Computational modeling of coupled blood-wall mass transport of LDL: effects of local wall shear stress

Olgaç, Ufuk; Kurtcuoglu, Vartan; Poulikakos, Dimos

doi:10.1152/ajpheart.01082.2007

Cited by 118 publications

(215 citation statements)

References 37 publications

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“…In order to specify a pressure drop across the arterial wall, a constant pressure of 2333.022 Pa (17.5 mmHg) was assumed at the intima-media interface [41,47]. The coupling of the flow dynamics in the artery lumen with that in the arterial wall is achieved by a three-pore model, and a transmural volumetric flux (J v (m s 21 )) through the endothelium is calculated by means of this theory, which takes into account the vesicular pathway, normal endothelial junctions and leaky junctions [41] where L p,nj is the hydraulic conductivity for the normal junction and L p,lj , the hydraulic conductivity for the leaky junction defined as…”

Section: Transmural Plasma Flow Throughout the Artery Wallmentioning

confidence: 99%

“…The correlation between WSS and f lj is obtained using published experimental data , and the number of mitotic cells that is directly related to the WSS. For more details, see Olgac et al [41].…”

Section: Transmural Plasma Flow Throughout the Artery Wallmentioning

confidence: 99%

“…The lumen-artery wall interface coupling of solute dynamics is achieved by a three-pore model that takes into account the vesicular pathway, normal endothelial junctions and leaky junctions. Thus, the solute flux of LDL at the endothelium was defined as a boundary condition by the Kedem & Katchalsky [18] [41,55]. Furthermore, because the entrance of LDL into the arterial wall cannot grow indefinitely, there is a natural saturation incorporated by the C th LDL in the denominator of equation (3.14).…”

Section: 22mentioning

confidence: 99%

“…Therefore, the dependence of fluid and mass transport through the endothelium on local blood flow characteristics has been modelled using a three-pore model, because this is more accurate than the use of a single pathway approach [39][40][41]. This model is represented by the vesicular pathway, normal junctions and leaky junctions.…”

Section: Introductionmentioning

confidence: 99%

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Mathematical modelling of atheroma plaque formation and development in coronary arteries

Cilla

Peña

Martı́nez

2014

J. R. Soc. Interface.

114

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Atherosclerosis is a vascular disease caused by inflammation of the arterial wall, which results in the accumulation of low-density lipoprotein (LDL) cholesterol, monocytes, macrophages and fat-laden foam cells at the place of the inflammation. This process is commonly referred to as plaque formation. The evolution of the atherosclerosis disease, and in particular the influence of wall shear stress on the growth of atherosclerotic plaques, is still a poorly understood phenomenon. This work presents a mathematical model to reproduce atheroma plaque growth in coronary arteries. This model uses the Navier-Stokes equations and Darcy's law for fluid dynamics, convectiondiffusion-reaction equations for modelling the mass balance in the lumen and intima, and the Kedem-Katchalsky equations for the interfacial coupling at membranes, i.e. endothelium. The volume flux and the solute flux across the interface between the fluid and the porous domains are governed by a three-pore model. The main species and substances which play a role in early atherosclerosis development have been considered in the model, i.e. LDL, oxidized LDL, monocytes, macrophages, foam cells, smooth muscle cells, cytokines and collagen. Furthermore, experimental data taken from the literature have been used in order to physiologically determine model parameters. The mathematical model has been implemented in a representative axisymmetric geometrical coronary artery model. The results show that the mathematical model is able to qualitatively capture the atheroma plaque development observed in the intima layer.

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Section: Transmural Plasma Flow Throughout the Artery Wallmentioning

confidence: 99%

Section: Transmural Plasma Flow Throughout the Artery Wallmentioning

confidence: 99%

Section: 22mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Mathematical modelling of atheroma plaque formation and development in coronary arteries

Cilla

Peña

Martı́nez

2014

J. R. Soc. Interface.

114

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“…on hemodynamics and its relationship to atherosclerosis [29][30][31]. Some of these models have been customized with individual patient data [32,33].…”

Section: Discussionmentioning

confidence: 99%

The Apoe-/- Mouse PhysioLab® Platform: A Validated Physiologically-based Mathematical Model of Atherosclerotic Plaque Progression in the Apoe-/- Mouse

Chan¹,

Vuillaume²,

Bever³

et al. 2012

Biodiscovery

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Directed glia‐assisted angiogenesis in a mature neurosensory structure: Pericytes mediate an adaptive response in human dental pulp that maintains blood‐barrier function

Farahani

Sarrafpour

Simonian

et al. 2012

J of Comparative Neurology

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The specialized tightly controlled microcirculation of craniofacial neurosensory organs is an essential evolutionary adaptation and yet a dilemma where angiogenic remodeling occurs. Despite extreme plasticity of neurosensory structures, the capacity to reconcile barrier phenotype of the microcirculation with an angiogenic cascade is not known. Here we provide primary evidence for such a response in an elemental neurosensory structure, human dental pulp, following chronic carious insult. In response to hypoxic challenge neurosensory odontoblasts express hypoxia-inducible factor-1α and notch-1. Associated radial rearrangement of astrocyte-like telacytes that communicate through a cell-poor zone with the microvasculature is observed. Activated pericytes characterized by expression of α-smooth muscle actin are located adjacent to the telacyte attachment to the vasculature. In this location, endothelial expression of sonic hedgehog parallels expression of notch-1 by pericytes. The angiogenic response is initiated by pericyte contraction and altered endothelial polarity and proliferation leading to intussusception of endothelial cells and extensive remodeling of basement membrane with upregulation of laminin-8 and laminin-5. These responses guide intravascular loop formation that maintains both intact basement membrane and tight junctions. This initial phase is followed by formation of anastomoses that enhance the hemodynamic capacity of the intravascular loops. The formation of anastomoses is mediated by extension of cytonemes from pericytes guided by MHC-II(+)/CD-163(+) microglia aligned with the telacytes. The cytonemes seek out pericytes on adjacent intravascular loops to initiate migration of endothelial cells. These findings support a new paradigm for understanding angiogenic capacity of neurosensory structures and aberrations of this response manifest as neurovasculopathies.

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Computational modeling of coupled blood-wall mass transport of LDL: effects of local wall shear stress

Cited by 118 publications

References 37 publications

Mathematical modelling of atheroma plaque formation and development in coronary arteries

Mathematical modelling of atheroma plaque formation and development in coronary arteries

The Apoe-/- Mouse PhysioLab® Platform: A Validated Physiologically-based Mathematical Model of Atherosclerotic Plaque Progression in the Apoe-/- Mouse

Directed glia‐assisted angiogenesis in a mature neurosensory structure: Pericytes mediate an adaptive response in human dental pulp that maintains blood‐barrier function

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