Robert E. Monticone
National Institutes of Health
Matrix metalloproteinaseInternal medicineEndocrinologyPathologyProinflammatory cytokineReceptorPlatelet-derived growth factor receptorChemistryExtracellular matrixIn vitroImmunologyIn vivoMyocyteVascular smooth muscleElastinAortaCalcificationPlatelet-derived growth factorAngiotensin IISignal transductionMedicineCell cultureBiologyCell biology
52Publications
28H-index
3,153Citations
Publications 52
Newest
#1Soo Hyuk Kim (NIH: National Institutes of Health)H-Index: 10
#2Robert E. Monticone (NIH: National Institutes of Health)H-Index: 28
Last. Mingyi Wang (NIH: National Institutes of Health)H-Index: 28
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Abstract Elastic fibers are the main components of the extracellular matrix of the large arterial wall. Elastic fiber remodeling is an intricate process of synthesis and degradation of the core elastin protein and microfibrils accompanied by the assembly and disassembly of accessory proteins. Age-related morphological, structural, and functional proinflammatory remodeling within the elastic fiber has a profound effect upon the integrity, elasticity, calcification, amyloidosis, and stiffness of t...
Source
#1Ni L (Peking Union Medical College)
#1Leng Ni (NIH: National Institutes of Health)H-Index: 2
Last. Wang m
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Angiotensin II (Ang II) and milk fat globule-epidermal growth factor VIII (MFG-E8) are increased in the aged arterial wall and are involved in remodeling. However, the precise interactions between Ang II and MFG-E8 in proinflammatory arterial remodeling remains unknown. In this study, both MFG-E8 knock out (KO) and wild-type (WT) mice were infused with Ang II via an osmotic mini-pump. After infusion with Ang II, increases in systolic blood pressure (SBP) and circulating Ang II were observed in a...
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#1Soo Hyuk Kim (NIH: National Institutes of Health)H-Index: 10
#2Lijuan Liu (NIH: National Institutes of Health)H-Index: 4
Last. Mingyi Wang (NIH: National Institutes of Health)H-Index: 28
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Abstract Objective The proinflammatory phenotypic shift of vascular smooth muscle cells (VSMCs) is closely linked to the elastolysis and calcification in the aging arterial wall. Degradation of tropoelastin (TPELN) is a key molecular event which often accompanies the proinflammatory phenotypic shift of VSMCs, arterial elastolysis and calcification with aging. Milk fat globule-EGF factor 8 (MFG-E8), secreted mainly from VSMCs, predominantly binds to degenerated elastin fibers, and alters VSMCs ph...
1 CitationsSource
#1Mingyi WangH-Index: 28
#2Robert E. MonticoneH-Index: 28
Last. Kimberly R. McGrawH-Index: 3
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Aging is a major risk factor for quintessential cardiovascular diseases, which are closely related to arterial proinflammation. The age-related alterations of the amount, distribution, and properties of the collagen fibers, such as cross-links and degradation in the arterial wall, are the major sequelae of proinflammation. In the aging arterial wall, collagen types I, II, and III are predominant, and are mainly produced by stiffened vascular smooth muscle cells (VSMCs) governed by proinflammator...
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#2Mingyi Wang (NIH: National Institutes of Health)H-Index: 28
Last. Shivakumar KailasamH-Index: 3
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Collagen accumulation and remodeling in the vascular wall is a cardinal feature of vascular fibrosis that exacerbates the complications of hypertension, aging, diabetes and atherosclerosis. With no specific therapy available to date, identification of mechanisms underlying vascular fibrogenesis is an important clinical goal. Here, we tested the hypothesis that Discoidin Domain Receptor 2 (DDR2), a collagen-specific receptor tyrosine kinase, is a determinant of arterial fibrosis. We report a sign...
4 CitationsSource
#1Mingyi WangH-Index: 28
#2Robert E. MonticoneH-Index: 28
Last. Kimberly R. McGrawH-Index: 3
view all 3 authors...
Source
#1Mingyi Wang (NIH: National Institutes of Health)H-Index: 28
#2Li Zhang (Southern Medical University)H-Index: 3
Last. Edward G. Lakatta (NIH: National Institutes of Health)H-Index: 166
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Background Aging exponentially increases the incidence of morbidity and mortality of quintessential cardiovascular disease mainly due to arterial proinflammatory shifts at the molecular, cellular, ...
11 CitationsSource
#1Gianfranco Pintus (Qatar University)H-Index: 32
#2Roberta Giordo (Qatar University)H-Index: 13
Last. Edward G. Lakatta (NIH: National Institutes of Health)H-Index: 166
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// Gianfranco Pintus 1, 2, * , Roberta Giordo 1, 2, * , Yushi Wang 1, 3 , Wanqu Zhu 1 , Soo Hyuk Kim 1 , Li Zhang 1, 4 , Leng Ni 1, 5 , Jing Zhang 1 , Richard Telljohann 1 , Kimberly R. McGraw 1 , Robert E. Monticone 1 , Chloe Ferris 1 , Lijuan Liu 1 , Mingyi Wang 1 and Edward G. Lakatta 1 1 Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Biomedical Research Center (BRC), Baltimore, MD, USA 2 Biomedical Research Center, Qatar University, Doha, Qa...
5 CitationsSource
#1Wanqu Zhu (Johns Hopkins University)H-Index: 6
#2Byoung Choul KimH-Index: 14
Last. Steven S. An (UNIST: Ulsan National Institute of Science and Technology)H-Index: 33
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Here we report exquisitely distinct material properties of primary vascular smooth muscle (VSM) cells isolated from the thoracic aorta of adult (8 months) vs. aged (30 months) F344XBN rats. Individual VSM cells derived from the aged animals showed a tense internal network of the actin cytoskeleton (CSK), exhibiting increased stiffness (elastic) and frictional (loss) moduli than those derived from the adult animals over a wide frequency range of the imposed oscillatory deformation. This discrete ...
14 CitationsSource
#1Mingyi WangH-Index: 28
#2Robert E. MonticoneH-Index: 28
Last. Kimberly R. McGrawH-Index: 3
view all 3 authors...
: Age-associated structural and functional remodeling of the arterial wall produces a productive environment for the initiation and progression of hypertension and atherosclerosis. Chronic aging stress induces low-grade proinflammatory signaling and causes cellular proinflammation in arterial walls, which triggers the structural phenotypic shifts characterized by endothelial dysfunction, diffuse intimal-medial thickening, and arterial stiffening. Microscopically, aged arteries exhibit an increas...
9 CitationsSource