TY - JOUR
T1 - Alterations in pulse pressure affect artery function
AU - Hayman, Danika M.
AU - Xiao, Yangming
AU - Yao, Qingping
AU - Jiang, Zonglai
AU - Lindsey, Merry L.
AU - Han, Hai Chao
N1 - Funding Information:
This work was supported by the National Science Foundation under award number CBET-0602834 (HCH) and the National Institutes of Health (HL095852 to HCH, F31HL096448 to DH, and HL075360 and NHLBI HHSN 268201000036C (N01-HV-00244) for the UTHSCSA Cardiovascular Proteomics Center to MLL). It was also partially supported by Grant 10928206 from the National Natural Science Foundation of China. We thank Dr. Colleen Witt and the UTSA Research Center in Minority Institution (RCMI) Advanced Imaging Core for providing us the access and technical support for confocal microscopy. We also thank Dr. John Zhang, Dr. Rogelio Zamilpa, Dr. Quixia Dai, Ms. Monica Gireud, Ms. Trevi Ramirez, Ms. Jamie Parra, and Ms. Erin Dunne for their help in this study.
PY - 2012/12
Y1 - 2012/12
N2 - Pulse pressure changes in response to cardiovascular diseases and interventions, but its effect on vascular wall structure and function is poorly understood. We examined the effect of increased or decreased pulse pressure on artery function, cellular function, and extracellular matrix remodeling. Porcine carotid arteries were cultured under non-pulsatile (100 mmHg), pulsatile (70-130 mmHg), or hyper-pulsatile pressure (50-150 mmHg) for 1-3 days. Vasomotor response, wall permeability, cell proliferation, apoptosis, extracellular matrix remodeling, and proteins involved in atherogenesis were examined. Our results showed that hyper-pulsatile pressure decreased the artery response to sodium nitroprusside, basal tone, and wall permeability after 3 days. Non-pulsatile pressure increased cell proliferation. Neither hyper-pulsatile nor non-pulsatile pressure caused a change in the extracellular matrix or in the expression of matrix metalloproteinase-2 (MMP-2), MMP-9, caveolin-1, or a-actin. Hyper-pulsatile pressure increased monocyte chemotactic protein-1 gene expression. Taken together, these changes indicate that pulse pressure has a limited effect on the artery immediately after its application. Specifically an increase in pulse pressure alters the artery tone and wall permeability while a decrease in pulse pressure alters cell proliferation. Overall these results provide insight into how the artery initially responds to changes in pulse pressure.
AB - Pulse pressure changes in response to cardiovascular diseases and interventions, but its effect on vascular wall structure and function is poorly understood. We examined the effect of increased or decreased pulse pressure on artery function, cellular function, and extracellular matrix remodeling. Porcine carotid arteries were cultured under non-pulsatile (100 mmHg), pulsatile (70-130 mmHg), or hyper-pulsatile pressure (50-150 mmHg) for 1-3 days. Vasomotor response, wall permeability, cell proliferation, apoptosis, extracellular matrix remodeling, and proteins involved in atherogenesis were examined. Our results showed that hyper-pulsatile pressure decreased the artery response to sodium nitroprusside, basal tone, and wall permeability after 3 days. Non-pulsatile pressure increased cell proliferation. Neither hyper-pulsatile nor non-pulsatile pressure caused a change in the extracellular matrix or in the expression of matrix metalloproteinase-2 (MMP-2), MMP-9, caveolin-1, or a-actin. Hyper-pulsatile pressure increased monocyte chemotactic protein-1 gene expression. Taken together, these changes indicate that pulse pressure has a limited effect on the artery immediately after its application. Specifically an increase in pulse pressure alters the artery tone and wall permeability while a decrease in pulse pressure alters cell proliferation. Overall these results provide insight into how the artery initially responds to changes in pulse pressure.
KW - Cell proliferation
KW - Ex vivo organ culture
KW - Matrix metalloproteinase
KW - Monocyte chemotactic protein-1
KW - Permeability
KW - Porcine artery
KW - Pulsatile pressure
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U2 - 10.1007/s12195-012-0251-x
DO - 10.1007/s12195-012-0251-x
M3 - Article
C2 - 23243477
AN - SCOPUS:84874108269
SN - 1865-5025
VL - 5
SP - 474
EP - 487
JO - Cellular and Molecular Bioengineering
JF - Cellular and Molecular Bioengineering
IS - 4
ER -