COX-2 is associated with cadmium-induced ICAM-1 expression in cerebrovascular endothelial cells

Seok, Sun Mi; Park, Dong Hyun; Kim, Young Chae; Moon, Chang Hyun; Jung, Yi Sook; Baik, Eun Joo; Moon, Chang Kiu; Lee, Soo Hwan

doi:10.1016/j.toxlet.2006.04.007

Cited by 34 publications

(32 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…4). In our previous report, however, only p38 MAPK, but not JNK or ERK, was activated by Cd in bEnd.3 cells (Seok et al, 2006). The reason for such discrepant results in the same cell line is due to treating cells with different concentrations of Cd; much lower Cd concentration (2 μM) was used and time points later than 4 h were not studied in our previous study.…”

Section: Discussionmentioning

confidence: 72%

Cadmium induces apoptotic cell death through p38 MAPK in brain microvessel endothelial cells

Jeong¹,

Park²,

Kim³

et al. 2008

European Journal of Pharmacology

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 72%

Cadmium induces apoptotic cell death through p38 MAPK in brain microvessel endothelial cells

Jeong¹,

Park²,

Kim³

et al. 2008

European Journal of Pharmacology

View full text Add to dashboard Cite

“…Prozialeck11 suggested E-cadherin, a C ++ -binding protein localized at the junctions between vascular endothelial cells, as a target for Cd toxicity. Cd is also able to induce the expression of intercellular adhesion molecule 1, an adhesion molecule playing an important role in inflammation 12. Furthermore, Cd was shown to indirectly generate superoxide and hydroxyl radicals 13.…”

Section: Introductionmentioning

confidence: 99%

Blood and urine levels of heavy metal pollutants in female and male patients with coronary artery disease

Sponder

Fritzer‐Szekeres

Marculescu

et al. 2014

VHRM

View full text Add to dashboard Cite

BackgroundHeavy metal pollutants such as cadmium (Cd), lead (Pb), and mercury (Hg) are rarely the subjects of cardiovascular research although they have been suspected for decades to negatively impact the circulatory system.MethodsApart from detailed anamnestic data, urinary levels of Cd and full blood levels of Pb and Hg were measured in 53 female (mean age: 68.04±7.03 years) and 111 male (mean age: 60.68±11.43 years) nonsmoking or never-smoking patients with angiographically verified and precisely quantified coronary artery disease (CAD).ResultsAlthough Cd was quantifiable in 68.3% of subjects, only 34.1% of these patients exceeded the critical 1 μg/L Human Biomonitoring (HBM)-I level. Median Pb (20 μg/L) and Hg (0.55 μg/L) levels were lower than the HBM-I, as well as reference levels of Pb. Wine consumption was the main source for Pb, fish and wine consumption for Hg, and previous nicotine abuse for Cd. There was no correlation between Cd, Pb, or Hg and severity of CAD although severity correlated positively with atherosclerosis parameters (uric acid, creatinine, triglycerides, blood urea nitrogen, C-reactive protein) and negatively with high density lipoprotein cholesterol.ConclusionCd levels detected in CAD patients were high compared to German and European reference levels but it could not be proven that urine levels of Cd and blood levels of Hg or Pb played a major role in the genesis of CAD, particularly when compared to well-known biomarkers such as blood pressure, glucose, and lipids.

show abstract

“…We previously have demonstrated that Cd induces ICAM-1 expression possibly through p38 mitogenactivated protein kinase (MAPK) activation in bEnd.3 cells (2,3), suggesting that ICAM-1 expression may be associated with inflammatory injury in the blood brain barrier (BBB). In this study, we investigated the effect of Cd on the expression VCAM-1 and its underlying mechanism, especially focusing on MAPKs signaling pathways.…”

mentioning

confidence: 99%

“…Chronic exposure to Cd (10 µg/ml) has been demonstrated to induce BBB dysfunction and increase BBB permeability in rats (8). Indeed, ICAM-1 has been reported to increase in bEnd.3 cells, implicating its potential role in Cd-induced BBB endothelial dysfunction (2,3). Furthermore, the present study demonstrates that 3 -10 µM Cd increases the expression of the VCAM-1 at both the protein and mRNA levels in a dose-and time-dependent manner in bEnd.3 cells.…”

mentioning

confidence: 99%

Cadmium Stimulates the Expression of Vascular Cell Adhesion Molecule-1 (VCAM-1) via p38 Mitogen-Activated Protein Kinase (MAPK) and JNK Activation in Cerebrovascular Endothelial Cells

et al. 2009

View full text Add to dashboard Cite

Abstract. In this study, we examined the effect of Cd on the expression of vascular cell adhesion molecule-1 (VCAM-1) and its mechanisms in bEnd.3 cells. The treatment with Cd increased protein and mRNA expressions of VCAM-1 and increased the phosphorylations of p38, JNK, and ERK. The Cd-induced VCAM-1 expression was significantly suppressed by either a specific p38 mitogen-activated protein kinase (MAPK) inhibitor (SB202190) or a JNK inhibitor (SP600125), but not by an ERK inhibitor (U0126). These results suggest that Cd induces the expression of VCAM-1, at least in part, via p38 and JNK pathways in bEnd.3 cells.

show abstract

COX-2 is associated with cadmium-induced ICAM-1 expression in cerebrovascular endothelial cells

Cited by 34 publications

References 40 publications

Cadmium induces apoptotic cell death through p38 MAPK in brain microvessel endothelial cells

Cadmium induces apoptotic cell death through p38 MAPK in brain microvessel endothelial cells

Blood and urine levels of heavy metal pollutants in female and male patients with coronary artery disease

Cadmium Stimulates the Expression of Vascular Cell Adhesion Molecule-1 (VCAM-1) via p38 Mitogen-Activated Protein Kinase (MAPK) and JNK Activation in Cerebrovascular Endothelial Cells

Contact Info

Product

Resources

About