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Increased expression of placenta growth factor in COPD.

Cheng SL, Wang HC, Yu CJ, Yang PC - Thorax (2008)

Bottom Line: Continuous concomitant treatment with PlGF, TNF-alpha and IL-8 stimulation reduced VEGF expression and induced cell death.This phenomenon was suppressed by VEGF receptor inhibitor (CBO-P11).Concomitant treatment with PlGF, TNF-alpha and IL-8 causes detrimental effects on airway epithelial cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, National Taiwan University Hospital, No. 7, Chung-Shan South Road, Taipei, Taiwan.

ABSTRACT

Background: Vascular endothelial growth factor (VEGF) and its receptor may have an important role in the pathogenesis of emphysema. The effect of another angiogenic factor, placenta growth factor (PlGF), in chronic obstructive pulmonary disease (COPD) is unknown.

Methods: The serum levels of VEGF and PlGF in patients with COPD (n = 184), smokers (n = 212) and non-smokers (n = 159) and the bronchoalveolar lavage (BAL) fluid levels of VEGF and PlGF in another group (20 patients with COPD, 18 controls) were measured. In vitro cell culture experiments were performed to investigate the effect of PlGF on VEGF.

Results: The mean (SE) serum levels of PlGF were significantly higher in patients with COPD than in controls (27.1 (7.4) pg/ml vs 12.3 (5.1) pg/ml in smokers and 10.8 (6.3) pg/ml in non-smokers, p = 0.005). The levels of PlGF in BAL fluid were also significantly higher in patients with COPD than in controls (45.7 (12.3) pg/ml vs 23.9 (7.6) pg/ml, p = 0.005), associated with an increase in the cytokines tumour necrosis factor-alpha (TNF-alpha) and interleukin-8 (IL-8). In patients with COPD the levels of PlGF correlated inversely with forced expiratory volume in 1 s (FEV(1)) in serum (r = -0.59, p = 0.002) and in BAL fluid (r = -0.51, p = 0.001). While the serum levels of VEGF were the same in patients with COPD and controls, the BAL fluid levels were significantly lower in patients with COPD than in controls (127.5 (30.1) pg/ml vs 237.8 (36.1) pg/ml, p = 0.002). In cultured bronchial epithelial cells, proinflammatory cytokines induced an increase in the protein expression of both PlGF and VEGF. Continuous concomitant treatment with PlGF, TNF-alpha and IL-8 stimulation reduced VEGF expression and induced cell death. This phenomenon was suppressed by VEGF receptor inhibitor (CBO-P11).

Conclusions: The serum and BAL fluid levels of PlGF are increased in patients with COPD and are inversely correlated with FEV(1). Concomitant treatment with PlGF, TNF-alpha and IL-8 causes detrimental effects on airway epithelial cells. These data suggest that bronchial epithelial cells can express PlGF, which may contribute to the pathogenesis of COPD.

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Related in: MedlinePlus

Correlation between the serum concentration of placenta growth factor (PlGF) and forced expiratory volume in 1 s (FEV1) percentage predicted in patients with COPD (r = −0.59, p = 0.002). The serum levels of PlGF were inversely correlated with FEV1.
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THX-63-06-0500-f01: Correlation between the serum concentration of placenta growth factor (PlGF) and forced expiratory volume in 1 s (FEV1) percentage predicted in patients with COPD (r = −0.59, p = 0.002). The serum levels of PlGF were inversely correlated with FEV1.

Mentions: There was no significant difference in the mean (SE) serum levels of VEGF between patients with COPD and controls (COPD: 282.7 (13.3) pg/ml; smokers: 318.4 (19.6) pg/ml; non-smoker controls: 296.8 (26.1) pg/ml, p = 0.35, F test between the three samples). However, the serum levels of PlGF were significantly higher in patients with COPD (27.1 (7.4) pg/ml than in the controls (smokers: 12.3 (5.1) pg/ml; non-smoker controls: 10.8 (6.3) pg/ml, p = 0.005). Moreover, the serum levels of PlGF correlated inversely with the value of FEV1 in patients with COPD (r = −0.59, p = 0.002; fig 1). Patients with higher PlGF levels tended to have lower FEV1 values.


Increased expression of placenta growth factor in COPD.

Cheng SL, Wang HC, Yu CJ, Yang PC - Thorax (2008)

Correlation between the serum concentration of placenta growth factor (PlGF) and forced expiratory volume in 1 s (FEV1) percentage predicted in patients with COPD (r = −0.59, p = 0.002). The serum levels of PlGF were inversely correlated with FEV1.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2571977&req=5

THX-63-06-0500-f01: Correlation between the serum concentration of placenta growth factor (PlGF) and forced expiratory volume in 1 s (FEV1) percentage predicted in patients with COPD (r = −0.59, p = 0.002). The serum levels of PlGF were inversely correlated with FEV1.
Mentions: There was no significant difference in the mean (SE) serum levels of VEGF between patients with COPD and controls (COPD: 282.7 (13.3) pg/ml; smokers: 318.4 (19.6) pg/ml; non-smoker controls: 296.8 (26.1) pg/ml, p = 0.35, F test between the three samples). However, the serum levels of PlGF were significantly higher in patients with COPD (27.1 (7.4) pg/ml than in the controls (smokers: 12.3 (5.1) pg/ml; non-smoker controls: 10.8 (6.3) pg/ml, p = 0.005). Moreover, the serum levels of PlGF correlated inversely with the value of FEV1 in patients with COPD (r = −0.59, p = 0.002; fig 1). Patients with higher PlGF levels tended to have lower FEV1 values.

Bottom Line: Continuous concomitant treatment with PlGF, TNF-alpha and IL-8 stimulation reduced VEGF expression and induced cell death.This phenomenon was suppressed by VEGF receptor inhibitor (CBO-P11).Concomitant treatment with PlGF, TNF-alpha and IL-8 causes detrimental effects on airway epithelial cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, National Taiwan University Hospital, No. 7, Chung-Shan South Road, Taipei, Taiwan.

ABSTRACT

Background: Vascular endothelial growth factor (VEGF) and its receptor may have an important role in the pathogenesis of emphysema. The effect of another angiogenic factor, placenta growth factor (PlGF), in chronic obstructive pulmonary disease (COPD) is unknown.

Methods: The serum levels of VEGF and PlGF in patients with COPD (n = 184), smokers (n = 212) and non-smokers (n = 159) and the bronchoalveolar lavage (BAL) fluid levels of VEGF and PlGF in another group (20 patients with COPD, 18 controls) were measured. In vitro cell culture experiments were performed to investigate the effect of PlGF on VEGF.

Results: The mean (SE) serum levels of PlGF were significantly higher in patients with COPD than in controls (27.1 (7.4) pg/ml vs 12.3 (5.1) pg/ml in smokers and 10.8 (6.3) pg/ml in non-smokers, p = 0.005). The levels of PlGF in BAL fluid were also significantly higher in patients with COPD than in controls (45.7 (12.3) pg/ml vs 23.9 (7.6) pg/ml, p = 0.005), associated with an increase in the cytokines tumour necrosis factor-alpha (TNF-alpha) and interleukin-8 (IL-8). In patients with COPD the levels of PlGF correlated inversely with forced expiratory volume in 1 s (FEV(1)) in serum (r = -0.59, p = 0.002) and in BAL fluid (r = -0.51, p = 0.001). While the serum levels of VEGF were the same in patients with COPD and controls, the BAL fluid levels were significantly lower in patients with COPD than in controls (127.5 (30.1) pg/ml vs 237.8 (36.1) pg/ml, p = 0.002). In cultured bronchial epithelial cells, proinflammatory cytokines induced an increase in the protein expression of both PlGF and VEGF. Continuous concomitant treatment with PlGF, TNF-alpha and IL-8 stimulation reduced VEGF expression and induced cell death. This phenomenon was suppressed by VEGF receptor inhibitor (CBO-P11).

Conclusions: The serum and BAL fluid levels of PlGF are increased in patients with COPD and are inversely correlated with FEV(1). Concomitant treatment with PlGF, TNF-alpha and IL-8 causes detrimental effects on airway epithelial cells. These data suggest that bronchial epithelial cells can express PlGF, which may contribute to the pathogenesis of COPD.

Show MeSH
Related in: MedlinePlus