Apoptosis as a creative agent of embryonic development of bucca, mentum and nasolacrimal duct. An in vivo study in rats

Lotz, Kristina; Proff, Peter; Bienengraeber, Volker; Fanghaenel, Jochen; Gedrange, Tomasz; Weingaertner, Jens

doi:10.1016/s1010-5182(06)60003-6

Cited by 27 publications

(15 citation statements)

References 19 publications

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“…Although previous studies have suggested that apoptosis plays a role in normal embryonic development (Brill et al, 1999;Lotz et al, 2006;Weingaertner et al, 2006), mechanistically diverse teratogens have been shown to induce excessive apoptosis in early embryos, leading to disrupted development (Chan, 2006;Detmar et al, 2006;Hsuuw et al, 2005;Huang et al, 2003;Shang and Wu, 2004).…”

Section: Introductionmentioning

confidence: 99%

Protective effects of resveratrol on ethanol-induced apoptosis in embryonic stem cells and disruption of embryonic development in mouse blastocysts

et al. 2007

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Section: Introductionmentioning

confidence: 99%

Protective effects of resveratrol on ethanol-induced apoptosis in embryonic stem cells and disruption of embryonic development in mouse blastocysts

et al. 2007

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“…Gewebe ausgebildet, nur bleibt die Verschmelzung der darunterliegenden mesenchymalen Gewebe aus, so dass Nerven, Gefäße, Muskeln und Faszien in abnormen Bahnen verlaufen und später bei chirurgischen Korrekturen einige Probleme bereiten können [59]. Als morphologische Ursache für den fehlenden embryonalen Schluss zweier miteinander verschmelzender Epithelien wird eine fehlende Apoptose der Epithelzellen angenommen [36,45,50,78]. Beide Fehlbildungen haben auch gemeinsam, dass sie durch die gleichen Ursachen induziert werden, aber auf Grund der Embryogenesereihenfolge zu einem unterschiedlichen Zeitpunkt entstehen.…”

Section: General Significance Of Vitaminsunclassified

“…Allerdings sues fail to fuse, so that nerves, blood vessels, muscles and fasciae follow abnormal pathways, which may create problems during surgical correction [59]. It is assumed that the absence of apoptosis of epithelial cells is the morphological cause for the failure of fusing of the two epithelial processes during embryonic development [36,45,50,78]. The two malformations also share the characteristic of being induced by the same factors, although they occur at different times during the embryonic sequence.…”

Section: Introductionmentioning

confidence: 99%

Induction and Prevention of Cleft Lip, Alveolus and Palate and Neural Tube Defects with Special Consideration of B Vitamins and the Methylation Cycle

et al. 2007

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Previous studies on the development of cleft lip, alveolus, palate, and velum and neural tube defects have revealed several shared multifactorial causes. Both anomalies emerge at different times during embryonic development and are not associated with each other unless there is a genetic component to the etiology. Vitamin deficiency disorders are one of several factors contributing to the etiology of these anomalies.Vitamins B6, folic acid and B12 play an essential role in the methylation cycle. A lack of or deficiency in these vitamins thus has severe consequences for the organism, especially the unborn child. Due to its short half-life, vitamin B6 is particularly important for undisturbed embryogenesis and should be taken along with folic acid as a periconceptional supplement to prevent embryonic deformities. This paper is intended to provide the orthodontist (as a member of the interdisciplinary cleft team) with an overview of the issues and etiological significance of vitamin B deficiencies as possible inducers of these embryopathies. This may encourage comprehensive counselling, particularly of parents of children born with deformities who wish to have more children.

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“…Apoptosis plays an important role in development and disease [21]. Several reports have confirmed the significance of apoptosis in normal embryonic development [22,23,24]. However, excessive apoptosis triggered in early embryos by mechanistically diverse teratogens can lead to developmental injury [13,18,25,26,27].…”

Section: Introductionmentioning

confidence: 99%

Cytotoxic Effects of Dillapiole on Embryonic Development of Mouse Blastocysts in Vitro and in Vivo

Chan

2014

IJMS

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We examined the cytotoxic effects of dillapiole, a phenylpropanoid with antileishmanial, anti-inflammatory, antifungal, and acaricidal activities, on the blastocyst stage of mouse embryos, subsequent embryonic attachment and outgrowth in vitro, and in vivo implantation via embryo transfer. Blastocysts treated with 2.5–10 μM dillapiole exhibited a significant increase in apoptosis and corresponding decrease in total cell number. Notably, the implantation success rates of blastocysts pretreated with dillapiole were lower than those of their control counterparts. Moreover, in vitro treatment with 2.5–10 μM dillapiole was associated with increased resorption of post-implantation embryos and decreased fetal weight. Our results collectively indicate that dillapiole induces apoptosis and retards early post-implantation development, both in vitro and in vivo. However, the extent to which this organic compound exerts teratogenic effects on early human development is not known at present. Further studies are required to establish effective protection strategies against the cytotoxic effects of dillapiole.

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Apoptosis as a creative agent of embryonic development of bucca, mentum and nasolacrimal duct. An in vivo study in rats

Cited by 27 publications

References 19 publications

Protective effects of resveratrol on ethanol-induced apoptosis in embryonic stem cells and disruption of embryonic development in mouse blastocysts

Protective effects of resveratrol on ethanol-induced apoptosis in embryonic stem cells and disruption of embryonic development in mouse blastocysts

Induction and Prevention of Cleft Lip, Alveolus and Palate and Neural Tube Defects with Special Consideration of B Vitamins and the Methylation Cycle

Cytotoxic Effects of Dillapiole on Embryonic Development of Mouse Blastocysts in Vitro and in Vivo

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