What Makes us Human? A Biased View from the Perspective of Comparative Embryology and Mouse Genetics

doi:10.1201/b12877-3

Cited by 25 publications

(50 citation statements)

References 12 publications

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“…Increased oxidative stress is widely accepted to be involved in the development and progression of diabetes and its complications (Maritim et al, 2003). Moreover, analysis of gene expression in mouse embryos with NTDs from a model of maternal diabetes revealed that there was an enrichment of genes containing binding sites for transcription factors involved in the response to oxidative stress (Pavlinkova et al, 2009). It is also well documented that oxidative stress inhibits the expression of Pax-3, which is essential for neural tube closure during embryogenesis (Chang et al, 2003).…”

Section: Homocysteinementioning

confidence: 99%

Association of neural tube defects in children of mothers with MTHFR 677TT genotype and abnormal carbohydrate metabolism risk: a case-control study

et al. 2014

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ABSTRACT. Abnormalities in maternal folate and carbohydrate 2201©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 13 (1): 2200-2207 (2014) Combination of risk factors in spina bifida metabolism have both been shown to induce neural tube defects (NTD) in humans and animal models. However, the relationship between these two factors in the development of NTDs remains unclear. Data from mothers of children with spina bifida seen at the Unidad de Espina Bífida del Hospital Infantil Virgen del Rocío (case group) were compared to mothers of healthy children with no NTD (control group) who were randomly selected from patients seen at the outpatient ward in the same hospital. There were 25 individuals in the case group and 41 in the control group. Analysis of genotypes for the methylenetetrahydrofolate reductase (MTHFR) 677CT polymorphism in women with or without risk factors for abnormal carbohydrate metabolism revealed that mothers who were homozygous for the MTHFR 677TT polymorphism and at risk of abnormal carbohydrate metabolism were more likely to have offspring with spina bifida and high levels of homocysteine, compared to the control group. The increased incidence of NTDs in mothers homozygous for the MTHFR 677TT polymorphism and at risk of abnormal carbohydrate metabolism stresses the need for careful metabolic screening in pregnant women, and, if necessary, determination of the MTHFR 677CT genotype in those mothers at risk of developing abnormal carbohydrate metabolism.

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Section: Homocysteinementioning

confidence: 99%

Association of neural tube defects in children of mothers with MTHFR 677TT genotype and abnormal carbohydrate metabolism risk: a case-control study

et al. 2014

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“…6 Fetal exposure to a hyperglycemic environment alters embryonic transcriptional program affecting normal development. 7 In addition, hyperglycemia-induced changes in the gene expression are associated with proliferation and cell-fate specification of embryonic neuronal stem cells. 8 Data also indicate that preexisting tissue damage and aberrant cell specialization due to hyperglycemia cannot be reversed even after normoglycemic levels are achieved during pregnancy.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol Prevents Impairment in Activation of Retinoic Acid Receptors and MAP Kinases in the Embryos of a Rodent Model of Diabetic Embryopathy

et al. 2012

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Diabetes induces impairments in gene expression during embryonic development that leads to premature and improper tissue specialization. Retinoic acid receptors (RARs and retinoid X receptor [RXRs]) and mitogen-activated protein kinases (MAPKs) play crucial roles during embryonic development, and their suppression or activation has been shown as a determinant of the fate of embryonic organogenesis. We studied the activation of RARs and MAPKs in embryonic day 12 (E12) in embryos of rats under normal, diabetic, and diabetic treated with resveratrol ([RSV]; 100 mg/kg body weight) conditions. We found downregulation of RARs and RXRs expressions as well as their DNA-binding activities in the embryos exhibiting developmental delays due to diabetes. Furthermore, the phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 was decreased and phosphorylation of c-Jun N-terminal kinase (JNK) 1/2 and p38 was increased. Interestingly, embryos of diabetic rats treated with RSV showed normalized patterns of RARs, RXRs, neuronal markers, and ERK, JNK and p38 phosphorylation.

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“…In addition, the neural tissue with defective patterning showed altered expression of several signalling molecules and transcription factors such as Shh, Nkx2.1, bafilomycin-1, transforming growth factor-β and Pax3 which are critical in forebrain patterning and neural tube closure [25][26][27][28] . Recently, high throughput gene expression profiling using cDNA microarray revealed the altered expression of several genes in the cranial neural tubes of embryos from diabetic pregnancy [20,[28][29][30] . Higher numbers of genes involved in metabolism and cellular process were found to be altered by maternal diabetes [20] .…”

Section: Characterisation Of Ntdsmentioning

confidence: 99%

“…Higher numbers of genes involved in metabolism and cellular process were found to be altered by maternal diabetes [20] . Microarray analysis on whole embryos from diabetic pregnancy has also revealed the altered expression of several genes involved in critical developmental pathways that could contribute to maternal diabetes-induced birth defects including genes known to cause NTDs [29] . These descriptive reports suggest that brain development is impaired due to the altered expression of developmental control genes caused by maternal diabetes-induced glucotoxicity.…”

Section: Characterisation Of Ntdsmentioning

confidence: 99%

Frontiers in research on maternal diabetes-induced neural tube defects: Past, present and future

Sudhaharan

Bay²,

Tay³

et al. 2012

WJD

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Diabetes mellitus rightly regarded as a silent-epidemic is continually on the rise and estimated to have a global prevalence of 6.4 % as of 2010. Diabetes during pregnancy is a well known risk factor for congenital anomalies in various organ systems that contribute to neonatal mortality, including cardiovascular, gastrointestinal, genitourinary and neurological systems, among which the neural tube defects are frequently reported. Over the last two to three decades, several groups around the world have focussed on identifying the molecular cues and cellular changes resulting in altered gene expression and the morphological defects and in diabetic pregnancy. In recent years, the focus has gradually shifted to looking at pre-programmed changes and activation of epigenetic mechanisms that cause altered gene expression. While several theories such as oxidative stress, hypoxia, and apoptosis triggered due to hyperglycemic conditions have been proposed and proven for being the cause for these defects, the exact mechanism or the link between how high glucose can alter gene expression/transcriptome and activate epigenetic mechanisms is largely unknown. Although preconceptual control of diabetes, (i.e., managing glucose levels during pregnancy), and in utero therapies has been proposed as an effective solution for managing diabetes during pregnancy, the impact that a fluctuating glycemic index can have on foetal development has not been evaluated in detail. A tight glycemic control started before pregnancy has shown to reduce the incidence of congenital abnormalities in diabetic mothers. On the other hand, a tight glycemic control after organogenesis and embryogenesis have begun may prove insufficient to prevent or reverse the onset of congenital defects. The importance of determining the extent to which glycemic levels in diabetic mothers should be regulated is critical as foetal hypoglycemia has also been shown to be teratogenic. Finally, the major question remaining is if this whole issue is negligible and not worthy of investigation as the efficient management of diabetes during pregnancy is well in place in many countries.

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What Makes us Human? A Biased View from the Perspective of Comparative Embryology and Mouse Genetics

Cited by 25 publications

References 12 publications

Association of neural tube defects in children of mothers with MTHFR 677TT genotype and abnormal carbohydrate metabolism risk: a case-control study

Association of neural tube defects in children of mothers with MTHFR 677TT genotype and abnormal carbohydrate metabolism risk: a case-control study

Resveratrol Prevents Impairment in Activation of Retinoic Acid Receptors and MAP Kinases in the Embryos of a Rodent Model of Diabetic Embryopathy

Frontiers in research on maternal diabetes-induced neural tube defects: Past, present and future

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