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Alexander W. Caulk
Yale University
AnatomyCardiologyArterial stiffnessEfavirenzBiology
21Publications
7H-index
107Citations
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Publications 25
Newest
#1Pei-Yu Chen (Yale University)H-Index: 14
#2Lingfeng Qin (Yale University)H-Index: 21
Last. Xinbo Zhang (Yale University)H-Index: 10
view all 25 authors...
Summary The etiology of aortic aneurysms is poorly understood, but it is associated with atherosclerosis, hypercholesterolemia, and abnormal transforming growth factor β (TGF-β) signaling in smooth muscle. Here, we investigated the interactions between these different factors in aortic aneurysm development and identified a key role for smooth muscle cell (SMC) reprogramming into a mesenchymal stem cell (MSC)-like state. SMC-specific ablation of TGF-β signaling in Apoe−/− mice on a hypercholester...
1 CitationsSource
#1Bart SpronckH-Index: 8
#2J. FerruzziH-Index: 13
Last. J. D. HumphreyH-Index: 5
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#1Bart SpronckH-Index: 8
#2J. FerruzziH-Index: 13
Last. J. D. HumphreyH-Index: 5
view all 6 authors...
OBJECTIVES: Increased central artery stiffness associates with cardiovascular disease. Among other factors, hypertension and aging are strong contributors to central artery stiffening, yet it has been difficult to separate their effects. Herein, we study isolated and combined effects of hypertension and aging on central artery remodeling in multiple mouse models as a function of sex. METHODS: We biomechanically phenotyped the aorta as a function of two different methods of inducing hypertension ...
1 CitationsSource
#1Guangxin LiH-Index: 8
#2Mo WangH-Index: 1
Last. Yang JiaoH-Index: 4
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Smooth muscle cell (SMC) proliferation has been thought to limit the progression of thoracic aortic aneurysm and dissection (TAAD) because loss of medial cells associates with advanced disease. We investigated effects of SMC proliferation in the aortic media by conditional disruption of Tsc1, which hyperactivates mTOR complex 1. Consequent SMC hyperplasia led to progressive medial degeneration and TAAD. In addition to diminished contractile and synthetic functions, fate-mapped SMCs displayed inc...
2 CitationsSource
#1Alexander W. Caulk (Yale University)H-Index: 7
#2Kevin A. Janes (UVA: University of Virginia)H-Index: 25
Simple multilinear methods, such as partial least squares regression (PLSR), are effective at interrelating dynamic, multivariate datasets of cell–molecular biology through high-dimensional arrays. However, data collected in vivo are more difficult, because animal-to-animal variability is often high, and each time-point measured is usually a terminal endpoint for that animal. Observations are further complicated by the nesting of cells within tissues or tissue sections, which themselves are nest...
Source
#1S-I. Murtada (Yale University)
#2Y. Kawamura (Yale University)
Last. D HumphreyJay (Yale University)H-Index: 56
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Hutchinson-Gilford Progeria Syndrome (HGPS) is an ultra-rare disorder with devastating sequelae resulting in early death, presently believed to stem primarily from heart failure secondary to central arterial stiffening. We analyze novel longitudinal cardiovascular data from a mouse model of HGPS (LmnaG609G/G609G) using allometric scaling and advanced computational modelling and show that a late-stage increase in pulse wave velocity, with associated diastolic dysfunction but preserved systolic fu...
Source
#1Bart Spronck (UM: Maastricht University)H-Index: 8
#2Alexander W. Caulk (Yale University)H-Index: 7
Last. D HumphreyJay (Yale University)H-Index: 56
view all 9 authors...
Objective: Many genetically-induced mutations affect aortic structure and function in mice, but little is known about the influence of background strain. This study quantifies the aortic phenotype in angiotensin II (AngII)-induced hypertension across different strains of wild-type mice. Approach and Results: Adult male C57BL/6J and 129SvEv mice were studied before and after induction of hypertension via subcutaneous infusion of AngII (1000 ng/kg/min) for two weeks, which elevated blood pressure ...
Source
#1Alexander W. Caulk (Yale University)H-Index: 7
#2D HumphreyJay (Yale University)H-Index: 56
Last. Sae-Il Murtada (Yale University)H-Index: 3
view all 3 authors...
3 CitationsSource
#1J. Ferruzzi (Yale University)H-Index: 13
#2D. Madziva (Yale University)H-Index: 1
Last. D HumphreyJay (Yale University)H-Index: 56
view all 5 authors...
Aging leads to central artery stiffening and associated hemodynamic sequelae. Because healthy arteries exhibit differential geometry, composition, and mechanical behaviors along the central vasculature, we sought to determine whether wall structure and mechanical function differ across five vascular regions—the ascending and descending thoracic aorta, suprarenal and infrarenal abdominal aorta, and common carotid artery—in 20 versus 100-week-old male wild-type mice. Notwithstanding generally cons...
7 CitationsSource
#1Alexander W. Caulk (Yale University)H-Index: 7
#2George Tellides (Yale University)H-Index: 45
Last. D HumphreyJay (Yale University)H-Index: 56
view all 3 authors...
Abstract Since the mid-1970s, it has been increasingly recognized that vascular cells—endothelial, smooth muscle, and fibroblasts—are highly sensitive to mechanical stimuli, changing their gene expression profile in response to changes in mechanics. Such changes explain many observed vascular adaptations to perturbations in hemodynamics and certain pathologies. Similar to mechanical loading, inflammation also affects the extent of many vascular adaptations and disease progression. In this chapte...
1 CitationsSource
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