on human umbilical vein endothelial cells (HUVEC). The adhesion of monocytic U937 cells to HUVEC and the expression of early (E- and P-selectins) and late (ICAM-1, PECAM-1, VCAM-1) adhesion molecules were tested. Adhesion of U937 cells to HUVEC was evaluated by coculture experiments using [3H]thymidine-labeled U937 cells and the expression of adhesion molecules was evaluated by flow cytometry. Tumor necrosis factor (TNF)-alpha was used as a positive control of endothelial activation. Our results showed that both PM2.5 and PM10 induced the adhesion of U937 cells to HUVEC, and their maximal effect was observed at 20 microg/cm2. This adhesion was associated with an increase in the expression of all adhesion molecules evaluated for PM10, and E-selectin, P-selectin, and ICAM-1 for PM2.5. In general, maximum expression of adhesion molecules induced by PM2.5 and PM10 was obtained with 20 microg/cm2; however, PM10-induced expression was observed from 5 microg/cm2. E-selectin and ICAM-1 had the strongest expression in response to particles. In conclusion, PM2.5 and PM10 induce the activation of HUVEC, leading to monocytic adhesion via the expression of adhesion molecules, suggesting that these particles may participate in the development of inflammatory diseases. The role of these events in the development of diseases such as atherosclerosis is likely to be evaluated.

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“…Cells were used within passages 4-10 and were identified as endothelial by their morphology and by uniform positive endoglin (CD105) surface antigen (BD Pharmigen) staining. Crystal violet stain allows the evaluation of cell viability as well as cellular proliferation in relation to the culture time [20,21]. Mitochondrial dehydrogenase activity was determined by the reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT, 5 mg/mL) in sterile PBS [22].…”

Section: Isolation and Culture Of Human Umbilical Vein Endothelial Cementioning

confidence: 99%

HUVECs from newborns with a strong family history of diabetes show diminished ROS synthesis in the presence of high glucose concentrations

Alvarado-Vásquez

Páez

Zapata

et al. 2006

Diabetes Metabolism Res

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Dehydroepiandrosterone inhibits the proliferation of human umbilical vein endothelial cells by enhancing the expression of p53 and p21, restricting the phosphorylation of retinoblastoma protein, and is androgen‐ and estrogen‐receptor independent

Cited by 43 publications

References 54 publications

Coordination of Id1 and p53 Activation by Oxidized LDL Regulates Endothelial Cell Proliferation and Migration

Coordination of Id1 and p53 Activation by Oxidized LDL Regulates Endothelial Cell Proliferation and Migration

PM_2.5and PM₁₀Induce the Expression of Adhesion Molecules and the Adhesion of Monocytic Cells to Human Umbilical Vein Endothelial Cells

HUVECs from newborns with a strong family history of diabetes show diminished ROS synthesis in the presence of high glucose concentrations

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Dehydroepiandrosterone inhibits the proliferation of human umbilical vein endothelial cells by enhancing the expression of p53 and p21, restricting the phosphorylation of retinoblastoma protein, and is androgen‐ and estrogen‐receptor independent

Cited by 43 publications

References 54 publications

Coordination of Id1 and p53 Activation by Oxidized LDL Regulates Endothelial Cell Proliferation and Migration

Coordination of Id1 and p53 Activation by Oxidized LDL Regulates Endothelial Cell Proliferation and Migration

PM2.5and PM10Induce the Expression of Adhesion Molecules and the Adhesion of Monocytic Cells to Human Umbilical Vein Endothelial Cells

HUVECs from newborns with a strong family history of diabetes show diminished ROS synthesis in the presence of high glucose concentrations

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PM_2.5and PM₁₀Induce the Expression of Adhesion Molecules and the Adhesion of Monocytic Cells to Human Umbilical Vein Endothelial Cells