Cardiovascular hemodynamics in mice with tumor necrosis factor receptor—associated factor 2 mediated cytoprotection in the heart
IntroductionMany studies in mice have demonstrated that cardiac-specific innate immune signaling pathways can be reprogrammed to modulate inflammation in response to myocardial injury and improve outcomes. While the echocardiography standard parameters of left ventricular (LV) ejection fraction, fra...
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Frontiers Media S.A.
2023-05-01
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Series: | Frontiers in Cardiovascular Medicine |
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Online Access: | https://www.frontiersin.org/articles/10.3389/fcvm.2023.1064640/full |
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author | Andrea G. Marshall Kit Neikirk Zer Vue Heather K. Beasley Edgar Garza-Lopez Larry Vang Taylor Barongan Zoe Evans Amber Crabtree Elsie Spencer Josephs Anudokem Josephs Anudokem Remi Parker Remi Parker Jamaine Davis Dominique Stephens Dominique Stephens Steven Damo Thuy T. Pham Jose A. Gomez Vernat Exil Vernat Exil Dao-fu Dai Sandra A. Murray Mark L. Entman George E. Taffet Antentor O. Hinton Anilkumar K. Reddy |
author_facet | Andrea G. Marshall Kit Neikirk Zer Vue Heather K. Beasley Edgar Garza-Lopez Larry Vang Taylor Barongan Zoe Evans Amber Crabtree Elsie Spencer Josephs Anudokem Josephs Anudokem Remi Parker Remi Parker Jamaine Davis Dominique Stephens Dominique Stephens Steven Damo Thuy T. Pham Jose A. Gomez Vernat Exil Vernat Exil Dao-fu Dai Sandra A. Murray Mark L. Entman George E. Taffet Antentor O. Hinton Anilkumar K. Reddy |
author_sort | Andrea G. Marshall |
collection | DOAJ |
description | IntroductionMany studies in mice have demonstrated that cardiac-specific innate immune signaling pathways can be reprogrammed to modulate inflammation in response to myocardial injury and improve outcomes. While the echocardiography standard parameters of left ventricular (LV) ejection fraction, fractional shortening, end-diastolic diameter, and others are used to assess cardiac function, their dependency on loading conditions somewhat limits their utility in completely reflecting the contractile function and global cardiovascular efficiency of the heart. A true measure of global cardiovascular efficiency should include the interaction between the ventricle and the aorta (ventricular-vascular coupling, VVC) as well as measures of aortic impedance and pulse wave velocity.MethodsWe measured cardiac Doppler velocities, blood pressures, along with VVC, aortic impedance, and pulse wave velocity to evaluate global cardiac function in a mouse model of cardiac-restricted low levels of TRAF2 overexpression that conferred cytoprotection in the heart.ResultsWhile previous studies reported that response to myocardial infarction and reperfusion was improved in the TRAF2 overexpressed mice, we found that TRAF2 mice had significantly lower cardiac systolic velocities and accelerations, diastolic atrial velocity, aortic pressures, rate-pressure product, LV contractility and relaxation, and stroke work when compared to littermate control mice. Also, we found significantly longer aortic ejection time, isovolumic contraction and relaxation times, and significantly higher mitral early/atrial ratio, myocardial performance index, and ventricular vascular coupling in the TRAF2 overexpression mice compared to their littermate controls. We found no significant differences in the aortic impedance and pulse wave velocity.DiscussionWhile the reported tolerance to ischemic insults in TRAF2 overexpression mice may suggest enhanced cardiac reserve, our results indicate diminished cardiac function in these mice. |
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spelling | doaj.art-7b33348424c54b3a9e0eeab706b782342023-05-09T05:37:27ZengFrontiers Media S.A.Frontiers in Cardiovascular Medicine2297-055X2023-05-011010.3389/fcvm.2023.10646401064640Cardiovascular hemodynamics in mice with tumor necrosis factor receptor—associated factor 2 mediated cytoprotection in the heartAndrea G. Marshall0Kit Neikirk1Zer Vue2Heather K. Beasley3Edgar Garza-Lopez4Larry Vang5Taylor Barongan6Zoe Evans7Amber Crabtree8Elsie Spencer9Josephs Anudokem10Josephs Anudokem11Remi Parker12Remi Parker13Jamaine Davis14Dominique Stephens15Dominique Stephens16Steven Damo17Thuy T. Pham18Jose A. Gomez19Vernat Exil20Vernat Exil21Dao-fu Dai22Sandra A. Murray23Mark L. Entman24George E. Taffet25Antentor O. Hinton26Anilkumar K. Reddy27Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, United StatesDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, United StatesDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, United StatesDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, United StatesDepartment of Internal Medicine, University of Iowa, Iowa City, IA, United StatesDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, United StatesDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, United StatesDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, United StatesDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, United StatesDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, United StatesDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, United StatesDepartment of Biochemistry and Cancer Biology, Meharry Medical College, Nashville, TN, United StatesDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, United StatesDepartment of Biochemistry and Cancer Biology, Meharry Medical College, Nashville, TN, United StatesDepartment of Biochemistry and Cancer Biology, Meharry Medical College, Nashville, TN, United StatesDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, United StatesDepartment of Life and Physical Sciences, Fisk University, Nashville, TN, United StatesDepartment of Life and Physical Sciences, Fisk University, Nashville, TN, United StatesDepartment of Medicine, Baylor College of Medicine, One Baylor Plaza, Houston, TX, United StatesDepartment of Medicine, Vanderbilt University Medical Center, Nashville, TN, United StatesDepartment of Pediatrics, Div. of Cardiology, St. Louis University School of Medicine, St. Louis, MO, United StatesDepartment of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, IA, United StatesDepartment of Pathology, Carver College of Medicine, University of Iowa, Iowa City, IA, United States0Department of Cell Biology, College of Medicine, University of Pittsburgh, Pittsburgh, United StatesDepartment of Medicine, Baylor College of Medicine, One Baylor Plaza, Houston, TX, United StatesDepartment of Medicine, Baylor College of Medicine, One Baylor Plaza, Houston, TX, United StatesDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, United StatesDepartment of Medicine, Baylor College of Medicine, One Baylor Plaza, Houston, TX, United StatesIntroductionMany studies in mice have demonstrated that cardiac-specific innate immune signaling pathways can be reprogrammed to modulate inflammation in response to myocardial injury and improve outcomes. While the echocardiography standard parameters of left ventricular (LV) ejection fraction, fractional shortening, end-diastolic diameter, and others are used to assess cardiac function, their dependency on loading conditions somewhat limits their utility in completely reflecting the contractile function and global cardiovascular efficiency of the heart. A true measure of global cardiovascular efficiency should include the interaction between the ventricle and the aorta (ventricular-vascular coupling, VVC) as well as measures of aortic impedance and pulse wave velocity.MethodsWe measured cardiac Doppler velocities, blood pressures, along with VVC, aortic impedance, and pulse wave velocity to evaluate global cardiac function in a mouse model of cardiac-restricted low levels of TRAF2 overexpression that conferred cytoprotection in the heart.ResultsWhile previous studies reported that response to myocardial infarction and reperfusion was improved in the TRAF2 overexpressed mice, we found that TRAF2 mice had significantly lower cardiac systolic velocities and accelerations, diastolic atrial velocity, aortic pressures, rate-pressure product, LV contractility and relaxation, and stroke work when compared to littermate control mice. Also, we found significantly longer aortic ejection time, isovolumic contraction and relaxation times, and significantly higher mitral early/atrial ratio, myocardial performance index, and ventricular vascular coupling in the TRAF2 overexpression mice compared to their littermate controls. We found no significant differences in the aortic impedance and pulse wave velocity.DiscussionWhile the reported tolerance to ischemic insults in TRAF2 overexpression mice may suggest enhanced cardiac reserve, our results indicate diminished cardiac function in these mice.https://www.frontiersin.org/articles/10.3389/fcvm.2023.1064640/fullsystolic and diastolic functionmyocardial performance indexventricular-vascular couplingarterial and left ventricular elastanceaortic impedance |
spellingShingle | Andrea G. Marshall Kit Neikirk Zer Vue Heather K. Beasley Edgar Garza-Lopez Larry Vang Taylor Barongan Zoe Evans Amber Crabtree Elsie Spencer Josephs Anudokem Josephs Anudokem Remi Parker Remi Parker Jamaine Davis Dominique Stephens Dominique Stephens Steven Damo Thuy T. Pham Jose A. Gomez Vernat Exil Vernat Exil Dao-fu Dai Sandra A. Murray Mark L. Entman George E. Taffet Antentor O. Hinton Anilkumar K. Reddy Cardiovascular hemodynamics in mice with tumor necrosis factor receptor—associated factor 2 mediated cytoprotection in the heart Frontiers in Cardiovascular Medicine systolic and diastolic function myocardial performance index ventricular-vascular coupling arterial and left ventricular elastance aortic impedance |
title | Cardiovascular hemodynamics in mice with tumor necrosis factor receptor—associated factor 2 mediated cytoprotection in the heart |
title_full | Cardiovascular hemodynamics in mice with tumor necrosis factor receptor—associated factor 2 mediated cytoprotection in the heart |
title_fullStr | Cardiovascular hemodynamics in mice with tumor necrosis factor receptor—associated factor 2 mediated cytoprotection in the heart |
title_full_unstemmed | Cardiovascular hemodynamics in mice with tumor necrosis factor receptor—associated factor 2 mediated cytoprotection in the heart |
title_short | Cardiovascular hemodynamics in mice with tumor necrosis factor receptor—associated factor 2 mediated cytoprotection in the heart |
title_sort | cardiovascular hemodynamics in mice with tumor necrosis factor receptor associated factor 2 mediated cytoprotection in the heart |
topic | systolic and diastolic function myocardial performance index ventricular-vascular coupling arterial and left ventricular elastance aortic impedance |
url | https://www.frontiersin.org/articles/10.3389/fcvm.2023.1064640/full |
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