Increase in Collagen Turnover But Not in Collagen Fiber Content Is Associated with Flow-Induced Arterial Remodeling

Sluijter, Joost P.G.; Smeets, Mirjam B.; Velema, Evelyn; Pasterkamp, Gérard; Kleijn, Dominique P.V. de

doi:10.1159/000081972

Cited by 22 publications

(15 citation statements)

References 57 publications

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“…With increased flow, an upregulation of ECM genes, including collagen genes in the pulmonary artery [37], an increase of spiraled collagen in coronary arteries [38] and in collagen turnover [39] has been reported. In vitro, the gene expression of TGFβ1, a cytokine well-known to enhance collagen deposition, was increased in vascular smooth muscle cells exposed to shear stress [40].…”

Section: Discussionmentioning

confidence: 99%

High-Flow-Induced Arterial Remodeling in Rats with Different Susceptibilities to Cerebral Aneurysms

Coutard

Osborne-Pellegrin²,

Fontaine³

et al. 2006

J Vasc Res

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Background: The higher incidence of cerebral aneurysms (CAs) induced by enhanced arterial blood flow in Long Evans (LE) compared to Brown Norway (BN) rats suggests that intrinsic differences in high-flow arterial remodeling may be involved in determining CA susceptibility. Some aspects of this remodeling were compared in LE and BN rats after creation of an abdominal aortocaval fistula (ACF). Methods and Results: At 4 days with ACF, aortic luminal cross-sectional area (LCSA) determined by morphometry was increased by 20% in LE but not in BN rats. mRNA levels, determined by RT-PCR, were higher in LE than in BN rats for collagen α1(I), collagen α1(III), MMP2 and its inhibitor TIMP1 at 19 days with ACF. Nitric oxide synthase (NOS) mRNA levels were higher in LE rats at 4 days for the inducible (NOS2) isoform and at 4 and 19 days for the neuronal (NOS1) isoform. Aortic LCSA and NOS1 mRNA levels were tightly correlated and NOS inhibition prevented ACF-induced aortic remodeling in the LE rat. MMP2 and MMP7 activity, evaluated by zymography at 4 days with ACF, did not greatly differ between BN and LE. Conclusions: These data suggest that a higher intrinsic ability for high-flow-induced arterial enlargement associated with NOS gene overexpression may be a possible genetic determinant in CA susceptibility.

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Section: Discussionmentioning

confidence: 99%

High-Flow-Induced Arterial Remodeling in Rats with Different Susceptibilities to Cerebral Aneurysms

Coutard

Osborne-Pellegrin²,

Fontaine³

et al. 2006

J Vasc Res

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“…Whereas rates of production of vascular collagen decrease dramatically from high levels in development to low basal levels in maturity (Note: the half-life of vascular collagen in maturity appears to be *70 days; [9]), slightly increased rates (up to 4.5-fold above basal values) can be recovered in maturity in cases of disease, injury, or altered mechanical loading (e.g. [127][128][129]). In addition to the amount and orientation of newly deposited collagen, one of the most important and yet overlooked issues is the value of stress/strain at which collagen is deposited (which in analogy to the cytoskeletal literature could be called a prestress or prestrain).…”

Section: Matrix Turnovermentioning

confidence: 99%

Vascular Adaptation and Mechanical Homeostasis at Tissue, Cellular, and Sub-cellular Levels

Humphrey

2007

Cell Biochem Biophys

362

323

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Blood vessels exhibit a remarkable ability to adapt throughout life that depends upon genetic programming and well-orchestrated biochemical processes. Findings over the past four decades demonstrate, however, that the mechanical environment experienced by these vessels similarly plays a critical role in governing their adaptive responses. This article briefly reviews, as illustrative examples, six cases of tissue level growth and remodeling, and then reviews general observations at cell-matrix, cellular, and sub-cellular levels, which collectively point to the existence of a "mechanical homeostasis" across multiple length and time scales that is mediated primarily by endothelial cells, vascular smooth muscle cells, and fibroblasts. In particular, responses to altered blood flow, blood pressure, and axial extension, disease processes such as cerebral aneurysms and vasospasm, and diverse experimental manipulations and clinical treatments suggest that arteries seek to maintain constant a preferred (homeostatic) mechanical state. Experiments on isolated microvessels, cell-seeded collagen gels, and adherent cells isolated in culture suggest that vascular cells and sub-cellular structures such as stress fibers and focal adhesions likewise seek to maintain constant a preferred mechanical state. Although much is known about mechanical homeostasis in the vasculature, there remains a pressing need for more quantitative data that will enable the formulation of an integrative mathematical theory that describes and eventually predicts vascular adaptations in response to diverse stimuli. Such a theory promises to deepen our understanding of vascular biology as well as to enable the design of improved clinical interventions and implantable medical devices.

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“…Additionally, we can only estimate relative collagen turnover by using radiocarbon birth dating as an indicator, since the total collagen content in human CA samples cannot be monitored over time. 33 However, since collagen I is the main constituent of CAs and since we generally excised and analyzed more than 2/3 of the aneurysm dome, the birth dating measurements are likely to reflect the majority of the aneurysmal mass. Further, the measurement precision in radiocarbon birth dating corresponds to a chronological uncertainty of 1 to 3 years and current technology does not allow for better temporal resolution in samples.…”

Section: Discussionmentioning

confidence: 99%

Age of Collagen in Intracranial Saccular Aneurysms

Etminan

Dreier

Buchholz

et al. 2014

Stroke

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Background and Purpose The chronological development and natural history of cerebral aneurysms (CA) remains incompletely understood. We used 14C birth dating of a main constituent of CAs, i.e. collagen type I, as an indicator for biosynthesis and turnover of collagen in CAs in relation to human cerebral arteries to further investigate this. Methods Forty-six ruptured and unruptured CA samples from 43 patients as well 10 cadaveric human cerebral arteries were obtained. The age of collagen, extracted and purified from excised CAs, was estimated using 14C birth dating and correlated with CA and patient characteristics, including the history of risk factors associated with atherosclerosis and potentially aneurysm growth and rupture. Results Nearly all CA samples contained collagen type I which was less than 5 years old, irrespective of patient age, aneurysm size, morphology, or rupture status. However, CAs from patients with a history of risk factors (smoking or hypertension), contained significantly younger collagen than CAs from patients with no risk factors (mean 1.6±1.2 years versus 3.9±3.3 years, respectively, p= 0.012). CAs and cerebral arteries did not share one dominant structural protein, such as collagen type I, which would allow comparison of their collagen turnover. Conclusions The abundant amount of relatively young collagen type I in CAs suggests that there is on-going collagen remodeling in aneurysms, which is significantly more rapid in patients with risk factors. These findings challenge the concept that cerebral aneurysms are present for decades and that they undergo only sporadic episodes of structural change.

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Increase in Collagen Turnover But Not in Collagen Fiber Content Is Associated with Flow-Induced Arterial Remodeling

Cited by 22 publications

References 57 publications

High-Flow-Induced Arterial Remodeling in Rats with Different Susceptibilities to Cerebral Aneurysms

High-Flow-Induced Arterial Remodeling in Rats with Different Susceptibilities to Cerebral Aneurysms

Vascular Adaptation and Mechanical Homeostasis at Tissue, Cellular, and Sub-cellular Levels

Age of Collagen in Intracranial Saccular Aneurysms

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