Developmental Stage Dependent Expression of the Endothelial Stress Fibers and Organization of Fibronectin Fibrils in the Aorta of Chick Embryos

Jinguji, Yoichi

doi:10.2108/zsj.20.1359

Cited by 5 publications

(4 citation statements)

References 26 publications

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“…Native endothelial cells normally reside on a matrix composed primarily of laminin and collagen IV (39). However, the subendothelial matrix in fetal or newborn arteries is enriched in fibronectin, with endothelial stress fibers connecting via focal adhesion complexes to fibronectin fibrils (3, 5, 6, 40). As endothelial cells mature during the immediate postnatal period, they reorganize their underlying matrix, decreasing the levels of fibronectin and increasing laminin and collagen IV (1, 3, 4, 40).…”

Section: The Normal Maturation Of Protective Arterial Endotheliummentioning

confidence: 99%

In Development—A New Paradigm for Understanding Vascular Disease

Flavahan

2017

Journal of Cardiovascular Pharmacology

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Under physiological conditions, the arterial endothelium exerts a powerful protective influence to maintain vascular homeostasis. However, during the development of vascular disease, these protective activities are lost and dysfunctional endothelial cells actually promote disease pathogenesis. Numerous investigations have analyzed the characteristics of dysfunctional endothelium with a view to understanding the processes responsible for the dysfunction and to determining their role in vascular pathology. The present review adopts an alternate approach: reviewing the mechanisms that contribute to the initial formation of a healthy protective endothelium and on how those mechanisms may be disrupted, precipitating the appearance of dysfunctional endothelial cells and the progression of vascular disease. This approach, which highlights the role of endothelial adherens junctions and VE-cadherin in endothelial maturation and endothelial dysfunction, provides new insight into the remarkable biology of this important cell layer and its role in vascular protection and vascular disease.

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Section: The Normal Maturation Of Protective Arterial Endotheliummentioning

confidence: 99%

In Development—A New Paradigm for Understanding Vascular Disease

Flavahan

2017

Journal of Cardiovascular Pharmacology

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“…Indeed, endothelial adhesion to fibronectin stimulates stress fiber formation, which is prevented by inhibiting Rho kinase (9). The subendothelial matrix of endothelial cells lining fetal or newborn arteries is enriched in fibronectin, with endothelial stress fibers connecting via focal adhesion complexes to fibronectin fibrils (4,5,14,23). As endothelial cells mature during the immediate postnatal period, they reorganize their underlying matrix, decreasing the levels of fibronectin and generating a normal subendothelial matrix (4,5,15,16).…”

Section: H630mentioning

confidence: 99%

The atypical structure and function of newborn arterial endothelium is mediated by Rho/Rho kinase signaling

Flavahan

2014

American Journal of Physiology-Heart and Circulatory Physiology

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Flavahan S, Flavahan NA. The atypical structure and function of newborn arterial endothelium is mediated by Rho/Rho kinase signaling. Am J Physiol Heart Circ Physiol 307: H628 -H632, 2014. First published June 20, 2014 doi:10.1152/ajpheart.00327.2014.-Endothelium of fetal or newborn arteries is atypical, displaying actin stress fibers and reduced nitric oxide (NO)-mediated dilatation. This study tested the hypothesis that Rho/Rho kinase signaling, which promotes endothelial stress fibers and inhibits endothelial dilatation, contributed to this phenotype. Carotid arteries were isolated from newborn [postnatal day 1 (P1)], P7, and P21 mice. Endothelial dilatation to acetylcholine (pressure myograph) was minimal at P1, increased at P7, and further increased at P21. Inhibition of Rho (C3 transferase) or Rho kinase (Y27632, fasudil) significantly increased dilatation to acetylcholine in P1 arteries but had no effect in P7 or P21 arteries. After inhibition of NO synthase (N G -nitro-L-arginine methyl ester), Rho kinase inhibition no longer increased acetylcholine responses in P1 arteries. Rho kinase inhibition did not affect dilatation to the NO donor DEA-NONOate. The endothelial actin cytoskeleton was labeled with phalloidin and visualized by laser-scanning microscopy. In P1 arteries, the endothelium had prominent transcytoplasmic stress fibers, whereas in P7 and P21 arteries, the actin fibers had a significantly reduced intensity and were restricted to cell borders. Phosphorylation of myosin light chains, a Rho kinase substrate, was highest in P1 endothelium and significantly reduced in P7 and P21 endothelium (laser-scanning microscopy). In P1 arteries, inhibition of Rho (C3 transferase) or Rho kinase (Y27632) significantly reduced the intensity of actin fibers, which were restricted to cell borders. Similarly, in P1 arteries, Rho inhibition significantly reduced endothelial levels of phosphorylated myosin light chains. These results indicate that the atypical function and morphology of newborn endothelium is mediated by Rho/Rho kinase signaling.

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“…Assembled FN also regulates phenotypic plasticity in smooth muscle cells223. Early studies suggested that ECs are involved in remodeling FN in the basal lamina and that FN organization, similar to actin stress fiber organization, shows flow dependency2425. In the descending aorta, an area of the vasculature that experiences laminar flow, FN fibrils are thick and align in the direction of flow.…”

mentioning

confidence: 99%

“…In the descending aorta, an area of the vasculature that experiences laminar flow, FN fibrils are thick and align in the direction of flow. However, at the renal artery bifurcation, an area of disturbed flow, FN fibrils are randomly distributed25. The role of FN assembly in vessel function was more definitively tested using a peptide that inhibits FN polymerization: when this peptide was utilised in a mouse model of partial carotid artery ligation (CAL), it inhibited intima-media thickening (IMT) and flow-mediated vascular remodeling2.…”

mentioning

confidence: 99%

Haemodynamics Regulate Fibronectin Assembly via PECAM

Chen

Givens

Reader

et al. 2017

Sci Rep

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Fibronectin (FN) assembly and fibrillogenesis are critically important in both development and the adult organism, but their importance in vascular functions is not fully understood. Here we identify a novel pathway by which haemodynamic forces regulate FN assembly and fibrillogenesis during vascular remodelling. Induction of disturbed shear stress in vivo and in vitro resulted in complex FN fibril assembly that was dependent on the mechanosensor PECAM. Loss of PECAM also inhibited the cell-intrinsic ability to remodel FN. Gain- and loss-of-function experiments revealed that PECAM-dependent RhoA activation is required for FN assembly. Furthermore, PECAM−/− mice exhibited reduced levels of active β1 integrin that were responsible for reduced RhoA activation and downstream FN assembly. These data identify a new pathway by which endothelial mechanotransduction regulates FN assembly and flow-mediated vascular remodelling.

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Developmental Stage Dependent Expression of the Endothelial Stress Fibers and Organization of Fibronectin Fibrils in the Aorta of Chick Embryos

Cited by 5 publications

References 26 publications

In Development—A New Paradigm for Understanding Vascular Disease

In Development—A New Paradigm for Understanding Vascular Disease

The atypical structure and function of newborn arterial endothelium is mediated by Rho/Rho kinase signaling

Haemodynamics Regulate Fibronectin Assembly via PECAM

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