Reduced laminin immunoreactivity in the blood vessel wall of ageing rats correlates with reduced innervation in vivo and following transplantation

Isabella Gavazzi; Karen S. Boyle; David Edgar; Timothy Cowen

doi:10.1007/bf00307955

Gene-Eluting Stents: Comparison of Adenoviral and Adeno- Associated Viral Gene Delivery to the Blood Vessel Wall In Vivo

Human Gene Therapy ◽

10.1089/hum.2006.17.741 ◽

2006 ◽

Vol 17 (7) ◽

pp. 741-750 ◽

Cited By ~ 37

Author(s):

Faisal Sharif ◽

Sean O. Hynes ◽

Jill McMahon ◽

Ronan Cooney ◽

Siobhan Conroy ◽

...

Keyword(s):

Gene Delivery ◽

Blood Vessel ◽

Vessel Wall ◽

Viral Gene ◽

Blood Vessel Wall ◽

Viral Gene Delivery

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Macrovascular thrombosis is driven by tissue factor derived primarily from the blood vessel wall

Blood ◽

10.1182/blood-2004-06-2225 ◽

2005 ◽

Vol 105 (1) ◽

pp. 192-198 ◽

Cited By ~ 212

Author(s):

Sharlene M. Day ◽

Jennifer L. Reeve ◽

Brian Pedersen ◽

Diana M Farris ◽

Daniel D. Myers ◽

...

Keyword(s):

Blood Vessel ◽

Tissue Factor ◽

Vessel Wall ◽

Thrombus Formation ◽

Vena Cava ◽

Vascular Wall ◽

Blood Vessel Wall ◽

Wild Type

Abstract Leukocytes and leukocyte-derived microparticles contain low levels of tissue factor (TF) and incorporate into forming thrombi. Although this circulating pool of TF has been proposed to play a key role in thrombosis, its functional significance relative to that of vascular wall TF is poorly defined. We tested the hypothesis that leukocyte-derived TF contributes to thrombus formation in vivo. Compared to wild-type mice, mice with severe TF deficiency (ie, TF–/–, hTF-Tg+, or “low-TF”) demonstrated markedly impaired thrombus formation after carotid artery injury or inferior vena cava ligation. A bone marrow transplantation strategy was used to modulate levels of leukocyte-derived TF. Transplantation of low-TF marrow into wild-type mice did not suppress arterial or venous thrombus formation. Similarly, transplantation of wild-type marrow into low-TF mice did not accelerate thrombosis. In vitro analyses revealed that TF activity in the blood was very low and was markedly exceeded by that present in the vessel wall. Therefore, our results suggest that thrombus formation in the arterial and venous macrovasculature is driven primarily by TF derived from the blood vessel wall as opposed to leukocytes.

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Gene-eluting stents: non-viral, liposome-based gene delivery of eNOS to the blood vessel wall in vivo results in enhanced endothelialization but does not reduce restenosis in a hypercholesterolemic model

Gene Therapy ◽

10.1038/gt.2011.92 ◽

2011 ◽

Vol 19 (3) ◽

pp. 321-328 ◽

Cited By ~ 26

Author(s):

F Sharif ◽

S O Hynes ◽

K J A McCullagh ◽

S Ganley ◽

U Greiser ◽

...

Keyword(s):

Gene Delivery ◽

Blood Vessel ◽

Vessel Wall ◽

Blood Vessel Wall

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Transmural strain distribution in the blood vessel wall

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00607.2004 ◽

2005 ◽

Vol 288 (2) ◽

pp. H881-H886 ◽

Cited By ~ 20

Author(s):

Xiaomei Guo ◽

Xiao Lu ◽

Ghassan S. Kassab

Keyword(s):

Blood Vessel ◽

Experimental Evidence ◽

Strain Distribution ◽

Vessel Wall ◽

Load Condition ◽

Opening Angle ◽

Stress And Strain ◽

Blood Vessel Wall ◽

Arterial Tree

The transmural distributions of stress and strain at the in vivo state have important implications for the physiology and pathology of the vessel wall. The uniform transmural strain hypothesis was proposed by Takamyzawa and Hayashi (Takamizawa K and Hayashi K. J Biomech 20: 7–17, 1987; Biorheology 25: 555–565, 1988) as describing the state of arteries in vivo. From this hypothesis, they derived the residual stress and strain at the no-load condition and the opening angle at the zero-stress state. However, the experimental evidence cited by Takamyzawa and Hayashi ( J Biomech 20: 7–17, 1987; and Biorheology 25: 555–565, 1988) to support this hypothesis was limited to arteries whose opening angles (θ) are <180°. It is well known, however, that θ > 180° do exist in the cardiovascular system. Our hypothesis is that the transmural strain distribution cannot be uniform when θ is >180°. We present both theoretical and experimental evidence for this hypothesis. Theoretically, we show that the circumferential stretch ratio cannot physically be uniform across the vessel wall when θ exceeds 180° and the deviation from uniformity will increase with an increase in θ beyond 180°. Experimentally, we present data on the transmural strain distribution in segments of the porcine aorta and coronary arterial tree. Our data validate the theoretical prediction that the outer strain will exceed the inner strain when θ > 180°. This is the converse of the gradient observed when the residual strain is not taken into account. Although the strain distribution may not be uniform when θ exceeds 180°, the uniformity of stress distribution is still possible because of the composite nature of the blood vessel wall, i.e., the intima-medial layer is stiffer than the adventitial layer. Hence, the larger strain at the adventitia can result in a smaller stress because the adventitia is softer at physiological loading.

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Gene-Eluting Stents: Comparison of Adenoviral and Adeno- Associated Viral Gene Delivery to the Blood Vessel Wall In Vivo

Human Gene Therapy ◽

10.1089/hum.2006.17.ft-223 ◽

2006 ◽

Vol 0 (0) ◽

pp. 060801084750030

Author(s):

Faisal Sharif ◽

Sean O. Hynes ◽

Jill McMahon ◽

Ronan Cooney ◽

Siobhan Conroy ◽

...

Keyword(s):

Gene Delivery ◽

Blood Vessel ◽

Vessel Wall ◽

Viral Gene ◽

Blood Vessel Wall ◽

Viral Gene Delivery

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The Intravascular Generation of Fibrinogen Derivatives and the Blood Vessel Wall in Venous Thrombosis and Disseminated Intravascular Coagulation

Thrombosis and Haemostasis ◽

10.1055/s-0038-1651902 ◽

1977 ◽

Vol 38 (04) ◽

pp. 0831-0849 ◽

Cited By ~ 1

Author(s):

Gwendolyn J. Stewart

Keyword(s):

Blood Vessel ◽

Venous Thrombosis ◽

Vessel Wall ◽

Fluid Phase ◽

Primary Site ◽

Blood Vessel Wall ◽

Fibrin Deposition ◽

Tissue Destruction ◽

Fibrin Formation ◽

Rich Material

SummaryBoth deep venous thrombosis and DIC are intermediate mechanisms of disease – both are a consequence of the deposition of fibrin-rich material in blood vessels some distance from the primary site of tissue destruction. The great difference in the sites of fibrin deposition may depend on the extent and site of activation of the clotting mechanism. DIC likely occurs in the fluid phase of the blood as a consequence of massive fibrin formation while thrombosis results from limited fibrin formation at the interface between blood and vessel wall. Leukocytes may be essential for attaching thrombi to the vessel wall in many places.

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