Developmental pattern of ANF gene expression reveals a strict localization of cardiac chamber formation in chicken.

In mouse, atrial natriuretic factor (ANF) gene expression was shown to be a marker for chamber formation within the embryonic heart. To gain insight into the process of chamber formation in the chicken embryonic heart, we analyzed the expression pattern of cANF during development. We found cANF to be specifically expressed in the myocardium of the morphologically distinguishable atrial and ventricular chambers, similar to ANF in mouse. cANF expression was never detected in the myocardium of the atrioventricular canal (AVC), inner curvature, and outflow tract (OFT), which is lined by endocardial cushions. Expression was strictly excluded from the interventricular myocardium and most proximal part of the bundle branches, as identified by the expression of Msx-2, whereas the rest of the bundle branches, trabeculae, and surrounding working myocardium did express cANF. The myocardium that forms de novo within the cushions after looping did not express cANF. At HH9 cANF expression was first observed in a subset of cardiomyocytes, which was localized ventrally in the fused heart tube and laterally in the unfused cardiac sheets. Together, these results show that cANF expression can be used to distinguish differentiated chamber (working) myocardium, including the peripheral ventricular conduction system, from embryonic myocardium. We conclude that differentiation of chamber myocardium takes place already at HH9 at the ventral side of the linear heart tube, possibly preceded by latero-medial signals in the unfused cardiac sheets.     

Expression of Muscle Segment Homeobox Genes in the Developing Myocardium

Msx1 and Msx2 are essential for the development of many organs. In the heart, they act redundantly in development of the cardiac cushions. Additionally, Msx2 is expressed in the developing conduction system. However, the exact expression of Msx1 has not been established. We show that Msx1 is expressed in the cardiac cushions, but not in the myocardium. In Msx2‐null mice, Msx1 is not ectopically expressed in the myocardium. The absence of myocardial defects in the Msx2 knock‐out can therefore not be attributed to a redundant action of Msx1 in the myocardium. Anat Rec, 2010. © 2010 Wiley‐Liss, Inc.     

Diversified expression patterns of autotaxin,a gene for phospholipid‐generating enzyme during mouse and chicken development

Autotaxin (ATX), or nucleotide pyrophosphatase‐phosphodiesterase 2, is a secreted lysophospholipase D that generates bioactive phospholipids that act on G protein–coupled receptors. Here we show the expression patterns of the ATX gene in mouse and chicken embryos. ATX has a dynamic spatial and temporal expression pattern in both species and the expression domains during neural development are quite distinct from each other. Murine ATX (mATX) is expressed immediately rostral to the midbrain‐hindbrain boundary, whereas chicken ATX (cATX) is expressed in the diencephalon and later in the parencephalon‐synencephalon boundary. In the neural tube, cATX is expressed in the alar plate in contrast to mATX in the floor plate. ATX is also expressed in the hindbrain and various organ primordia such as face anlagen and skin appendages of the mouse and chicken. These results suggest conserved and non‐conserved roles for ATX during neural development and organogenesis in these species. Developmental Dynamics 236:1134–1143, 2007. © 2007 Wiley‐Liss, Inc.     

Developmental regulation of cation pumps in skeletal and cardiac muscle

The prenatal and early postnatal periods are critical stages during which long-term development can be affected. For example, retardation of growth during these periods is closely linked to the occurrence of adult degenerative diseases. Appropriate development of muscle is essential for numerous functions, including movement, posture, thermogenesis, breathing and maintenance of the circulation. Defects in normal muscle development could thus impair any of these functions in the neonate and may also have long-term consequences for the health of the individual. Central to normal muscle structure and function is the appropriate development not only of the sarcomeric proteins but also of the sarcolemma, transverse-tubules, sarcoplasmic reticulum and associated membrane-bound ATPases. Long-term regulation of these ATPases is by changes in their concentration, whereas short-term regulation is mediated by alterations in enzyme activity. This review focuses on changes in total concentrations of Na⁺, K⁺- and Ca²⁺-ATPases during prenatal and postnatal life, in functionally diverse muscles of mammalian species born at different stages of maturity. Both these cation pumps belong to multigene families and changes in relative abundance of their specific isoforms are also considered because they may have important consequences for contractile performance during distinct stages of development. Finally, potential regulatory mechanisms which alter markedly during normal ontogeny are discussed. These include intrinsic factors such as hormones and contractile activity, extrinsic factors such as nutrition and environmental temperature, and interactions between these variables which are known to be especially important during postnatal development.     

Disrupted blastocoele formation reveals a critical developmental role for long-chain acyl-CoA dehydrogenase

Long-chain acyl-CoA dehydrogenase (LCAD) deficiency has not been found in human patients. There has been an LCAD deficient (LCAD-/-) mouse model developed via gene targeting strategies that has gestational loss as a part of its phenotype. We tested the hypothesis that LCAD deficiency disrupts normal embryonic development and explains at least in part the gestational loss in the mouse and may suggest a mechanism to explain the lack of any human patients with this inherited enzyme deficiency. We cultured and evaluated embryos with three different genotypes: LCAD+/+, LCAD+/-, and LCAD-/-. We found a significantly increased rate of death (P<0.012) in LCAD-/- embryos at the morula-to-blastocyst conversion indicating a deficient ability to complete the development of a blastocoele and formation of a blastocyst. Furthermore, we hypothesized that we could rescue LCAD-/- embryos in culture by supplying excess fatty acids of chain-lengths that could be readily oxidized by them despite their inherited enzyme deficiency. We were unable, however, to demonstrate any rescue by supplementing the culture medium with fatty acids of a wide-range of chain-lengths. Therefore, overall we demonstrated a severely deficient capacity for LCAD-/- embryos to develop past the morula stage with intermediate rates of development found in the LCAD+/- embryos as compared to the LCAD+/+ embryos. Furthermore, we were unable to rescue the LCAD-/- embryos with any fatty acid supplementation.     

细胞外基质在大鼠胚胎心脏的时相性分布

采用酶免疫组织化学法检测 ECM及其受体 β1 在胎龄 11至 19天胚鼠心脏中的表达 ,结果显示 ECM中 FN、L MN、Vn及受体 β1 均于 ED11起在胚鼠心脏存在表达 ,但其表达高峰及在流出道、心内膜垫、心室肌及室间隔中表达持续时间各不相同 ,Co IV在胚胎各期均为阴性表达 ,提示不同的 ECM在胚胎心脏的不同部位有着不同的时相性表达规律 ,ECM(主要是 FN与 L MN)及其受体 β1 在胚胎心脏的发生发育中起着一定的介导作用     

Platelet‐derived growth factor is involved in the differentiation of second heart field‐derived cardiac structures in chicken embryos

For the establishment of a fully functional septated heart, addition of myocardium from second heart field‐derived structures is important. Platelet‐derived growth factors (PDGFs) are known for their role in cardiovascular development. In this study, we aim to elucidate this role of PDGF‐A, PDGF‐C, and their receptor PDGFR‐α. We analyzed the expression patterns of PDGF‐A, ‐C, and their receptor PDGFR‐α during avian heart development. A spatiotemporal pattern of ligands was seen with colocalization of the PDGFR‐α. This was found in second heart field‐derived myocardium as well as the proepicardial organ (PEO) and epicardium. Mechanical inhibition of epicardial outgrowth as well as chemical disturbance of PDGFR‐α support a functional role of the ligands and the receptor in cardiac development. Developmental Dynamics 238:2658–2669, 2009. © 2009 Wiley‐Liss, Inc.