Coordination of fibronectin adhesion with contraction and relaxation in microvascular smooth muscle

Hong, Zhongkui; Sun, Zhe; Li, Zhaohui; Mesquitta, Walatta-Tseyon; Trzeciakowski, Jerome P.; Meininger, Gerald A.

doi:10.1093/cvr/cvs239

Cited by 64 publications

(72 citation statements)

References 43 publications

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“…Conversely, the VSMC stiffness level may be influencing the adhesion properties, as recently published work supports a mechanistic link between, stiffness and adhesion. Hong et al 43,44 demonstrated that treatment of VSMCs with the vasoactive agents angiotensin II or adenosine, respectively increase and decrease VSMC stiffness and adhesion in a coordinated manor. It may be that the interplay of these two mechanisms, VSMC stiffness and VSMC adhesion, contributes to the interaction of hypertension and aging in accelerating vascular stiffness.…”

Section: Discussionmentioning

confidence: 99%

Augmented Vascular Smooth Muscle Cell Stiffness and Adhesion When Hypertension Is Superimposed on Aging

et al. 2015

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Hypertension and aging are both recognized to increase aortic stiffness, but their interactions are not completely understood. Most prior studies have attributed increased aortic stiffness to changes in extracellular matrix proteins that alter mechanical properties of the vascular wall. Alternatively, we hypothesized that a significant component of increased vascular stiffness in hypertension is due to changes in the mechanical and adhesive properties of vascular smooth muscle cells, and that aging would augment the contribution from vascular smooth muscle cells compared to the extracellular matrix. Accordingly, we studied aortic stiffness in young (16 wks) and old (64 wks) spontaneously hypertensive rats and Wistar-Kyoto wild-type controls. Systolic and pulse pressures were significantly increased in young spontaneously hypertensive rats, compared to young Wistar-Kyoto rats, and these continued to rise in old spontaneously hypertensive rats, compared to age-matched controls. Excised aortic ring segments exhibited significantly greater elastic moduli in both young and old spontaneously hypertensive rats vs. Wistar-Kyoto rats. Vascular smooth muscle cells were isolated from the thoracic aorta, and stiffness and adhesion to fibronectin were measured by atomic force microscopy. Hypertension increased both vascular smooth muscle cell stiffness and vascular smooth muscle cell adhesion, and these increases were both augmented with aging. By contrast, hypertension did not affect histological measures of aortic collagen and elastin, which were predominantly changed by aging. This supports the concept that stiffness and adhesive properties of vascular smooth muscle cells are novel mechanisms contributing to the increased aortic stiffness occurring with hypertension superimposed on aging.

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Section: Discussionmentioning

confidence: 99%

Augmented Vascular Smooth Muscle Cell Stiffness and Adhesion When Hypertension Is Superimposed on Aging

et al. 2015

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“…Angiotensin II (AngII), a well characterized vasoconstrictor in the renin-angiotensin system, contributes to smooth muscle proliferation through increased integrin activation and enhanced application of mechanical forces to integrin adhesions [192, 193]. AngII induces smooth muscle adhesion to collagen and fibronectin through the AT1 receptor [192–194], resulting in FAK-dependent ERK activation and enhanced cell proliferation [195, 196].…”

Section: Integrins In Smooth Muscle Migration and Proliferationmentioning

confidence: 99%

“…AngII induces smooth muscle adhesion to collagen and fibronectin through the AT1 receptor [192–194], resulting in FAK-dependent ERK activation and enhanced cell proliferation [195, 196]. Cytoskeletal stiffening and contraction of smooth muscle cells treated with AngII results in elevated blood pressure [192, 193, 197], thereby enhancing mechanical load on the smooth muscle integrins. However, integrin signaling may also contribute to vasoconstriction, as treatment with the integrin inhibitor RGDS reduced vasoconstriction to AngII but not other vasoconstrictors [198].…”

Section: Integrins In Smooth Muscle Migration and Proliferationmentioning

confidence: 99%

Integrin signaling in atherosclerosis

Finney

Stokes

Pattillo

et al. 2017

Cell. Mol. Life Sci.

112

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Atherosclerosis, a chronic lipid-driven inflammatory disease affecting large arteries, represents the primary cause of cardiovascular disease in the world. The local remodeling of the vessel intima during atherosclerosis involves the modulation of vascular cell phenotype, alteration of cell migration and proliferation, and propagation of local extracellular matrix remodeling. All of these responses represent targets of the integrin family of cell adhesion receptors. As such, alterations in integrin signaling affect multiple aspects of atherosclerosis, from the earliest induction of inflammation to the development of advanced fibrotic plaques. Integrin signaling has been shown to regulate endothelial phenotype, facilitate leukocyte homing, affect leukocyte function, and drive smooth muscle fibroproliferative remodeling. In addition, integrin signaling in platelets contributes to the thrombotic complications that typically drive the clinical manifestation of cardiovascular disease. In this review, we examine the current literature on integrin regulation of atherosclerotic plaque development and the suitability of integrins as potential therapeutic targets to limit cardiovascular disease and its complications.

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“…AngII also strongly regulates vascular remodeling via VSMC hypertrophy and hyperplasia (70). In addition, AngII increases VSMC stiffness via increased VSMC E-modulus and adhesion to ECM proteins (59, 71). AngII-mediated vascular remodeling has been extensively studied and is mediated by a plethora of intracellular pathways downstream of the AngII type 1 receptor (AT 1 R); this triggers proproliferative, profibrotic, and pro-inflammatory signals, all contributing to progression of the disease.…”

Section: Renin-angiotensin System (Ras)mentioning

confidence: 99%

Coronary microvascular disease as an early culprit in the pathophysiology of diabetes and metabolic syndrome

Labazi

Trask

2017

Pharmacological Research

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Metabolic syndrome (MetS) is a group of cardio-metabolic risk factors that includes obesity, insulin resistance, hypertension, and dyslipidemia; these are also a combination of independent coronary artery disease (CAD) risk factors. Alarmingly, the prevalence of MetS risk factors are increasing and a leading cause for mortality. In the vasculature, complications from MetS and type 2 diabetes (T2D) can be divided into microvascular (retinopathy and nephropathy) and macrovascular (cardiovascular diseases and erectile dysfunction). In addition to vascular and endothelial dysfunction, vascular remodeling and stiffness are also hallmarks of cardiovascular disease (CVD), and well-characterized vascular changes that are observed in the early stages of hypertension, T2D, and obesity (1-3). In the heart, the link between obstructive atherosclerosis of coronary macrovessels and myocardial ischemia (MI) is well established. However, recent studies show that abnormalities in the coronary microcirculation are associated with functional and structural changes in coronary microvessels (classically defined as being <150-200 μm internal diameter), which may cause or contribute to MI even in the absence of obstractive CAD. This suggests a prognostic value of an abnormal coronary microcirculation as an early sub-clinical culprit in the pathogenesis and progression of heart disease in T2D and MetS. The aim of this review is to summarize recent studies investigating the coronary microvascular remodeling in an early pre-atherosclerotic phase of MetS and T2D, and to explore potential mechanisms associated with the timing of coronary microvascular remodeling relative to that of the macrovasculature.

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Coordination of fibronectin adhesion with contraction and relaxation in microvascular smooth muscle

Cited by 64 publications

References 43 publications

Augmented Vascular Smooth Muscle Cell Stiffness and Adhesion When Hypertension Is Superimposed on Aging

Augmented Vascular Smooth Muscle Cell Stiffness and Adhesion When Hypertension Is Superimposed on Aging

Integrin signaling in atherosclerosis

Coronary microvascular disease as an early culprit in the pathophysiology of diabetes and metabolic syndrome

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