Immunohistochemical identification of arteriolar development using markers of smooth muscle differentiation. Evidence that capillary arterialization proceeds from terminal arterioles.

Price, Richard J.; Owens, Gary K.; Skalak, Thomas C.

doi:10.1161/01.res.75.3.520

Cited by 107 publications

(127 citation statements)

References 16 publications

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“…We investigated growth of arterioles by counting the number of vessels stained with fluorescently labelled a smooth muscle actin (aSMA) and myosin heavy chain (MHC) antibodies. The former were shown to stain terminal arterioles in younger animals while more mature arterioles showed staining for both (Price et al 1994); in our experience small venules are not stained.…”

contrasting

confidence: 45%

Cardiovascular/Respiratory Control

1995

The Journal of Physiology

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contrasting

confidence: 45%

Cardiovascular/Respiratory Control

1995

The Journal of Physiology

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“…For example, SM α-actin can be expressed by pericytes, immature smooth muscle cells, which express SM α-actin and not SM myosin heavy chain, and mature smooth muscle cells, which express both contractile proteins (Nehls and Drenckhahn, 1991;Price et al, 1994;Van Gieson et al, 2003;Yoshida and Owens, 2005). Desmin and PDGF-β can also be expressed by smooth muscle cells and interstitial fibroblasts (Nehls et al, 1992).…”

Section: Role For Perivascular Cells In Hypertensionmentioning

confidence: 99%

Chapter 12 Structure of Microvascular Networks in Genetic Hypertension

Murfee

Schmid‐Schönbein

2008

Methods in Enzymology

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Microvascular rarefaction, defined by a loss of terminal arterioles, small venules and/or capillaries, is a common characteristic of the hypertension syndrome. While rarefaction has been associated with vessel specific free radical production, deficient leukocyte adhesion, and cellular apoptosis, the relationships of rarefaction with structural alterations at the network and cellular level remain largely unexplored. The objective of this study was to examine the architecture and perivascular cell phenotypes along microvascular networks in hypertensive versus normotensive controls in the context of imbalanced angiogenesis. Mesenteric tissues from age-matched adult male spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats were harvested and immnolabeled for PECAM and neuron-glia antigen 2 (NG2). Evaluation of intact rat mesenteric microvascular networks rats suggests that network alterations associated with hypertension are more complex than just a loss of vessels. Typical SHR versus WKY networks demonstrate a reduced branching architecture marked by more proximal arteriole/venous anastomoses and an absence of NG2 labeling along arterioles. Although less frequent, larger SHR microvascular networks display regions of dramatically increased vascular density. SHR and WKY lymphatic networks demonstrate increased vessel diameters and vascular density compared to networks in normotensive Wistar rats (the strain from which both the SHR and WKY originated). These observations provide a rationale for investigating the presence of local angiogenic factors and response of microvascular networks to therapies aimed at reversing rarefaction in genetic hypertension.

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“…Angiogenesis refers to the process of blood vessel sprouting from preexisting capillaries, and includes subsequent remodeling processes such as pruning, vessel enlargement, and intussusception (vessel splitting) to form stable vessel networks [2,[11][12][13][14]. Arteriogenesis mainly denotes the enlargement of arterial vessels to adjust for lost flow in other vessels [11,15], and this term is also used at times to include the process of remodeling of existing capillaries to form arterioles [16].…”

Section: Introductionmentioning

confidence: 99%

Spatiotemporal control over growth factor signaling for therapeutic neovascularization☆

Cao

Mooney

2007

Advanced Drug Delivery Reviews

110

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Many of the qualitative roles of growth factors involved in neovascularization have been delineated, but it is unclear yet from an engineering perspective how to use these factors as therapies. We propose that an approach that integrates quantitative spatiotemporal measurements of growth factor signaling using 3-D in vitro and in vivo models, mathematic modeling of factor tissue distribution, and new delivery technologies may provide an opportunity to engineer neovascularization on demand.

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Immunohistochemical identification of arteriolar development using markers of smooth muscle differentiation. Evidence that capillary arterialization proceeds from terminal arterioles.

Cited by 107 publications

References 16 publications

Cardiovascular/Respiratory Control

Cardiovascular/Respiratory Control

Chapter 12 Structure of Microvascular Networks in Genetic Hypertension

Spatiotemporal control over growth factor signaling for therapeutic neovascularization☆

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