scholarly journals Maternal B cell signaling orchestrates fetal development in mice

Development ◽  
2021 ◽  
Author(s):  
Mandy Busse ◽  
Stefanie Langwisch ◽  
Kerry Tedford ◽  
Klaus-Dieter Fischer ◽  
Ana Claudia Zenclussen
Keyword(s):  
B Cell ◽  
Fetal Development ◽  
Uterine Artery ◽  
Flow Regulation ◽  
Early Embryo ◽  
Uterine Blood Flow ◽  
B Cell Signaling ◽  
In Utero Development ◽  
Placental Thickness ◽  
Specific Deletion

B cell participation in early embryo/fetal development and the underlying molecular pathways have not been explored. To understand whether maternal B cell absence or impaired signaling interferes with placental and fetal growth, we paired CD19-deficient (CD19−/-) mice, females with B cell-specific MyD88 (BMyD88−/-) or IL-10 (BIL-10−/-) deficiency as well as WT and MyD88−/- controls on C57Bl/6 background with BALB/c males. Pregnancies were followed by ultrasound and Doppler measurements. Implantation number was reduced in BMyD88−/- and MyD88−/- mice. Loss of MyD88 or B cell-specific deletion of MyD88 or IL-10 resulted in decreased implantation areas at gestation days (gd)5, 8 and 10, accompanied by reduced placental thickness, diameter and areas at gd10. Uterine artery resistance was enhanced in BIL-10−/- dams at gd10. Challenge with 0.4mg LPS/kg BW at gd16 revealed that BMyD88−/-, BIL-10−/- and CD19−/- mothers delivered preterm while controls maintained their pregnancy. B cell specific MyD88 and IL-10 expression is essential for appropriate in utero development. IL-10+B cells are involved in uterine blood flow regulation during pregnancy. Finally, B cell-specific CD19, MyD88 and IL-10 expression influences susceptibility towards preterm birth.

Estrogen Induced Uterine Artery Endothelial Nitrosyl-Proteome: Potential Roles of Protein Nitrosylation in Uterine Blood Flow Regulation.

2009 ◽  
Vol 81 (Suppl_1) ◽  
pp. 149-149
Author(s):  
Honghai Zhang ◽  
Lin Feng ◽  
Jeong-Kyu Hoh ◽  
Jae-Yoon Shim ◽  
Itamar Livnat ◽  
...  
Keyword(s):  
Blood Flow ◽  
Uterine Artery ◽  
Flow Regulation ◽  
Uterine Blood Flow ◽  
Blood Flow Regulation

B‐cell signaling in persistent polyclonal B lymphocytosis (PPBL)

2016 ◽  
Vol 94 (9) ◽  
pp. 830-837 ◽  
Author(s):  
Nadine Voelxen ◽  
Claudia Wehr ◽  
Sylvia Gutenberger ◽  
Baerbel Keller ◽  
Miriam Erlacher ◽  
...  
Keyword(s):  
Cell Signaling ◽  
B Cell ◽  
B Cell Signaling

scholarly journals Follicular Helper T Cell Differentiation Requires Continuous Antigen Presentation that Is Independent of Unique B Cell Signaling

Immunity ◽  
2010 ◽  
Vol 33 (2) ◽  
pp. 241-253 ◽  
Author(s):  
Elissa K. Deenick ◽  
Anna Chan ◽  
Cindy S. Ma ◽  
Dominique Gatto ◽  
Pamela L. Schwartzberg ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
T Cell ◽  
Cell Signaling ◽  
B Cell ◽  
Antigen Presentation ◽  
T Cell Differentiation ◽  
Helper T Cell ◽  
B Cell Signaling ◽  
Follicular Helper ◽  
Follicular Helper T Cell

Uterine artery pseudoaneurysm and embolisation during pregnancy

2020 ◽  
Vol 13 (5) ◽  
pp. e234058
Author(s):  
Jared T Roeckner ◽  
Adetola F Louis-Jacques ◽  
Bruce R Zwiebel ◽  
Judette M Louis
Keyword(s):  
Blood Flow ◽  
Uterine Artery ◽  
Thrombin Injection ◽  
Uterine Blood Flow ◽  
Coil Embolisation ◽  
Artery Pseudoaneurysm ◽  
Healthy Young Woman ◽  
Dangerous Condition ◽  
Uterine Artery Pseudoaneurysm ◽  
In Pregnancy

Uterine artery pseudoaneurysm in pregnancy is a dangerous condition as rupture can be catastrophic due to the large volume of uterine blood flow. We present a case of a healthy, young woman with a desired pregnancy at 15 weeks of gestation incidentally discovered to have a pseudoaneurysm of the uterine artery during a routine prenatal ultrasound. She underwent initial thrombin injection followed by endovascular coil embolisation of the left uterine artery and carried the pregnancy to term without further complications.

Functional role of angiotensin II type 1 and 2 receptors in regulation of uterine blood flow in nonpregnant sheep

2000 ◽  
Vol 278 (2) ◽  
pp. H353-H359 ◽  
Author(s):  
Donna S. Lambers ◽  
Suzanne G. Greenberg ◽  
Kenneth E. Clark
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Uterine Artery ◽  
Receptor Subtype ◽  
Ang Ii ◽  
Uterine Blood Flow ◽  
Response Curves ◽  
Vascular Responses

The objective was to determine the receptor subtype of angiotensin II (ANG II) that is responsible for vasoconstriction in the nonpregnant ovine uterine and systemic vasculatures. Seven nonpregnant estrogenized ewes with indwelling uterine artery catheters and flow probes received bolus injections (0.1, 0.3 and 1 μg) of ANG II locally into the uterine artery followed by a systemic infusion of ANG II at 100 ng ⋅ kg−1 ⋅ min−1for 10 min to determine uterine vasoconstrictor responses. Uterine ANG II dose-response curves were repeated following administration of the ANG II type 2 receptor (AT2) antagonist PD-123319 and then repeated again in the presence of an ANG II type 1 receptor (AT1) antagonist L-158809. In a second experiment, designed to investigate the mechanism of ANG II potentiation that occurred in the presence of AT2 blockade, nonestrogenized sheep received a uterine artery infusion of L-158809 (3 mg/min for 5 min) prior to the infusion of 0.03 μg/min of ANG II for 10 min. ANG II produced dose-dependent decreases in uterine blood flow ( P < 0.03), which were potentiated in the presence of the AT2 antagonist ( P < 0.02). Addition of the AT1 antagonist abolished the uterine vascular responses and blocked ANG II-induced increases in systemic arterial pressure ( P < 0.01). Significant uterine vasodilation ( P < 0.01) was noted with AT1 blockade in the second experiment, which was reversed by administration of the AT2 antagonist or by the nitric oxide synthetase inhibitor N ω-nitro-l-arginine methyl ester. We conclude that the AT1- receptors mediate the systemic and uterine vasoconstrictor responses to ANG II in the nonpregnant ewe. AT2-receptor blockade resulted in a potentiation of the uterine vasoconstrictor response to ANG II, suggesting that the AT2-receptor subtype may modulate uterine vascular responses to ANG II potentially by release of nitric oxide.

scholarly journals Role of ETS1 in the Transcriptional Network of Diffuse Large B Cell Lymphoma of the Activated B Cell-Like Type

Cancers ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1912
Author(s):  
Valdemar Priebe ◽  
Giulio Sartori ◽  
Sara Napoli ◽  
Elaine Yee Lin Chung ◽  
Luciano Cascione ◽  
...  
Keyword(s):  
B Cell ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
B Cell Differentiation ◽  
Sequencing Data ◽  
B Cell Signaling ◽  
Large B Cell Lymphoma ◽  
Novel Target ◽  
Signaling Activation ◽  
Large B Cell

Diffuse large B cell lymphoma (DLBCL) is a heterogenous disease that has been distinguished into at least two major molecular entities, the germinal center-like B cell (GCB) DLBCL and activated-like B cell (ABC) DLBCL, based on transcriptome expression profiling. A recurrent ch11q24.3 gain is observed in roughly a fourth of DLBCL cases resulting in the overexpression of two ETS transcription factor family members, ETS1 and FLI1. Here, we knocked down ETS1 expression by siRNA and analyzed expression changes integrating them with ChIP-seq data to identify genes directly regulated by ETS1. ETS1 silencing affected expression of genes involved in B cell signaling activation, B cell differentiation, cell cycle, and immune processes. Integration of RNA-Seq (RNA sequencing) data and ChIP-Seq (chromatin immunoprecipitation sequencing) identified 97 genes as bona fide, positively regulated direct targets of ETS1 in ABC-DLBCL. Among these was the Fc receptor for IgM, FCMR (also known as FAIM3 or Toso), which showed higher expression in ABC- than GCB-DLBCL clinical specimens. These findings show that ETS1 is contributing to the lymphomagenesis in a subset of DLBCL and identifies FCMR as a novel target of ETS1, predominantly expressed in ABC-DLBCL.

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