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Lois Kelsey Ann M. Flenniken Dawei Qu Alister P. W. Funnell Richard Pearson Yu-Qing Zhou Irina Voronina Zorana Berberovic Geoffrey Wood Susan Newbigging Edward S. Weiss Michael Wong Ivan Quach S. Y. Sandy Yeh Ashish R. Deshwar Ian C. Scott Colin McKerlie Mark Henkelman Peter Backx Jeremy Simpson Lucy Osborne Janet Rossant Merlin Crossley Benoit Bruneau S. Lee Adamson 《PLoS genetics》2013,9(7)
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The etiology of congenital heart disease is multifactorial, with genetics and nutritional deficiencies recognized as causative
agents. Maternal zinc (Zn) deficiency is associated with an increased risk for fetal heart malformations; however, the contributing
mechanisms have yet to be identified. In this study, we fed pregnant rats a Zn-adequate diet (ZnA), a Zn-deficient (ZnD),
or a restricted amount of Zn adequate diet (RF) beginning on gestation day (GD) 4.5, to examine whether increased cell death
and changes in cardiac neural crest cells (NCC) play a role in Zn deficiency-induced heart defects. Fetuses were collected
on GD 13.5, 15.5, and 18.5 and processed for GATA-4, FOG-2, connexin-43 (Cx43), HNK-1, smooth muscle α-actin (SMA) and cleaved
caspase-3 protein expression. Fetuses from ZnA-fed dams showed normal heart development, whereas fetuses from dams fed with
the ZnD diet exhibited a variety of heart anomalies, particularly in the region of the outflow tract. HNK-1 expression was
lower than normal in the hearts of GD13.5 and 15.5 ZnD fetuses, particularly in the right atrium and in the distal tip of
the interventricular septum. Conversely, Cx43 immunoreactivity was increased throughout the heart in fetuses from ZnD dams
compared to fetuses from control dams. The distribution and intensity of expression of SMA, GATA-4, FOG-2, and markers of
apoptosis were similar among the three groups. We propose that Zn deficiency induced alterations in the distribution of Cx43
and HNK-1 in fetal hearts contribute to the occurrence of the developmental heart anomalies. 相似文献
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Kozuka T Sugita M Shetzline S Gewirtz AM Nakata Y 《Journal of immunology (Baltimore, Md. : 1950)》2011,187(11):5974-5982
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Heart malformations are common congenital defects in humans. Many congenital heart defects involve anomalies in cardiac septation or valve development, and understanding the developmental mechanisms that underlie the formation of cardiac septal and valvular tissues thus has important implications for the diagnosis, prevention and treatment of congenital heart disease. The development of heart septa and valves involves multiple types of progenitor cells that arise either within or outside the heart. Here, we review the morphogenetic events and genetic networks that regulate spatiotemporal interactions between the cells that give rise to septal and valvular tissues and hence partition the heart. 相似文献
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Krüppel样因子(Krüppel-like factors, KLFs)是一类C-末端含有3个C2H2锌指结构的转录因子,N-末端为转录调控结构域,能够结合多种特异蛋白质,介导转录调控。目前在人体基因组中共发现18种KLFs,它们在多种类型人类细胞的分化、表型维持和生理功能调控中发挥重要作用。多个KLFs参与了对人和动物的心肌、平滑肌和骨骼肌的发育和功能的调控。在心肌中,KLF4、KLF10、KLF11和KLF15参与心肌肥大的负调控,KLF6参与调控心脏纤维化,KLF13调控胚胎时期的心肌发育。在血管平滑肌中,KLF4受促增殖或促分化因子调控,介导调控血管平滑肌表型转换;KLF5促进血管平滑肌增殖,KLF8和KLF15抑制血管平滑肌增殖。在骨骼肌中,KLF2、KLF3、KLF4、KLF10和KLF15调控骨骼肌发育,此外,KLF15是肌肉组织能量代谢的调节因子。本文综述了KLFs在心肌、平滑肌和骨骼肌中的功能研究进展,为进一步揭示KLFs在肌肉组织中的作用和肌肉相关疾病的分子机制提供参考。 相似文献