Isozyme patterns in erythrocytes from human fetuses

Chen, Shi‐Han; Anderson, Jeanne E.; Giblett, Eloise R.; Stamatoyannopoulos, George

doi:10.1002/ajh.2830030103

Cited by 12 publications

(3 citation statements)

References 18 publications

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“…8 Since then, numerous studies have focused on the regulation of fetal specific isogenes. The fetal gene program is regulated in response to developmental, hormonal, and hemodynamic stimuli.…”

Section: Razeghi Et Al Metabolic Gene Expression In Fetal and Failingmentioning

confidence: 99%

Metabolic Gene Expression in Fetal and Failing Human Heart

et al. 2001

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Background-Previous studies suggest that the failing heart reactivates fetal genes and reverts to a fetal pattern of energy substrate metabolism. We tested this hypothesis by examining metabolic gene expression profiles in the fetal, nonfailing, and failing human heart. Methods and Results-Human left ventricular tissue (apex) was obtained from 9 fetal, 10 nonfailing, and 10 failing adult hearts. Using quantitative reverse transcription-polymerase chain reaction, we measured transcript levels of atrial natriuretic factor, myosin heavy chain-␣ and -␤, and 13 key regulators of energy substrate metabolism, of which 3 are considered "adult" isoforms (GLUT4, mGS, mCPT-I) and 3 are considered "fetal" isoforms (GLUT1, lGS, and lCPT-I), primarily through previous studies in rodent models. Compared with the nonfailing adult heart, steady-state mRNA levels of atrial natriuretic factor were increased in both the fetal and the failing heart. The 2 myosin heavy chain isoforms showed the highest expression level in the nonfailing heart. Transcript levels of most of the metabolic genes were higher in the nonfailing heart than the fetal heart. Adult isogenes predominated in all groups and always showed a greater induction than the fetal isogenes in the nonfailing heart compared with the fetal heart. In the failing heart, the expression of metabolic genes decreased to the same levels as in the fetal heart. Conclusions-In the human heart, metabolic genes exist as constitutive and inducible forms. The failing adult heart reverts to a fetal metabolic gene profile by downregulating adult gene transcripts rather than by upregulating fetal genes.

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Section: Razeghi Et Al Metabolic Gene Expression In Fetal and Failingmentioning

confidence: 99%

Metabolic Gene Expression in Fetal and Failing Human Heart

et al. 2001

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“…Our in vitro studies with fetal RBC have shown that an increase in oxygen tension is associated with an increased release of ATP from fetal RBC. The difference in the effect of oxygen on ATP release between fetal and mature RBC may be due to a loss of enzymes of oxidative phosphorylation in mature RBC (5). Thus fetal RBC appear to be uniquely suited to facilitate the birth-related transition in the pulmonary circulation.…”

Section: Discussionmentioning

confidence: 99%

Role of oxidative phosphorylation and ATP release in mediating birth-related pulmonary vasodilation in fetal lambs

Konduri

Mattei

2002

American Journal of Physiology-Heart and Circulatory Physiology

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We investigated the hypothesis that birth-related pulmonary vasodilation is mediated in part by an increase in oxidative phosphorylation and ATP release in response to oxygen exposure at birth. Studies were done in fetal lambs to evaluate the independent effects of oxygen, lung distension alone, or lung distension accompanied by oxygenation and shear stress on fetal pulmonary blood flow and resistance and plasma ATP levels in the pulmonary artery. The effect of each intervention was evaluated in lambs assigned to one of three groups: control or pretreatment with 2,4-dinitrophenol or antimycin-A, inhibitors of oxidative phosphorylation. Exposure to oxygen alone or with lung distension was associated with increases in plasma ATP levels and pulmonary blood flow and a decrease in pulmonary vascular resistance. Plasma ATP levels did not change during lung distension alone. 2,4-Dinitrophenol and antimycin-A attenuated the pulmonary vasodilator response to oxygen but did not attenuate the response to lung distension alone. An increase in oxidative phosphorylation and ATP release during oxygen exposure may contribute to birth-related pulmonary vasodilation in fetal lambs.

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“…The cardiac transcriptome regulatory network of the embryonic murine heart has previously been described 10 , 11 , providing information on transcription factor expression profiles and their role in cardiac pathogenesis. The existence of a ‘fetal gene programme’ is well established 12 and analysis of individual genes relating to health and disease or metabolic processes has provided support for the concept, and insights into the development of pathologies 13 .…”

Section: Introductionmentioning

confidence: 99%

The developmental transcriptome of the human heart

Pervolaraki

Dachtler

Anderson

et al. 2018

Sci Rep

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The human heart develops through complex mechanisms producing morphological and functional changes during gestation. We have recently demonstrated using diffusion tensor MRI that over the relatively short space of 40 days, between 100–140 days gestational age, the ventricular myocardium transforms from a disorganised tissue to the ordered structure characteristic of mature cardiac tissue. However, the genetic basis underpinning this maturation is unclear. Herein, we have used RNA-Seq to establish the developmentally-regulated transcriptome of gene expression in the developing human heart across three gestational ages in the first and second trimester. By comparing 9 weeks gestational age (WGA) with 12 WGA, we find 288 genes show significant differential expression. 305 genes were significantly altered comparing 12 and 16 WGA, and 806 genes differentially expressed between 9 and 16 WGA. Network analysis was used to identify genetic interactions, node properties and gene ontology categories. In summary, we present a comprehensive transcriptomic analysis of human heart development during early gestation, and identify differentially expressed genes during heart development between 9 and 16 weeks, overlapping the first and early second trimester.

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Isozyme patterns in erythrocytes from human fetuses

Cited by 12 publications

References 18 publications

Metabolic Gene Expression in Fetal and Failing Human Heart

Metabolic Gene Expression in Fetal and Failing Human Heart

Role of oxidative phosphorylation and ATP release in mediating birth-related pulmonary vasodilation in fetal lambs

The developmental transcriptome of the human heart

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