Function of RARγ and RARα2 at the initiation of retinoid signaling is essential for avian embryo survival and for distinct events in cardiac morphogenesis

Romeih, Mahmoud; Cui, Jian; Michaille, Jean‐Jacques; Jiang, Weihong; Zile, Michael R.

doi:10.1002/dvdy.10419

Cited by 29 publications

(35 citation statements)

References 66 publications

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“…On the other hand, many reports have demonstracted that VAD suppressed RALDHs, RARs and RXRs mRNA expression in many organs of VAD rats [40,41]. Moreover, the expressions of RAR-a and RAR-b are also severely downregulated in the VAD embryo in the avian [41,42]. Our results also have observed that VAD suppressed RALDHs and RARs mRNA expression in the liver and vertebral body of VAD neonatal rats at the day of birth.…”

Section: Discussionsupporting

confidence: 75%

Vitamin A Deficiency Induces Congenital Spinal Deformities in Rats

Shen

2013

The Spine Journal

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Section: Discussionsupporting

confidence: 75%

Vitamin A Deficiency Induces Congenital Spinal Deformities in Rats

Shen

2013

The Spine Journal

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“…Although it was known that Rarβ is expressed in somites and lateral plate mesoderm Ruberte et al, 1991;Romeih et al, 2003;Bayha et al, 2009), its role in somitogenesis was not addressed. A phenotype we observed with 100% penetrance in Rarβ2 MO-injected embryos is the loss of chevron-shaped somite morphology, the appearance of thicker and fewer, U-shaped somites and inhibition of hypaxial muscle migration.…”

Section: Rarβ2 Loss Of Function Reduces Somite Number and Increases Smentioning

confidence: 99%

“…In chick and zebrafish, loss of individual RARs causes specific phenotypes (Romeih et al, 2003;Garnaas et al, 2012;He et al, 2011;D'Aniello et al, 2013). RARα or RARγ knockdown in the frog, Xenopus laevis, produces specific defects in neuronal differentiation, pre-placodal ectoderm formation and axial elongation (Janesick et al, 2014(Janesick et al, , 2013(Janesick et al, , 2012Koide et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, RA-regulated processes such as neural tube patterning, hindbrain boundary setting, somite differentiation, limb development, and heart and lung morphogenesis (Maden, 2007;Niederreither and Dollé, 2008) likely rely on RARα or RARβ. Although RARβ is expressed in the somites and lateral plate mesoderm, positioning it to regulate somitogensis in chick and mouse Ruberte et al, 1991;Romeih et al, 2003;Bayha et al, 2009), the functionality of RARβ in early somitic development had not been explored.…”

Section: Introductionmentioning

confidence: 99%

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RARβ2 is required for vertebrate somitogenesis

et al. 2017

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During vertebrate somitogenesis, retinoic acid is known to establish the position of the determination wavefront, controlling where new somites are permitted to form along the anteroposterior body axis. Less is understood about how RAR regulates somite patterning, rostral-caudal boundary setting, specialization of myotome subdivisions or the specific RAR subtype that is required for somite patterning. Characterizing the function of RARβ has been challenging due to the absence of embryonic phenotypes in murine loss-offunction studies. Using the Xenopus system, we show that RARβ2 plays a specific role in somite number and size, restriction of the presomitic mesoderm anterior border, somite chevron morphology and hypaxial myoblast migration. Rarβ2 is the RAR subtype whose expression is most upregulated in response to ligand and its localization in the trunk somites positions it at the right time and place to respond to embryonic retinoid levels during somitogenesis. RARβ2 positively regulates Tbx3 a marker of hypaxial muscle, and negatively regulates Tbx6 via Ripply2 to restrict the anterior boundaries of the presomitic mesoderm and caudal progenitor pool. These results demonstrate for the first time an early and essential role for RARβ2 in vertebrate somitogenesis.

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“…The heart abnormality arising from knockout RAR or RXR embryos has a similar expression. RAR␣-null mutants all display an agenesis of the compact layer of the ventricular myocardium (11), while RAR␥ has a distinct role in cardiac asymmetry and looping information (22). However, there has been less research work on the expression of RARs and RXRs at the same time in VAD embryo heart development with the change of GATA-4 gene expression.…”

Section: Ectopic Expression Of Retinoic Acid Receptors and Change Of mentioning

confidence: 99%

Ectopic Expression of Retinoic Acid Receptors and Change of Myocardial Structure in the Offspring Heart with Vitamin A Deficiency

Feng

Yin

et al. 2012

J Nutr Sci Vitaminol

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309Vitamin A (VA) and its biological derivatives (the retinoids) play diverse roles in physiology, ranging from incorporation into vision pigments to controlling transcription of a host of important genes, as evidenced by the myriad of disorders that accompany defi ciency or excess states. Vitamin A defi ciency (VAD) is a public health problem in more than half of all countries, especially in developing countries, hitting hardest young children and pregnant women. According to the data from WHO, approximately 15% of pregnant women are estimated to be VAD all over the world (1). Maternal insuffi ciency of VA during pregnancy results in fetal death or severe abnormalities in the offspring, including aberrant heart development (2-4).The VA active form, retinoic acid (RA), which acts as a ligand for the nuclear receptors the retinoic acid receptors (RARs) (RAR␣, -␤, and -␥) and the retinoic X receptors (RXRs) (RXR␣, -␤, and -␥), distinctly regulates embryonic development. It is an accepted fact that RARs and RXRs are indispensable for embryonic patterning and organogensis, including cardiogenesis (5-8). Some studies show that the RAR␥ gene is at very high levels in the endocardial cushions of the midgestation embryo (9). Data from Mangelsdorf et al. (10) show that the expression of RXR␣ and RXR␤ are highest in the whole embryo at midgestion (embryonic days 11.5-12.5), while RXR␥ expression peaks slightly later (embryonic days 13.5-14.5). Kastner et al. indicate that at least four distinct retinoid receptors (RXR␣, RXR␤, RAR␣ and RAR␤) are likely involved in controlling the ventricular myocardium development (11). Ectopic Expression of Retinoic Acid Receptors and Change of Myocardial Structure in the Offspring Heart withVitamin A Defi ciency Summary Vitamin A is a key micronutrient required during crucial stages of embryonic development and vitamin A defi ciency (VAD) results in embryonic heart malformation. The pleiotropic functions of vitamin A are mediated by specifi c nuclear receptors: the retinoic acid receptors (RAR␣, -␤, and -␥) and the retinoic X receptors (RXR␣, -␤, and -␥). The action of nuclear receptors has been implicated in controlling of cell proliferation, differentiation and apoptosis, and the expressions of these receptor genes are regulated by retinoic acid levels during the early stages of embryonic development. GATA-4 is one of the earliest transcription factors expressed in developing cardiac cells. However, the functional links of specifi c nuclear receptors to heart development in VAD embryos are not clearly understood. In our study, weaning female Sprague-Dawley rats were fed a modifi ed diet containing different concentrations of vitamin A according to the American Institute of Nutrition 93 Growth Purifi ed Diet. After 10-wk feeding, the female rats were mated with normal male rats, and a portion of them were transferred to a diet with enough added vitamin A for the pregnancy cycle. The embryo hearts were dissected out at embryonic day 13.5 (E13.5) to study the expression of RARs, RXRs and...

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Function of RARγ and RARα2 at the initiation of retinoid signaling is essential for avian embryo survival and for distinct events in cardiac morphogenesis

Cited by 29 publications

References 66 publications

Vitamin A Deficiency Induces Congenital Spinal Deformities in Rats

Vitamin A Deficiency Induces Congenital Spinal Deformities in Rats

RARβ2 is required for vertebrate somitogenesis

Ectopic Expression of Retinoic Acid Receptors and Change of Myocardial Structure in the Offspring Heart with Vitamin A Deficiency

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