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6. Abstract 18753: Dynamic Phenotypic Transition of Smooth Muscle Cells During Human Ascending Thoracic Aortic Disease Progression: From Compensation in Aortic Aneurysm to Decompensation in Aortic Dissection

Author

Li, Yanming, Zhang, Chen, Vasquez, Hernan, Li, Yang, Chakraborty, Abhijit, Rebello, Kimberly, Xu, Samantha, Zhang, Lin, Sawada, Hisashi, Zhou, Zhen, Chen, Rui, li, yumei, Saeys, Yvan, eisenberg, steven, Lu, Hong S, Cassis, Lisa A, Coselli, Joseph S, Daugherty, Alan, Milewicz, Dianna M, Shen, Ying H, and Lemaire, Scott A

Published
2023
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13. Neutrophil Elastase Inhibition by Sivelestat (ONO-5046) Attenuates AngII-Induced Abdominal Aortic Aneurysms in Apolipoprotein E-Deficient Mice.

Author

Hada, Yoshiko, Uchida, Haruhito A, Okamoto, Shugo, Otaka, Nozomu, Katayama, Katsuyoshi, Subramanian, Venkateswaran, Daugherty, Alan, and Wada, Jun

Subjects
LEUCOCYTE elastase, ABDOMINAL aortic aneurysms, ARTERIAL diseases, ANGIOTENSIN II, MUSCLE cells, ELASTASES
Abstract

BACKGROUND Abdominal aortic aneurysm (AAA) is an arterial disease characterized by dilatation of the aortic wall. It has been suggested that neutrophil counts and neutrophil elastase activity are associated with AAA. We investigated whether a neutrophil elastase (NE) inhibitor, sivelestat (Siv), had a protective effect against angiotensin II (AngII)-induced AAAs. METHODS Male apolipoprotein E-deficient mice were assigned into three groups: Vehicle + saline, AngII + saline, and AngII + Siv. All mice were administered intraperitoneally with either Siv or vehicle twice daily after AngII infusion. RESULTS In the 4-week AngII infusion study, plasma NE concentration (P  = 0.041) and its activity (P  = 0.011) were elevated by AngII. These increases were attenuated by Siv (concentration: P  = 0.010, activity: P  = 0.027). Further, plasma elastase activity was closely correlated with aortic width (R  = 0.6976, P  < 0.001). In the 1-week AngII infusion study, plasma and tissue elastase activity increased by AngII (plasma: P  = 0.034, tissue: P  < 0.001), but were reduced by Siv (plasma: P  = 0.014, tissue: P  = 0.024). AngII increased aortic width (P  = 0.011) but was attenuated by co-administration of Siv (P  = 0.022). Moreover, Siv decreased the incidence of AAAs (P  = 0.009). Elastin fragmentation induced by AngII was reduced by Siv. Many inflammatory cells that were either CD68 or Gr-1 positive were observed in the AngII + saline group, whereas few inflammatory cells were accumulated in the AngII + Siv group. MMP-2 and MMP-9 were enhanced by AngII, but were reduced by Siv. In vitro , MMP-2 activity was induced by human NE (medium: P  < 0.001, cells: P  = 0.001), which was attenuated by co-incubation of Siv in medium (P  < 0.001) and protein of human aortic smooth muscle cells (P  = 0.001). CONCLUSIONS Siv attenuated AngII-induced AAA through the inhibition of NE. [ABSTRACT FROM AUTHOR]

Published
2024
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16. Exome-wide evaluation of rare coding variants using electronic health records identifies new gene–phenotype associations

Author

Park, Joseph, Lucas, Anastasia M., Zhang, Xinyuan, Chaudhary, Kumardeep, Cho, Judy H., Nadkarni, Girish, Dobbyn, Amanda, Chittoor, Geetha, Josyula, Navya S., Katz, Nathan, Breeyear, Joseph H., Ahmadmehrabi, Shadi, Drivas, Theodore G., Chavali, Venkata R. M., Fasolino, Maria, Sawada, Hisashi, Daugherty, Alan, Li, Yanming, Zhang, Chen, Bradford, Yuki, Weaver, JoEllen, Verma, Anurag, Judy, Renae L., Kember, Rachel L., Overton, John D., Reid, Jeffrey G., Ferreira, Manuel A. R., Li, Alexander H., Baras, Aris, LeMaire, Scott A., Shen, Ying H., Naji, Ali, Kaestner, Klaus H., Vahedi, Golnaz, Edwards, Todd L., Chen, Jinbo, Damrauer, Scott M., Justice, Anne E., Do, Ron, Ritchie, Marylyn D., and Rader, Daniel J.

Published
2021
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20. Adropin: An endocrine link between the biological clock and cholesterol homeostasis

Author

Ghoshal, Sarbani, Stevens, Joseph R., Billon, Cyrielle, Girardet, Clemence, Sitaula, Sadichha, Leon, Arthur S., Rao, D.C., Skinner, James S., Rankinen, Tuomo, Bouchard, Claude, Nuñez, Marinelle V., Stanhope, Kimber L., Howatt, Deborah A., Daugherty, Alan, Zhang, Jinsong, Schuelke, Matthew, Weiss, Edward P., Coffey, Alisha R., Bennett, Brian J., Sethupathy, Praveen, Burris, Thomas P., Havel, Peter J., and Butler, Andrew A.

Published
2018
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24. American Heart Association Vascular Disease Strategically Focused Research Network

Author

Barnett, Joey V., Beckman, Joshua A., Bonaca, Marc P., Carnethon, Mercedes R., Cassis, Lisa A., Creager, Mark A., Daugherty, Alan, Feinberg, Mark W., Freiberg, Matthew S., Goodney, Philip P., Greenland, Philip, Leeuwenburgh, Christiaan, LeMaire, Scott A., McDermott, Mary M., Sabatine, Marc S., Shen, Ying H., Wasserman, David H., Webb, Nancy R., and Wells, Quinn S.

Published
2020
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25. Honoring the Life and Legacy of Dr David A. Dichek.

Author

Aikawa, Elena, Allison, Matthew A., Iruela Arispe, Luisa, Bendeck, Michelle P., Yabing Chen, Gardiner, Elizabeth E., Golledge, Jonathan, Suzuki-Inoue, Katsue, Marelli-Berg, Federica, Powell, Janet T., Ramasamy, Ravichandran, Sarpong, Daniel F., Sorci-Thomas, Mary G., Daugherty, Alan, Hegele, Robert A., and Schmidt, Ann Marie

Published
2024
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30. Abstract 15530: Single-cell Analysis in Aortic Aneurysmal Tissue From Patients With Marfan Syndrome Reveals Increased Tgf-beta Production but Downregulation of Downstream Canonical Tgf-beta Signaling Pathways

Author

Dawson, Ashley, Li, Yanming, Ren, Pingping, Vasquez, Hernan, Zhang, Chen, Appel, Richard, Ageedi, Waleed, Luo, Wei, Zhang, Lin, Li, Yang, Sheppard, Mary B, Lu, Hong S, Cassis, Lisa A, Coselli, Joseph S, Daugherty, Alan, Shen, Ying H, and Lemaire, Scott A

Published
2020
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33. Lipoproteins, inflammation, and vascular disease

Author

Daugherty, Alan

Subjects
616.13
Abstract

The major focus of the studies described in this thesis is the interaction of lipoproteins and inflammation in vascular diseases. Early studies describe the role of postprandial lipoproteins in the development of lipid-laden macro phages that are a hallmark of atherosclerotic lesions. These studies paved the way for subsequent studies on the role of lipoprotein modification in atherosclerosis. These included the discovery that LDL present in atherosclerotic lesions had properties that were consistent with oxidative modification. To determine whether this modification was a cause or consequence of the disease, studies were performed using antioxidants. These studies defined the effects of antioxidants on early and mature atherosclerotic lesions, as well as on iatrogenic vascular lesions. My laboratory also studied two potential enzymes that have the potential to generate oxidized lipoprotein; myeloperoxidase and 15-lipoxygenase. The effects of pharmacological inhibition and regulation on the latter enzyme were defined. Studies have also addressed the regulation and function of a major receptor for oxidized LDL, class A scavenger receptor. These include regulation, structure-function, and the effects of cell selective overexpression. These lipoprotein modifications have a well characterized role on the infiltration of macro phages and their subsequent engorgement with lipid. Aberrant lipoprotein metabolism may be a factor underlying the recruitment of T Iymphocytes into lesions. Generally, T Iymphocytes have an under appreciated role in the atherogenic process. Studies using mice deficient in Iymphocyte subclasses and specific cytokines are addressing the issue of this cell type in lesion formation. Finally, we have recently discovered a pronounced inflammatory role of angiotensin II that is associated with the development of atherosclerosis and abdominal aortic aneurysms

Published
2002

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