PDGF signalling controls the migration of mesoderm cells during chick gastrulation by regulating N-cadherin expression

Yang, Xuesong; Chrisman, Holly; Weijer, Cornelis J.

doi:10.1242/dev.023416

Cited by 99 publications

(86 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…3B). In response to PDGFA, PSM cells express N-cadherin (Cdh2), an essential molecule for this cell migration (Tallquist et al, 2000;Yang et al, 2008). Indeed, mouse embryos lacking Cdh2 are embryonic lethal (by E10) and show somite disorganization and cell-adhesion defects in the primitive heart (Horikawa et al, 1999;Radice et al, 1997), consistent with a malformation of the early mesoderm.…”

Section: Kidney Morphogenesis In Mammalsmentioning

confidence: 99%

The origin of the mammalian kidney: implications for recreating the kidney in vitro

2015

View full text Add to dashboard Cite

The mammalian kidney, the metanephros, is a mesodermal organ classically regarded as arising from the intermediate mesoderm (IM). Indeed, both the ureteric bud (UB), which gives rise to the ureter and the collecting ducts, and the metanephric mesenchyme (MM), which forms the rest of the kidney, derive from the IM. Based on an understanding of the signalling molecules crucial for IM patterning and kidney morphogenesis, several studies have now generated UB or MM, or both, in vitro via the directed differentiation of human pluripotent stem cells. Although these results support the IM origin of the UB and the MM, they challenge the simplistic view of a common progenitor for these two populations, prompting a reanalysis of early patterning events within the IM. Here, we review our understanding of the origin of the UB and the MM in mouse, and discuss how this impacts on kidney regeneration strategies and furthers our understanding of human development.

show abstract

Section: Kidney Morphogenesis In Mammalsmentioning

confidence: 99%

The origin of the mammalian kidney: implications for recreating the kidney in vitro

2015

View full text Add to dashboard Cite

show abstract

“…Whole-mount in situ hybridization of chick embryos was performed according to standard in situ hybridization protocols (Henrique et al, 1995). Digoxigenin-labeled probes were synthesized against VE-cadherin (Yang et al, 2008). The whole-mount stained embryos were photographed and frozen sections were prepared by sectioning at a thickness of 15-20 μm on a cryostat microtome (Leica CM1900).…”

Section: Blood Island Formation In Chick Embryosmentioning

confidence: 99%

The impact of high salt exposure on cardiovascular development in the early chick embryo

Wang

Zhang

Wei

et al. 2015

Journal of Experimental Biology

Self Cite

View full text Add to dashboard Cite

In this study, we show that high-salt exposure dramatically increases chick mortality during embryo development. As embryonic mortality at early stages mainly results from defects in cardiovascular development, we focused on heart formation and angiogenesis. We found that high-salt exposure enhanced the risk of abnormal heart tube looping and blood congestion in the heart chamber. In the presence of high salt, both ventricular cell proliferation and apoptosis increased. The high osmolarity induced by high salt in the ventricular cardiomyocytes resulted in incomplete differentiation, which might be due to reduced expression of Nkx2.5 and GATA4. Blood vessel density and diameter were suppressed by exposure to high salt in both the yolk sac membrane (YSM) and chorioallantoic membrane models. In addition, high-salt-induced suppression of angiogenesis occurred even at the vasculogenesis stage, as blood island formation was also inhibited by high-salt exposure. At the same time, cell proliferation was repressed and cell apoptosis was enhanced by high-salt exposure in YSM tissue. Moreover, the reduction in expression of HIF2 and FGF2 genes might cause high-saltsuppressed angiogenesis. Interestingly, we show that high-salt exposure causes excess generation of reactive oxygen species (ROS) in the heart and YSM tissues, which could be partially rescued through the addition of antioxidants. In total, our study suggests that excess generation of ROS might play an important role in high-saltinduced defects in heart and angiogenesis.

show abstract

“…58,59 Generally, the embryos were fixed with 4% paraformaldehyde (PFA) at 4 C overnight, and unspecific immunoreactions was blocked with 2% Bovine Serum Albumin (BSA) C 1% Triton-X C 1% Tween 20 in PBS for 2 hours at room temperature, followed by a brief wash in PBS. The embryos were incubated with primary monoclonal antibody mixture raised against Atg7 (Sigma, 1:100), ECad (BD Transduction Laboratories, 1:100) and Laminin (Developmental Studies Hybridoma Bank, 1:100) overnight at 4 C with shaking.…”

Section: Immunofluorescent Stainingmentioning

confidence: 99%

Autophagy functions on EMT in gastrulation of avian embryo

Wang

et al. 2014

Cell Cycle

Self Cite

View full text Add to dashboard Cite

y These authors contributed equally to this work.Keywords: autophagy, Atg7, EMT and chick embryo, gastrulation Abbreviations: 3-MA, 3-Methyladenine; BF, bright-field; DAPI, 49-6-Diamidino-2-phenylindole; EB, embryoid bodies; E-Cad, E-cadherin; EMTs, epithelial-mesenchymal transitions; GFP, green fluorescent protein; HN, Hensen's node; MAPILC3(LC3), microtubule-associated protein 1 light chain 3; mTOR, mammalian target of rapamycin; N-Cad, N-cadherin; NT, neural tube; PBS, phosphate-buffered saline; PCD, Programmed cell death; PD, idiopathic Parkinson's Disease; PI3K, phosphoinositide-3-kinase; PPIA, peptidylprolyl isomerase A; PS, primitive streak; RAPA, Rapamycin; RT-PCR, reverse transcription PCR; shh, sonic hedgehog.Autophagy is important for cell renewing for its contribution to the degradation of bulk cytoplasm, long-lived proteins, and entire organelles and its role in embryonic development is largely unknown. In our study, we investigated the function of autophagy in gastrulation of the chick embryo using both in vivo and in vitro approaches, especially in the EMT process, and we found that autophagy gene Atg7 was expressed on the apical side of the ectoderm and endoderm. Over-expression of Atg7 could enhance the expression of Atg8 and the E-cadherin, the latter of which is a crucial marker of the EMT process. We also found that the disturbance of autophagy could retard the development of chick embryos in HH4 with shorter primitive steak than that in the control group, which is a newly formed structure during EMT process. So we assumed that autophagy could affect EMT process by adhesion molecule expression. Moreover, more molecules, such as slug, chordin, shh et., which were all involved in EMT process, were detected to address the mechanism of this phenomena. We established that the inhibition of autophagy could cause developmental delay by affecting EMT process in gastrulation of chick embryos.

show abstract

PDGF signalling controls the migration of mesoderm cells during chick gastrulation by regulating N-cadherin expression

Cited by 99 publications

References 35 publications

The origin of the mammalian kidney: implications for recreating the kidney in vitro

The origin of the mammalian kidney: implications for recreating the kidney in vitro

The impact of high salt exposure on cardiovascular development in the early chick embryo

Autophagy functions on EMT in gastrulation of avian embryo

Contact Info

Product

Resources

About