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Endothelial dysfunction induced by antibodies against angiotensin AT1 receptor in immunized rats.

Zhang SL, Du YH, Wang J, Yang LH, Yang XL, Zheng RH, Wu Y, Wang K, Zhang MS, Liu HR - Acta Pharmacol. Sin. (2010)

Bottom Line: Lactate dehydrogenase (LDH) activity was regarded as an indicator of cell necrotic death.IgGs in the immunized group significantly increased the LDH activity (0.84±0.17 vs 0.39±0.12, P<0.01 vs vehicle group IgGs)in incubated human umbilical vein endothelial cells through AT1 receptor.In addition, aortic endothelium-dependent vasodilatation was attenuated; endothelial ICAM-1 level was markedly increased and cardiac capillary endothelium was damaged following immunization.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Shanxi Medical University, Taiyuan, China.

ABSTRACT

Aim: To investigate the association between autoantibodies against angiotensin AT1 receptor (AT1-AAs) and endothelial dysfunction in vivo.

Methods: Rat models with AT1 receptor antibodies (AT1-Abs) were established by active immunization for nine months. Lactate dehydrogenase (LDH) activity was regarded as an indicator of cell necrotic death. Endothelin-1 (ET-1) in the sera of rats was determined and endothelium-dependent vasodilatation was detected in isolated thoracic aorta. Endothelial intercellular adhesion molecule-1 (ICAM-1) expression in aorta endothelium was assessed using confocal microscopy. Coronary artery endothelial ultrastructure was observed.

Results: IgGs in the immunized group significantly increased the LDH activity (0.84±0.17 vs 0.39±0.12, P<0.01 vs vehicle group IgGs)in incubated human umbilical vein endothelial cells through AT1 receptor. Higher content of ET-1 occurred in the immunized rats than that of the vehicle group, and reached two peaks at month 3 (27±4 ng/L, P<0.01) and month 7 (35±5 ng/L, P<0.01), respectively. In addition, aortic endothelium-dependent vasodilatation was attenuated; endothelial ICAM-1 level was markedly increased and cardiac capillary endothelium was damaged following immunization.

Conclusion: Our study demonstrated that AT1-Abs contributed to endothelial dysfunction in vivo, which was a potential mechanism through which the antibodies play vital roles in related diseases.

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Related in: MedlinePlus

Upregulation of the expression ICAM-1 in thoracic aortic endothelium in the immunized rats. At the end of the immunization, the expressions of thoracic aortic endothelial ICAM-1 in the two groups of rats were measured under a laser scanning confocal microscope. A FITC-labeled anti-rat ICAM-1 antibody produced the red stain (5A, 5C). 5B and 5D were the corresponding structure charts of vascular lying on left, respectively.
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fig5: Upregulation of the expression ICAM-1 in thoracic aortic endothelium in the immunized rats. At the end of the immunization, the expressions of thoracic aortic endothelial ICAM-1 in the two groups of rats were measured under a laser scanning confocal microscope. A FITC-labeled anti-rat ICAM-1 antibody produced the red stain (5A, 5C). 5B and 5D were the corresponding structure charts of vascular lying on left, respectively.

Mentions: The expression of endothelial ICAM-1 was determined by laser scanning confocal microscopy. Compared with the vehicle group (Figure 5C, 5D), enhanced fluorescence intensity were observed in immunized rats at month 9 after initial immunization (Figure 5A, 5B), which indicated that expressions of ICAM-1 increased in rats that contained high levels of AT1-Abs for a long term.


Endothelial dysfunction induced by antibodies against angiotensin AT1 receptor in immunized rats.

Zhang SL, Du YH, Wang J, Yang LH, Yang XL, Zheng RH, Wu Y, Wang K, Zhang MS, Liu HR - Acta Pharmacol. Sin. (2010)

Upregulation of the expression ICAM-1 in thoracic aortic endothelium in the immunized rats. At the end of the immunization, the expressions of thoracic aortic endothelial ICAM-1 in the two groups of rats were measured under a laser scanning confocal microscope. A FITC-labeled anti-rat ICAM-1 antibody produced the red stain (5A, 5C). 5B and 5D were the corresponding structure charts of vascular lying on left, respectively.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4012898&req=5

fig5: Upregulation of the expression ICAM-1 in thoracic aortic endothelium in the immunized rats. At the end of the immunization, the expressions of thoracic aortic endothelial ICAM-1 in the two groups of rats were measured under a laser scanning confocal microscope. A FITC-labeled anti-rat ICAM-1 antibody produced the red stain (5A, 5C). 5B and 5D were the corresponding structure charts of vascular lying on left, respectively.
Mentions: The expression of endothelial ICAM-1 was determined by laser scanning confocal microscopy. Compared with the vehicle group (Figure 5C, 5D), enhanced fluorescence intensity were observed in immunized rats at month 9 after initial immunization (Figure 5A, 5B), which indicated that expressions of ICAM-1 increased in rats that contained high levels of AT1-Abs for a long term.

Bottom Line: Lactate dehydrogenase (LDH) activity was regarded as an indicator of cell necrotic death.IgGs in the immunized group significantly increased the LDH activity (0.84±0.17 vs 0.39±0.12, P<0.01 vs vehicle group IgGs)in incubated human umbilical vein endothelial cells through AT1 receptor.In addition, aortic endothelium-dependent vasodilatation was attenuated; endothelial ICAM-1 level was markedly increased and cardiac capillary endothelium was damaged following immunization.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Shanxi Medical University, Taiyuan, China.

ABSTRACT

Aim: To investigate the association between autoantibodies against angiotensin AT1 receptor (AT1-AAs) and endothelial dysfunction in vivo.

Methods: Rat models with AT1 receptor antibodies (AT1-Abs) were established by active immunization for nine months. Lactate dehydrogenase (LDH) activity was regarded as an indicator of cell necrotic death. Endothelin-1 (ET-1) in the sera of rats was determined and endothelium-dependent vasodilatation was detected in isolated thoracic aorta. Endothelial intercellular adhesion molecule-1 (ICAM-1) expression in aorta endothelium was assessed using confocal microscopy. Coronary artery endothelial ultrastructure was observed.

Results: IgGs in the immunized group significantly increased the LDH activity (0.84±0.17 vs 0.39±0.12, P<0.01 vs vehicle group IgGs)in incubated human umbilical vein endothelial cells through AT1 receptor. Higher content of ET-1 occurred in the immunized rats than that of the vehicle group, and reached two peaks at month 3 (27±4 ng/L, P<0.01) and month 7 (35±5 ng/L, P<0.01), respectively. In addition, aortic endothelium-dependent vasodilatation was attenuated; endothelial ICAM-1 level was markedly increased and cardiac capillary endothelium was damaged following immunization.

Conclusion: Our study demonstrated that AT1-Abs contributed to endothelial dysfunction in vivo, which was a potential mechanism through which the antibodies play vital roles in related diseases.

Show MeSH
Related in: MedlinePlus