scholarly journals Effective Cell Immunoablation in Undisrupted Developing Avian Embryos

2016 ◽  
Author(s):  
Maríacruz López-Díaz ◽  
Julia Buján-Varela ◽  
Carlos Cadórniga-Valiño
Keyword(s):  
Germ Cells ◽  
Primordial Germ Cells ◽  
Rabbit Serum ◽  
Dependent Manner ◽  
Specific Antibodies ◽  
Avian Embryos ◽  
Complete Ablation ◽  
Summary Statement ◽  
Dose Dependent ◽  
Cellular Destruction

ABSTRACTIn birds the construction of germline chimeras by grafting exogenous primordial germ cells (PGCs) during embryonic development is feasible since they migrate to the gonads through the blood. Up to date, the efficiencies are highly variable, in part dependent on the destruction of endogenous PGCs in the recipient embryo. We show an almost complete ablation of the endogenous PGCs in stage X embryos using a baby rabbit serum (BRS), with previous cellular signaling by specific antibodies (SSEA1). The application of the treatments, either on epiblast or subgerminaly, produced the reduction of the PGCs in the embryos in a dose dependent manner. No malformations or damages were detected in the treated embryos. However, subgerminal injection of this cocktail produced a massive cellular destruction in all embryos. Therefore, sequential application is a selective and effective method to produce receptor embryos. Nevertheless, it can also be highly destructive if the mixture is applied locally, this could be useful in the treatment of malignancies.SUMMARY STATEMENTAn immunosurgery procedure is described that yields an almost complete ablation of primordial germ cells in early developing chick embryos, thus increasing the expected rates of chimerism when foreign PGCs are grafted onto these embryos

scholarly journals DNase II mediates a parthanatos-like developmental cell death pathway in Drosophila primordial germ cells

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Lama Tarayrah-Ibraheim ◽  
Elital Chass Maurice ◽  
Guy Hadary ◽  
Sharon Ben-Hur ◽  
Alina Kolpakova ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Germ Cells ◽  
Nuclear Translocation ◽  
Primordial Germ Cells ◽  
Nuclear Accumulation ◽  
Dependent Manner ◽  
Dnase Ii ◽  
Cell Death Pathway ◽  
Parp 1

AbstractDuring Drosophila embryonic development, cell death eliminates 30% of the primordial germ cells (PGCs). Inhibiting apoptosis does not prevent PGC death, suggesting a divergence from the conventional apoptotic program. Here, we demonstrate that PGCs normally activate an intrinsic alternative cell death (ACD) pathway mediated by DNase II release from lysosomes, leading to nuclear translocation and subsequent DNA double-strand breaks (DSBs). DSBs activate the DNA damage-sensing enzyme, Poly(ADP-ribose) (PAR) polymerase-1 (PARP-1) and the ATR/Chk1 branch of the DNA damage response. PARP-1 and DNase II engage in a positive feedback amplification loop mediated by the release of PAR polymers from the nucleus and the nuclear accumulation of DNase II in an AIF- and CypA-dependent manner, ultimately resulting in PGC death. Given the anatomical and molecular similarities with an ACD pathway called parthanatos, these findings reveal a parthanatos-like cell death pathway active during Drosophila development.

scholarly journals Enhancement of in vitro and in vivo antigen-specific antibody responses by interleukin 11.

1992 ◽  
Vol 175 (1) ◽  
pp. 211-216 ◽  
Author(s):  
T G Yin ◽  
P Schendel ◽  
Y C Yang
Keyword(s):  
T Cells ◽  
Antibody Titer ◽  
Specific Antibody ◽  
Antibody Responses ◽  
Rabbit Serum ◽  
Dependent Manner ◽  
Dose Dependent ◽  
Interleukin 11

The availability of large quantities of highly purified recombinant interleukin 11 (rhuIL-11) has allowed us to investigate the effects of rhuIL-11 on sheep red blood cell (SRBC)-specific antibody responses in the murine system. The results showed that rhuIL-11 was effective in enhancing the generation of mouse spleen SRBC-specific plaque-forming cells (PFC) in the in vitro cell culture system in a dose-dependent manner. These effects of rhuIL-11 were abrogated completely by the addition of anti-rhuIL-11 antibody, but not by the addition of preimmunized rabbit serum. Cell-depletion studies revealed that L3T4 (CD4)+ T cells, but not Lyt-2 (CD8)+ T cells, are required in the rhuIL-11-stimulated augmentation of SRBC-specific antibody responses. The effects of rhuIL-11 on the SRBC-specific antibody responses in vivo were also examined. RhuIL-11 administration to normal C3H/HeJ mice resulted in a dose-dependent increase in the number of spleen SRBC-specific PFC as well as serum SRBC-specific antibody titer in both the primary and secondary immune responses. In mice immunosuppressed by cyclophosphamide treatment, rhuIL-11 administration significantly augmented the number of spleen SRBC-specific PFC as well as serum SRBC-specific antibody titer when compared with the cyclophosphamide-treated mice without IL-11 treatment. These results demonstrated that IL-11 is a novel cytokine involved in modulating antigen-specific antibody responses in vitro as well as in vivo.

scholarly journals EPH/EPHRIN SIGNALING CONTROLS PROGENITOR IDENTITIES IN THE VENTRAL SPINAL CORD

2016 ◽  
Author(s):  
Julien Laussu ◽  
Christophe Audouard ◽  
Anthony Kischel ◽  
Poincyane Assis-Nascimento ◽  
Nathalie Escalas ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Sonic Hedgehog ◽  
Cell Communication ◽  
Dependent Manner ◽  
Eph Receptors ◽  
Loss Of Function ◽  
Summary Statement ◽  
Dose Dependent ◽  
Ventral Spinal Cord

SUMMARY STATEMENTThis article by Laussu et al. describes a role for Eph:ephrin signaling in controlling the identity of neural progenitors in the ventral spinal cord.Early specification of progenitors of the ventral spinal cord involves the morphogen Sonic Hedgehog which induces distinct progenitor identities in a dose-dependent manner. Following these initial patterning events, progenitor identities have to be maintained in order to generate appropriate numbers of progeny. Here we provide evidence that communication via Eph:ephrin signaling is required to maintain progenitor identities in the ventral spinal cord. We show that ephrinB2 and ephrinB3 are expressed in restricted progenitor domains in the ventral spinal cord while several Eph receptors are more broadly expressed. Further, we provide evidence that expression of Efnb3 and EphA4 is controlled by Shh. Genetic loss-of-function analyses indicate that expression of ephrinB2 and ephrinB3 is required to control progenitor identities and in vitro experiments reveal that activation of Eph forward signaling in spinal progenitors up-regulates the expression of the identity transcription factor Nkx2.2. Altogether our results indicate that cell-to-cell communication is necessary to control progenitor identity in the ventral spinal cord.

scholarly journals Specification of the germline by Nanos-dependent down-regulation of the somatic synMuvB transcription factor LIN-15B

2017 ◽  
Author(s):  
Chih-Yung S. Lee ◽  
Tu Lu ◽  
Geraldine Seydoux
Keyword(s):  
Transcription Factor ◽  
Germ Cells ◽  
Rna Binding ◽  
Primordial Germ Cells ◽  
Somatic Cells ◽  
Rna Binding Protein ◽  
Dependent Manner ◽  
Embryonic Cells ◽  
C Elegans ◽  
Underlying Mechanisms

AbstractThe Nanos RNA-binding protein has been implicated in the specification of primordial germ cells (PGCs) in metazoans, but the underlying mechanisms remain poorly understood. We have profiled the transcriptome of PGCs lacking the nanos homologues nos-1 and nos-2 iC. elegans. nos-1nos-2 PGCs fail to silence hundreds of genes normally expressed in oocytes and somatic cells, a phenotype reminiscent of PGCs lacking the repressive PRC2 complex. The nos-1nos-2 phenotype depends on LIN-15B, a broadly expressed synMuvB class transcription factor known to antagonize PRC2 activity in somatic cells. LIN-15B is maternally-inherited by all embryonic cells and is down-regulated specifically in PGCs in a nos-1nos-2-dependent manner. Consistent with LIN-15B being a critical target of Nanos regulation, inactivation of maternal LIN-15B restores fertility to nos-1nos-2 mutants. These studies demonstrate a central role for Nanos in reprogramming the transcriptome of PGCs away from an oocyte/somatic fate by down-regulating an antagonist of PRC2 activity.

Protective Effect of Pantethine on Experimental Thrombocytopenia in the Rat

1975 ◽  
Vol 33 (03) ◽  
pp. 528-539 ◽  
Author(s):  
Shin-ichiro Ashida ◽  
Yasushi Abiko
Keyword(s):  
Nitrogen Mustard ◽  
Experimental Period ◽  
Significant Degree ◽  
Rabbit Serum ◽  
Dependent Manner ◽  
Essentially Normal ◽  
And Function ◽  
Dose Dependent ◽  
Platelet Functions

SummaryThe effects of pantethine on circulating platelet counts and platelet functions were studied in normal and experimentally produced thrombocytopenic rats.Administration of pantethine to normal animals did not cause any alterations in both platelet count and function except for a slight enhancement of intravascular platelet aggregation induced by collagen or neuraminidase.Injection of anti-rat platelet rabbit serum into rats resulted in acute thrombocytopenia. Administration of pantethine prior to the antiserum promoted recovery from the thrombocytopenia in a dose dependent manner, but administration of the drug after development of the thrombocytopenia was not effective. A similar result was obtained with a transient thrombocytopenia induced by exchange transfusion with platelet poor blood. Regardless of whether animals were treated with pantethine or not, the platelets newly generated during the course of recovery from thrombocytopenia were essentially normal in the function tested in vitro.A more chronic thrombocytopenia induced by repeated injections of the antiserum was prevented, to some significant degree, by daily administration of pantethine throughout the experimental period.In contrast to these, such effect of pantethine was not observed with the thrombocytopenia models produced by nitrogen mustard N-oxide and neuraminidase.These findings were discussed in relation to mechanism of the action of pantethine and to possible clinical application of the drug to thrombocytopenia.

Is the embryo culture system useful for collecting primordial germ cells from endangered avian embryos?

Zoo Biology ◽  
2002 ◽  
Vol 21 (3) ◽  
pp. 287-294 ◽  
Author(s):  
Takaharu Kawashima ◽  
Rika Sakai ◽  
Koichiro Kano ◽  
Yoshinori Tamaki ◽  
Koichiro Hashimoto
Keyword(s):  
Germ Cells ◽  
Embryo Culture ◽  
Culture System ◽  
Primordial Germ Cells ◽  
Avian Embryos

Three further triterpenoid saponins from Gleditsia caspica fruits and protective effect of the total saponin fraction on cyclophosphamide-induced genotoxicity in mice

2015 ◽  
Vol 70 (1-2) ◽  
pp. 31-37 ◽  
Author(s):  
Farouk R. Melek ◽  
Fawzia A. Aly ◽  
Iman A.A. Kassem ◽  
Mona A.M. Abo-Zeid ◽  
Ayman A. Farghaly ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Germ Cells ◽  
Chromosomal Aberrations ◽  
Human Tumor ◽  
Tumor Cell Line ◽  
Dependent Manner ◽  
Triterpenoid Saponins ◽  
Saponin Fraction ◽  
Dose Dependent

Abstract Three triterpenoidal saponins were isolated from the saponin fraction derived from a Gleditsia caspica Desf. methanolic fruit extract. The isolated saponins were identified as gleditsiosides B, C, and Q based on spectral data. The saponin-containing fraction was evaluated in vivo for genotoxic and antigenotoxic activities. The fraction caused no DNA damage in Swiss albino male mice treated with a dose of 45 mg/kg body weight for 24 h, although it significantly inhibited the number of chromosomal aberrations induced by cyclophosphamide (CP) in bone marrow and germ cells when applied before or after CP administration. The inhibitory indices in chromosomal aberrations were 59% and 41% for bone marrow and 48% and 43% for germ cells, respectively. In addition, the saponin fraction was found to reduce the viability of the human tumor cell line MCF-7 in a dose-dependent manner with an extrapolated IC50 value in the range of 220 μg/mL.

A Reporter Mouse for In Vivo Detection of DNA Damage in Embryonic Germ Cells

2020 ◽  
Author(s):  
Jordana C. Bloom ◽  
John C. Schimenti
Keyword(s):  
Dna Damage ◽  
Germ Cells ◽  
Primordial Germ Cells ◽  
Strand Break ◽  
Dependent Manner ◽  
Dna Double Strand Breaks ◽  
Specific Expression ◽  
Exogenous Dna ◽  
Embryonic Germ Cells

AbstractMaintaining genome integrity in the germline is essential for survival and propagation of a species. In both mouse and human, germ cells originate during fetal development and are hypersensitive to both endogenous and exogenous DNA damaging agents. Currently, mechanistic understanding of how primordial germ cells respond to DNA damage is limited in part by the tools available to study these cells. We developed a mouse transgenic reporter strain expressing a 53BP1-mCherry fusion protein under the control of the Oct4ΔPE embryonic germ cell-specific promoter. This reporter binds sites of DNA double strand breaks (DSBs) on chromatin, forming foci. Using ionizing radiation as a DNA double strand break-inducing agent, we show that the transgenic reporter expresses specifically in the embryonic germ cells of both sexes and forms DNA damage induced foci in both a dose- and time-dependent manner. The dynamic time-sensitive and dose-sensitive DNA damage detection ability of this transgenic reporter, in combination with its specific expression in embryonic germ cells, makes it a versatile and valuable tool for increasing our understanding of DNA damage responses in these unique cells.

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