Maternal vasoactive intestinal peptide and the regulation of embryonic growth in the rodent.

Hill, Joanna M.; McCune, Susan K.; Alvero, Ruben J.; Glazner, Gordon W.; Henins, K A; Stanziale, Stephen F.; Keimowitz, J R; Brenneman, Douglas E.

doi:10.1172/jci118391

Cited by 65 publications

(60 citation statements)

References 31 publications

(51 reference statements)

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“…VIP has previously been shown to be a maternal factor acting on early brain development in rodents (80). Similarly, some data also suggest that maternal VIP could act on the embryonic and fetal brain in humans (41).…”

Section: Figure 10mentioning

confidence: 91%

VIP blockade leads to microcephaly in mice via disruption of Mcph1-Chk1 signaling

Passemard¹,

Ghouzzi²,

Nasser³

et al. 2011

J. Clin. Invest.

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Section: Figure 10mentioning

confidence: 91%

VIP blockade leads to microcephaly in mice via disruption of Mcph1-Chk1 signaling

Passemard¹,

Ghouzzi²,

Nasser³

et al. 2011

J. Clin. Invest.

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“…65 It is now known that VIP levels rise at the fetal-maternal interface at early gestation peaking at placentation begin. 66 Its role in embryogenesis was revealed after observing that its blockade during midgestation ends in induced growth retardation and microcephaly. 66 This is further confirmed in VIP À/À fetuses that highlights the role of maternal VIP for early neural development.…”

Section: Modulators Of the Immune Responses During Pregnancymentioning

confidence: 99%

Adaptive Immune Responses During Pregnancy

Zenclussen

2013

American J Rep Immunol

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It has long been believed that there is no immune interaction between mother and conceptus during pregnancy. This concept changed after evidence was provided that the maternal immune system is aware of the semiallogeneic conceptus and develops strategies to tolerate it. Since then, finely regulated mechanisms of active tolerance toward the fetus have been described. This Special Issue of the American Journal of Reproductive Immunology deals with these mechanisms. It begins with the description of minor histocompatibility antigens in the placenta; it further goes through adaptive immune responses toward paternal fetal antigens, mostly concentrating on regulatory T cells and molecules modulating the Th1/Th2 balance. The participation of antibody‐producing B cells in normal and pathological pregnancies is also discussed. This introductory chapter resumes the concepts presented throughout the Issue and discusses the clinical applications raised from these concepts.

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“…The source of VIP may be extrapancreatic embryonic tissues that express VIP mRNA during embryonic life (41). Maternal tissue may be another source of VIP acting on VIP binding sites in the embryo: VIP levels are high in maternal blood, and VIP can be transported from the maternal blood to the embryo (42). …”

Section: Discussionmentioning

confidence: 99%

Role for VPAC2 Receptor-Mediated Signals in Pancreas Development

Rachdi

Marie²,

Scharfmann³

2003

Diabetes

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T he pancreas originates from the dorsal and ventral regions of the foregut endoderm immediately behind the stomach. The endoderm evaginates to form epithelial buds that subsequently enlarge. During this period, exocrine and endocrine cells that will constitute the functional pancreatic unit undergo differentiation.Inductive signals have been shown to be important for normal pancreatic development. Such signals derive from various sources, such as the primitive streak mesoderm, notochord, blood vessels, cardiogenic mesoderm, septum transversum mesenchyme, mesoderm, and mesenchyme (1-6). Research has been conducted to define the exact nature of the inductive signals involved in pancreatic development, and several secreted factors have emerged as likely candidates. These factors belong to a variety of families. A large number of ligands for receptor tyrosine kinases such as fibroblast growth factor-1, -2, -4, -7, and -10; vascular endothelial growth factor; epidermal growth factor; and hepatocyte growth factor have been shown to be involved at various steps of pancreatic development (2,6 -13). Several members of the transforming growth factor (TGF)-␤ superfamily (e.g., activin, bone morphogenetic proteins, TGF-␤) have also been implicated in pancreas development (3,8,14,15).Various ligands of protein G-coupled receptors that increase cAMP accumulation have been shown to exert an important influence on pancreatic function and regeneration during postnatal life (16 -19). In other tissues, these ligands are important for normal development (20,21). However, to our knowledge, few data are available on their role in prenatal pancreas development. In the present study, we used a recently described in vitro system of immature embryonic pancreatic epithelium to look for evidence that ligands of protein G-coupled receptors that increase cAMP accumulation may contribute to the control of pancreas development.Our data indicate that embryonic pancreatic epithelial cells are sensitive to vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP). These factors signal via the VPAC2 receptor, which is highly expressed in the pancreatic epithelium between embryonic days 12 and 16. They increase the proliferation and survival of immature pancreatic epithelial cells, leading to a final increase in the number of insulin-expressing cells. RESEARCH DESIGN AND METHODSAnimals. Pregnant Wistar rats were purchased from the Janvier breeding center (Le Genet, France). The morning of the discovery of the vaginal plug was designated embryonic day 0.5 (E0.5). The animals had free access to food pellets and water. Pregnant rats at different stages of gestation were killed by CO 2 asphyxiation. Dissection of pancreatic epithelium. E13.5 embryos were harvested, and their dorsal pancreatic buds were dissected. The pancreatic epithelium was separated from its surrounding mesenchyme as described previously (22), with minor modifications. Briefly, the stomach, pancreas, and a small portion of the intestine were...

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Maternal vasoactive intestinal peptide and the regulation of embryonic growth in the rodent.

Cited by 65 publications

References 31 publications

VIP blockade leads to microcephaly in mice via disruption of Mcph1-Chk1 signaling

VIP blockade leads to microcephaly in mice via disruption of Mcph1-Chk1 signaling

Adaptive Immune Responses During Pregnancy

Role for VPAC2 Receptor-Mediated Signals in Pancreas Development

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