Abnormal development of the sinuatrial venous valve and posterior hindbrain may contribute to late fetal resorption of vitamin A-deficient rat embryos

White, Jeffrey C.; Highland, Margaret A.; Clagett‐Dame, Margaret

doi:10.1002/1096-9926(200012)62:6<374::aid-tera4>3.0.co;2-5

Cited by 29 publications

(10 citation statements)

References 54 publications

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“…Early in the 1940s, Warkany et al [3][4][5] had found a large array of congenital malformation in embryos isolated from VA-deficient (VAD) pregnant rats and categorized these defects as symptoms of the VAD syndrome, which involves ocular, genitourinary tract, kidneys, diaphragm, lung, aortic arch and heart. Subsequently, White et al [6][7][8] reported additional abnormalities involved in the craniofacial region, postotic cranial nerves, pharyngeal arches, otic vesicle, cardinal vein and sinuatrial valve. The homozygous null mutant mice of retinaldehyde dehydrogenases-2 (RALDH2), an important dehydrogenase in the generation of retinoic acid (RA), displayed severe embryonic abnormalities including lack of heart looping and chamber morphogenesis, incomplete neural tube closure, shortening of the trunk region and absence of limb buds, all of which are similar to the VAD phenotype [9].…”

Section: Introductionmentioning

confidence: 55%

“…Furthermore, RA response elements (RAREs) have been identified in the flanking regions of several Hox genes, including Hoxa1, Hoxb1, Hoxa4, and Hoxd4 both in vitro and in vivo [18][19][20][21][22][23][24], which manifests that at least some Hox genes are directly involved as the RA target genes during embryonic development. More directly, both the deficiency and the excess of VA have been shown to influence the spatiotemporal expression pattern of Hox genes resulting in various developmental defects [8,9]. In a study involving the distribution of RARs and cellular retinoid binding proteins (CRBP), it was shown that the CRBP functions as controllers to regulate the concentration of RA by interacting with the RAR distribution pattern.…”

Section: Introductionmentioning

confidence: 99%

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Suppression of retinoic acid receptors may contribute to embryonic skeleton hypoplasia in maternal rats with chronic vitamin A deficiency

Sun

Wang

et al. 2010

The Journal of Nutritional Biochemistry

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Section: Introductionmentioning

confidence: 55%

Section: Introductionmentioning

confidence: 99%

Suppression of retinoic acid receptors may contribute to embryonic skeleton hypoplasia in maternal rats with chronic vitamin A deficiency

Sun

Wang

et al. 2010

The Journal of Nutritional Biochemistry

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“…This provides a major impediment to these studies, as most neurite outgrowth and pathfinding does not occur until after this time. White et al (1998White et al ( , 2000a showed that embryos from pregnant vitamin A deficient (VAD) rats receiving a low level of atRA (12 mg/g diet) exhibit early hindbrain defects and die in utero. When the pregnant rats were provided with a higher amount of atRA (250 mg/g diet) starting as late as E8.5 (pre-somite stage), embryonic hindbrain patterning and cranial nerve development was rescued when examined at the 34-40 somite stage, and fetuses survived to birth.…”

Section: Does a Deficiency Of Ra Impair Neurite Outgrowth And/or Pathmentioning

confidence: 99%

Role of all‐trans retinoic acid in neurite outgrowth and axonal elongation

2006

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The vitamin A metabolite, all-trans retinoic acid (atRA) plays essential roles in nervous system development, including neuronal patterning, survival, and neurite outgrowth. Our understanding of how the vitamin A acid functions in neurite outgrowth comes largely from cultured embryonic neurons and model neuronal cell systems including human neuroblastoma cells. Specifically, atRA has been shown to increase neurite outgrowth from embryonic DRG, sympathetic, spinal cord, and olfactory receptor neurons, as well as dissociated cerebra and retina explants. A role for atRA in axonal elongation is also supported by a limited number of studies in vivo, in which a deficiency in retinoid signaling produced either by dietary or genetic means has been shown to alter neurite outgrowth from the spinal cord and hindbrain regions. Human neuroblastoma cells also show enhanced numbers of neurites and longer processes in response to atRA. The mechanism whereby retinoids regulate neurite outgrowth includes, but is not limited to, the regulation of the transcription of neurotrophin receptors. More recent evidence supports a role for atRA in regulating components of other signaling pathways or candidate neurite-regulating factors. Some of these effects, such as that on neuron navigator 2 (NAV2), may be direct, whereas others may be secondary to other atRA-induced changes in the cell. This review focuses on what is currently known about neurite initiation and growth, with emphasis on the manner in which atRA may influence these events.

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“…Supplementation of severely VAD female rats with atRA will support fertilization, implantation, and embryonic development to at least Embryonic Day 10.5 (E10.5). The addition of retinol after this time enables the generation of normal offspring [5], whereas the provision of low levels of atRA after E10.5 leads to a state of lateembryonic vitamin A deficiency (late VAD) [6].…”

Section: Introductionmentioning

confidence: 99%

Vitamin A Deficiency Blocks the Initiation of Meiosis of Germ Cells in the Developing Rat Ovary In Vivo1

Clagett‐Dame

2009

Biology of Reproduction

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Vitamin A (retinol) is required for male and female reproduction as well as to support many developmental processes. In the male, meiotic entry of germ cells occurs after birth and throughout adulthood, whereas in the female, the entry into meiosis I occurs during embryonic development. Evidence from cultured embryonic ovaries suggests that the vitamin A metabolite, all-trans retinoic acid (atRA), initiates this process. However, in vivo evidence to support a normal role for atRA in meiotic entry is lacking. The present study demonstrates that although germ cell number is normal in ovaries from both vitamin A-sufficient (VAS) embryos and those that are deficient in atRA, the majority of germ cells in the most severely atRA-deficient group fail to enter meiosis and remain in an undifferentiated state. In contrast, in a group that is only moderately deficient in atRA, a small number of ovarian germ cells enter meiosis (30%) compared with 75% of cells in the VAS control group. The expression of the atRA-responsive gene, Stra8, is reduced by approximately 90% and 50% in the severely and moderately atRA-deficient ovaries, respectively, compared with the VAS controls. These results provide the first in vivo evidence that vitamin A regulates the entry of germ cells into meiosis in the developing ovary.

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Abnormal development of the sinuatrial venous valve and posterior hindbrain may contribute to late fetal resorption of vitamin A-deficient rat embryos

Cited by 29 publications

References 54 publications

Suppression of retinoic acid receptors may contribute to embryonic skeleton hypoplasia in maternal rats with chronic vitamin A deficiency

Suppression of retinoic acid receptors may contribute to embryonic skeleton hypoplasia in maternal rats with chronic vitamin A deficiency

Role of all‐trans retinoic acid in neurite outgrowth and axonal elongation

Vitamin A Deficiency Blocks the Initiation of Meiosis of Germ Cells in the Developing Rat Ovary In Vivo1

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