Structure of mammalian portal vein: Postnatal establishment of two mutually perpendicular medial muscle zones in the rat

Ts’ao, Chung-hsin; Glagov, Seymour; Kelsey, Billy F.

doi:10.1002/ar.1091710403

Cited by 18 publications

(11 citation statements)

References 16 publications

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“…The rat portal vein provides a more physiologically relevant system to study the mechanisms of phenotypic modulation compared to a cultured cell system, where a fully differentiated VSM phenotype is not possible. In the neonatal portal vein (rat and human) smooth muscle cells are in an undifferentiated, proliferating (hyperplastic) state and resemble myoblasts [22]. At 2 -4 days the neonatal portal vein is contractile although has lower levels of smooth muscle-specific proteins [15] and expresses known markers of proliferation [19] as previously demonstrated by our group.…”

Section: Discussionsupporting

confidence: 70%

PDGF-induced signaling in proliferating and differentiated vascular smooth muscle: Effects of altered intracellular Ca regulation

Egan

Wainwright

Wadsworth

et al. 2005

Cardiovascular Research

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Section: Discussionsupporting

confidence: 70%

PDGF-induced signaling in proliferating and differentiated vascular smooth muscle: Effects of altered intracellular Ca regulation

Egan

Wainwright

Wadsworth

et al. 2005

Cardiovascular Research

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“…22 Two to 4 days after birth, the smooth muscle cells are myoblasts, and development is essentially complete at Ϸ28 days. 22 Morphological studies of aortic development 23 have shown that at birth, the aorta is still undergoing structural development, including hypertrophy and hyperplasia. 23 This also includes a doubling in vessel wall thickness produced primarily by the growth of the extracellular matrix.…”

Section: Discussionmentioning

confidence: 99%

Expression and Distribution of the Type 1 and Type 3 Inositol 1,4,5-Trisphosphate Receptor in Developing Vascular Smooth Muscle

Tasker

Michelangeli

Nixon

1999

Circulation Research

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Abstract-The recent discoveries of inositol 1,4,5-trisphosphate (IP 3 ) receptor subtypes with different affinities for IP 3 and their potential involvement in development has important consequences for vascular smooth muscle. This study has examined the expression and distribution of the type 1 and type 3 IP 3 receptor subtypes in developing rat vascular smooth muscles. Immunoblotting of portal vein and aorta from neonatal (2 to 4 days) and fully developed (6 weeks) rats revealed significantly higher levels of the type 3 IP 3 receptor expression in neonatal, compared with developed, vascular smooth muscles. concentration. 1 It is now well established that a major pathway for increasing intracellular Ca 2ϩ in smooth muscle is the activation of phospholipase C via activation of a plasma membrane receptor, which leads to the production of inositol 1,4,5-trisphosphate (IP 3 ). 2 IP 3 binds to specific IP 3 receptors in the smooth muscle cell, which produces a release of Ca 2ϩ from the intracellular stores. 3,4 Several investigators have isolated full-length cDNA clones that encode at least 3 distinct IP 3 receptors: type 1, 5 type 2, 6 and type 3. 7,8 Type 1 IP 3 receptor is expressed in many cell types, 9 type 2 IP 3 receptor is expressed in brain and heart, 10 and type 3 IP 3 receptor is expressed predominantly in nonneural tissues. 7 Messenger RNA for type 1, 2, and 3 IP 3 receptors has been detected in nonvascular smooth muscle, 11,12 and in a vascular smooth muscle cell line, only mRNA for type 1 and type 3 receptors was detected. 13 In smooth muscle, the type 1 IP 3 receptor has been localized to the sarcoplasmic reticulum throughout the cell. 14 The role of the different IP 3 receptor subtypes in smooth muscle remains to be established, although distinct functions of the type 1 and type 3 IP 3 receptors are suggested by their different binding affinities for IP 3 ; type 3 receptor has a 10-fold lower affinity than type 1 receptor. 12 In vascular smooth muscle cells, alterations in the IP 3 receptor subtype expression and/or localization could have functional implications for Ca 2ϩ homeostasis in blood vessels. To date, no studies have investigated the IP 3 receptor subtypes expressed in vascular smooth muscle or examined possible circumstances in which these may be altered. There is evidence that the expression of IP 3 receptor subtypes changes during differentiation in some cell types, which suggests a possible involvement in cell development. 15,16 Developmentally associated alterations in messenger RNA levels for IP 3 receptors have also been observed in the mouse cerebellum. 17 These developmental changes may occur in vascular smooth muscle, which given the difference in IP 3 affinities of the different subtypes, 12 could potentially have functional implications for the regulation of blood vessel development.This study examined the expression and distribution of the type 1 and type 3 IP 3 receptor in vascular smooth muscle from neonatal and fully developed rats. We reveal a significant

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“…Rat portal venous smooth muscle differentiation occurs within the first 3 wk of the neonatal period, and by 5 wk of age the rat PV displays characteristic phasic contractile activity (116,217). In species that are more mature at birth such as cat, guinea pig, and human this process may begin prenatally but extends well into the postnatal period (31,134).…”

Section: Blood Vessel Developmentmentioning

confidence: 99%

Vascular smooth muscle phenotypic diversity and function

Fisher

2010

Physiological Genomics

141

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The control of force production in vascular smooth muscle is critical to the normal regulation of blood flow and pressure, and altered regulation is common to diseases such as hypertension, heart failure, and ischemia. A great deal has been learned about imbalances in vasoconstrictor and vasodilator signals, e.g., angiotensin, endothelin, norepinephrine, and nitric oxide, that regulate vascular tone in normal and disease contexts. In contrast there has been limited study of how the phenotypic state of the vascular smooth muscle cell may influence the contractile response to these signaling pathways dependent upon the developmental, tissue-specific (vascular bed) or disease context. Smooth, skeletal, and cardiac muscle lineages are traditionally classified into fast or slow sublineages based on rates of contraction and relaxation, recognizing that this simple dichotomy vastly underrepresents muscle phenotypic diversity. A great deal has been learned about developmental specification of the striated muscle sublineages and their phenotypic interconversions in the mature animal under the control of mechanical load, neural input, and hormones. In contrast there has been relatively limited study of smooth muscle contractile phenotypic diversity. This is surprising given the number of diseases in which smooth muscle contractile dysfunction plays a key role. This review focuses on smooth muscle contractile phenotypic diversity in the vascular system, how it is generated, and how it may determine vascular function in developmental and disease contexts.

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Structure of mammalian portal vein: Postnatal establishment of two mutually perpendicular medial muscle zones in the rat

Cited by 18 publications

References 16 publications

PDGF-induced signaling in proliferating and differentiated vascular smooth muscle: Effects of altered intracellular Ca regulation

PDGF-induced signaling in proliferating and differentiated vascular smooth muscle: Effects of altered intracellular Ca regulation

Expression and Distribution of the Type 1 and Type 3 Inositol 1,4,5-Trisphosphate Receptor in Developing Vascular Smooth Muscle

Vascular smooth muscle phenotypic diversity and function

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