Smooth Muscle Myosin Heavy Chain Isoforms Are Developmentally Regulated in Male Fetal and Neonatal Sheep

Chern, Jennifer; Kamm, Kristine E.; Rosenfeld, Charles R.

doi:10.1203/00006450-199511000-00011

Cited by 31 publications

(23 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similar differences occur in the maturational changes in smooth muscle proteins and the switch from a synthetic to a contractile phenotype (29,32,39). We also observed that the regulation of AT subtype expression seems to differ between vessels.…”

Section: Discussionsupporting

confidence: 68%

“…In VSM, cellular differentiation is followed by maturational events that are organ and vessel specific (29,32,38,39). We therefore hypothesized that similar changes might occur in the RAS and, in particular, in VSM AT subtype expression.…”

Section: Discussionmentioning

confidence: 99%

“…In pregnant animals, the fetus was rapidly delivered, dried, weighed, and measured to confirm gestational age. A 6-to 8-cm segment of umbilical cord was obtained, and both umbilical arteries were dissected, placed into chilled physiologic based saline, and maintained on ice as previously described (29,32). Residual blood was expressed, and Wharton's jelly and adventitia were removed using blunt and sharp dissection.…”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Vessel-Specific Regulation of Angiotensin II Receptor Subtypes During Ovine Development

et al. 2005

Self Cite

View full text Add to dashboard Cite

Umbilical and systemic responses to angiotensin II differ in term fetal sheep, and peripheral vascular responses are attenuated or absent before and after birth. These observations may reflect developmental differences in angiotensin II receptor (AT) subtypes in vascular smooth muscle (VSM). Studies of AT subtype ontogeny and regulation are generally limited to the aorta, which may not be extrapolated to other arteries, and neither is completely described during ovine development. We therefore characterized VSM AT subtype expression and regulation throughout an extended period of development in umbilical and carotid artery and aorta from fetal (85-146 d gestation), postnatal (5-23 d), and adult sheep, measuring AT 1 and AT 2 mRNA and protein and performing immunohistochemistry. Parallel increases in umbilical AT 1 mRNA and protein began early in gestation and continued to term, and although AT 2 mRNA was unchanged, protein levels decreased Ͼ90% at term. Fetal carotid AT 1 mRNA was Ͻ40% of adult values and unchanged before birth; however, AT 1 protein rose Ͼ2-fold at term. After birth, AT 1 mRNA increased to 85% of adult values and was associated with another 2-fold rise in protein. In contrast, carotid AT 2 mRNA and protein fell in parallel throughout development and were barely detectable in the newborn and the adult. Immunostaining was consistent with observations in both arteries. A third pattern occurred in aortic VSM. The ontogeny of AT subtype expression and regulation is vessel specific, with changes in umbilical VSM beginning very early in development. Although the mechanisms that regulate mRNA and protein expression are unclear, these changes parallel differences in VSM maturation and function and local blood flow. The renin-angiotensin system (RAS) is expressed early in gestation and considered an important modulator of cardiovascular development, adaptation, and blood pressure control before and after birth (1-4). In fetal and neonatal sheep, hemorrhage and hypovolemia increase circulating angiotensin II (Ang II) (5-7). Although inhibition of Ang II receptors (AT) or converting enzyme accentuates hypovolemic episodes (3,7), their effects on basal arterial pressure are inconsistent (8,9). AT blockade also modifies the baroreflex and reflex control of renal sympathetic nerve activity after birth (10,11). Recent evidence suggests the RAS also contributes to the differentiation, maturation, and/or growth of vascular smooth muscle (VSM) (12-15). Thus, prevailing evidence suggests the RAS contributes to the regulation of vascular function, maturation, and growth during development.The effects of the RAS are mediated primarily by Ang II activation of ATs, which belong to the superfamily of seven transmembrane receptors (12,16,17). They are present in mammalian fetal and adult VSM and demonstrate similar binding characteristics during development and in the adult (18 -20). In fetal sheep, AT binding density and affinity in aorta and placental arteries are unchanged in the last third of gestation and resemble ...

show abstract

Section: Discussionsupporting

confidence: 68%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Vessel-Specific Regulation of Angiotensin II Receptor Subtypes During Ovine Development

et al. 2005

Self Cite

View full text Add to dashboard Cite

show abstract

“…The mechanisms regulating VSM maturation and thus blood pressure and tissue perfusion in early development remain to be determined. myosin heavy chain isoforms; nonmuscle myosin; fetal development; receptor and nonreceptor function; smooth muscle growth; angiotensin II SMOOTH MUSCLE DEVELOPMENT normally proceeds in a wellorchestrated manner before and after birth (5,6,11,14,41,53). These changes occur in three phases: cellular differentiation, functional maturation, and growth (42).…”

mentioning

confidence: 99%

“…Thus observations of VSM function and maturation during development are likely to be specific to the vascular bed under study, and results cannot be generalized. Furthermore, this has not been thoroughly examined early in development.Maturational changes in VSM function are associated with changes in cellular protein expression in near term and newborn animals (6,11,17,43); however, this is not described in midgestation, e.g., Ͻ100 days gestation in the sheep and Յ28 wk in the human. Recent clinical advances have resulted in survival of neonates born at Յ28 wk (33).…”

mentioning

confidence: 99%

Vascular development in early ovine gestation: carotid smooth muscle function, phenotype, and biochemical markers

Hutanu¹,

Cox²,

DeSpain³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Vascular smooth muscle (VSM) maturation is developmentally regulated and differs between vascular beds. The maturation and contribution of VSM function to tissue blood flow and blood pressure regulation during early gestation are unknown. The carotid artery (CA) contributes to fetal cerebral blood flow regulation and well being. We studied CA VSM contractility, protein contents, and phenotype beginning in the midthird of ovine development. CAs were collected from early (88 -101 day of gestation) and late (138 -150 day; term ϭ day 150) fetal (n ϭ 14), newborn (6 -8 day old; n ϭ 7), and adult (n ϭ 5) sheep to measure forces in endothelium-denuded rings with KCl, phenylephrine, and ANG II; changes in cellular proteins, including total and soluble protein, actin and myosin, myosin heavy chain isoforms (MHC), filamin, and proliferating cell nuclear antigen; and vascular remodeling. KCl and phenylephrine elicited age-and dose-dependent contraction responses (P Ͻ 0.001) at all ages except early fetal, which were unresponsive. In contrast, ANG II elicited dose responses only in adults, with contractility increasing greater than fivefold vs. that shown in fetal or neonatal animals (P Ͻ 0.001). Increased contractility paralleled age-dependent increases (P Ͻ 0.01) in soluble protein, actin and myosin, filamin, adult smooth muscle MHC-2 (SM2) and medial wall thickness and reciprocal decreases (P Ͻ 0.001) in nonmuscle MHC-B, proliferating cell nuclear antigen and medial cellular density. VSM nonreceptor-and receptor-mediated contractions are absent or markedly attenuated in midgestation and increase age dependently, paralleling the transition from synthetic to contractile VSM phenotype and, in the case of ANG II, paralleling the switch to the AT1 receptor. The mechanisms regulating VSM maturation and thus blood pressure and tissue perfusion in early development remain to be determined. myosin heavy chain isoforms; nonmuscle myosin; fetal development; receptor and nonreceptor function; smooth muscle growth; angiotensin II SMOOTH MUSCLE DEVELOPMENT normally proceeds in a wellorchestrated manner before and after birth (5,6,11,14,41,53). These changes occur in three phases: cellular differentiation, functional maturation, and growth (42). During differentiation, progenitor cells derived from the mesenchyme are transformed into immature smooth muscle cells (SMC) localized to either visceral or vascular sites. The subsequent maturational changes result in developmentally regulated improvements in specific organ or vascular function essential for the well being and growth of the developing fetus and newborn. For example, functional maturation of the ovine bladder and umbilical artery smooth muscle occurs early in development (4, 6). The former is required for maintenance of fetal fluid balance and establishment of amniotic fluid volume, which permit normal lung development. The latter is essential in the regulation of fetal oxygen and nutrient uptake from the maternal placental circulation and probably blood pressure (4, 32). In co...

show abstract

Changes in detrusor smooth muscle myosin heavy chain mRNA expression following spinal cord injury in the mouse

Wilson

Aziz

Vazques

et al. 2004

Neurourology and Urodynamics

View full text Add to dashboard Cite

show abstract

Smooth Muscle Myosin Heavy Chain Isoforms Are Developmentally Regulated in Male Fetal and Neonatal Sheep

Cited by 31 publications

References 23 publications

Vessel-Specific Regulation of Angiotensin II Receptor Subtypes During Ovine Development

Vessel-Specific Regulation of Angiotensin II Receptor Subtypes During Ovine Development

Vascular development in early ovine gestation: carotid smooth muscle function, phenotype, and biochemical markers

Changes in detrusor smooth muscle myosin heavy chain mRNA expression following spinal cord injury in the mouse

Contact Info

Product

Resources

About