Редактирование: FGR

Tyrosine-protein kinase Fgr (EC 2.7.10.2) (Gardner-Rasheed feline sarcoma viral (v-fgr) oncogene homolog) (Proto-oncogene c-Fgr) (p55-Fgr) (p58-Fgr) (p58c-Fgr) [SRC2]

==Publications==

{{medline-entry
|title=Aurora kinase mRNA expression is reduced with increasing gestational age and in severe early onset fetal growth restriction.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32452402
|abstract=Oxidative damage and biochemical ageing are implicated in placental dysfunction and potentially fetal death. Cellular senescence may play a role in the pathophysiology of fetal growth restriction ([[FGR]]) and preeclampsia (PE). Aurora kinases ([[AURKA]], B and C) are important regulators of cellular division in mitosis and meiosis with implications in cellular senescence. We aimed to investigate whether aurora kinase expression is altered with placental dysfunction or placental ageing. Placenta and blood was obtained across gestation from pregnancies complicated by PE, [[FGR]] or both PE and [[FGR]], as well as gestation-matched control samples. Expression of [[AURKA]], B and C mRNA was examined using real time qPCR in both the placenta and maternal circulation. Placental aurora kinase expression decreased as gestation progressed: [[AURKA]] and [[AURKB]] were significantly reduced at 37-40 weeks, whereas [[AURKC]] was significantly reduced at 34-37 weeks, when compared to <34 weeks. In the maternal circulation, the mRNA level of [[AURKB]] was significantly reduced at >40 weeks compared to <34 weeks gestation. A significant reduction in [[AURKC]] was seen in [[FGR]] pregnancies <34 weeks compared to gestation-matched controls. Placental AURK expression is reduced with increased gestation. Circulating [[AURKB]] mRNA reduces at >40 weeks gestation, when compared to <34 weeks. [[AURKC]] is significantly reduced in placentas from pregnancies complicated by severe early onset (<34 weeks) [[FGR]] compared with gestation-matched controls. The functional role of aurora kinase in the placenta and in gestational age warrants further investigation.

|keywords=* Aurora kinase
* Cellular senescence
* FGR
* Preeclampsia
|full-text-url=https://sci-hub.do/10.1016/j.placenta.2020.04.012
}}
{{medline-entry
|title=Premature Vascular Aging in Guinea Pigs Affected by Fetal Growth Restriction.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31311132
|abstract=Cardiovascular risk associated with fetal growth restriction ([[FGR]]) could result from an early impaired vascular function. However, whether this effect results in premature vascular aging has not been addressed. We studied the ex vivo reactivity of carotid and femoral arteries in fetal (near term), adults (eight months-old) and aged (16 months-old) guinea pigs in normal (control) and [[FGR]] offspring. Additionally, an epigenetic marker of vascular aging (i.e., LINE-1 DNA methylation) was evaluated in human umbilical artery endothelial cells (HUAEC) from control and [[FGR]] subjects. Control guinea pig arteries showed an increased contractile response (KCl-induced) and a progressive impairment of NO-mediated relaxing responses as animals get older. [[FGR]] was associated with an initial preserved carotid artery reactivity as well as a later significant impairment in NO-mediated responses. Femoral arteries from [[FGR]] fetuses showed an increased contractility but a decreased relaxing response compared with control fetuses, and both responses were impaired in [[FGR]]-adults. Finally, [[FGR]]-HUAEC showed decreased LINE-1 DNA methylation compared with control-HUAEC. These data suggest that the aging of vascular function occurs by changes in NO-mediated responses, with limited alterations in contractile capacity. Further, these effects are accelerated and imposed at early stages of development in subjects exposed to a suboptimal intrauterine environment.
|mesh-terms=* Aging
* Animals
* Carotid Arteries
* Cells, Cultured
* DNA Methylation
* Endothelium, Vascular
* Female
* Femoral Artery
* Fetal Growth Retardation
* Guinea Pigs
* Humans
* Long Interspersed Nucleotide Elements
* Nitric Oxide
* Vasoconstriction
* Vasodilation
|keywords=* Cardiovascular Diseases
* Early Vascular Aging
* Endothelial Dysfunction
* Fetal Growth Restriction
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6678381
}}
{{medline-entry
|title=Premature placental aging in term small-for-gestational-age and growth-restricted fetuses.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30125412
|abstract=To perform a comprehensive assessment of the placental aging process in small term fetuses classified as being small-for-gestational age (SGA) or having fetal growth restriction ([[FGR]]) through analysis of senescence and apoptosis markers. This was a prospective nested case-control study of singleton pregnancies delivered at term, including 21 control pregnancies with normally grown fetuses and 36 with a small fetus classified as SGA (birth weight between the 3  and 9  percentiles and normal fetoplacental Doppler; n = 18) or [[FGR]] (birth weight < 3  percentile and/or abnormal cerebroplacental ratio and/or uterine artery Doppler; n = 18). Telomerase activity, telomere length (quantified by comparing the amount of amplification product for the telomere sequence (T) to that of a single copy of the gene 36B4 (S)) and RNA expression of senescence (Sirtuins 1, 3 and 6) and apoptosis (p53, p21, [[BAX]] and Caspases 3 and 9) markers (analyzed using the 2  method) were determined in placental samples collected at birth and compared between the three groups. Compared to pregnancies with a normally grown fetus, both SGA and [[FGR]] pregnancies presented signs of accelerated placental aging, including lower telomerase activity (mean ± SD, 12.8 ± 6.6% in controls vs 7.98 ± 4.2% in SGA vs 7.79 ± 4.6% in [[FGR]]; P = 0.008), shorter telomeres (mean ± SD T/S ratio, 1.20 ± 0.6 in controls vs 1.08 ± 0.9 in SGA vs 0.66 ± 0.5 in [[FGR]]; P = 0.047) and reduced Sirtuin-1 RNA expression (mean ± SD 2  , 1.55 ± 0.8 in controls vs 0.91 ± 0.8 in SGA vs 0.63 ± 0.5 in [[FGR]]; P = 0.001) together with increased p53 RNA expression (median (interquartile range) 2  , 1.07 (0.3-3.3) in controls vs 5.39 (0.6-15) in SGA vs 3.75 (0.9-7.8) in [[FGR]]; P = 0.040). [[FGR]] cases presented signs of apoptosis, with increased Caspase-3 RNA levels (median (interquartile range) 2  , 0.94 (0.7-1.7) in controls vs 3.98 (0.9-31) in [[FGR]]; P = 0.031) and Caspase-9 RNA levels (median (interquartile range) 2  , 1.21 (0.6-4.0) in controls vs 3.87 (1.5-9.0) in [[FGR]]; P = 0.037) compared with controls. In addition, Sirtuin-1 RNA expression, telomerase activity, telomere length and Caspase-3 activity showed significant linear trends across groups as severity of the condition increased. Accelerated placental aging was observed in both clinical forms of late-onset fetal smallness (SGA and [[FGR]]), supporting a common pathophysiology and challenging the concept of SGA fetuses being constitutionally small. Copyright © 2018 ISUOG. Published by John Wiley