Oxidative stress effect on progesterone-induced blocking factor (PIBF) binding to PIBF-receptor in lymphocytes

Haba, Carlos de la; Palacio, J.; Palkovics, Tamas; Szekeres-Barthó, Júlia; Morros, Antoni; Martı́nez, Paz

doi:10.1016/j.bbamem.2013.08.006

Cited by 7 publications

(4 citation statements)

References 69 publications

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“…However, several other shorter splice variants have been recognized with tissue-specific intra- and extra-cellular expression (255–257). These short isoforms are also thought to be ligands for the PIBF receptor (256, 258). Highly proliferative cells such as trophoblast, mesenchymal stem cells, and tumor cells all express PIBF (257, 259, 260).…”

Section: P4-induced Blocking Factor (Pibf)mentioning

confidence: 99%

Progesterone-Related Immune Modulation of Pregnancy and Labor

et al. 2019

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Pregnancy involves a complex interplay between maternal neuroendocrine and immunological systems in order to establish and sustain a growing fetus. It is thought that the uterus at pregnancy transitions from quiescent to laboring state in response to interactions between maternal and fetal systems at least partly via altered neuroendocrine signaling. Progesterone (P4) is a vital hormone in maternal reproductive tissues and immune cells during pregnancy. As such, P4 is widely used in clinical interventions to improve the chance of embryo implantation, as well as reduce the risk of miscarriage and premature labor. Here we review research to date that focus on the pathways through which P4 mediates its actions on both the maternal reproductive and immune system. We will dissect the role of P4 as a modulator of inflammation, both systemic and intrinsic to the uterus, during human pregnancy and labor.

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Section: P4-induced Blocking Factor (Pibf)mentioning

confidence: 99%

Progesterone-Related Immune Modulation of Pregnancy and Labor

et al. 2019

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“…PIBF expression has been described in several cells with a high proliferation rate [ 9 , 17 , 37 ]. It has been suggested that PIBF isoforms act as ligands implicated in the activation of proliferation signaling pathways including JAK1/STAT6 [ 9 , 10 , 12 , 38 ], through the interaction with a receptor heterocomplex consisting of PIBF-R, which is attached to the plasma membrane by a glycosylphosphatidylinositol [ 13 ], and membrane receptor IL-4R α [ 10 , 12 ]. In previous studies, PIBF (200 ng/mL) increased the number of astrocytoma cells through the activation of the IL-4R α /JAK1/STAT6 pathway [ 10 ].…”

Section: Discussionmentioning

confidence: 99%

“…The shorter PIBF isoforms present a tissue-specific expression and have been located in the intra- and extracellular compartments [ 9 , 10 ]. These short isoforms have been proposed as ligands of the PIBF receptor/interleukin 4 receptor α (PIBF-R/IL-4R α ) heterocomplex that activates diverse proliferative signaling pathways [ 12 , 13 ]. The most studied pathway is the IL-4R/JAK1/STAT6 [ 10 , 12 , 14 ], associated with the differentiation of Th2 cells, to produce a cytokine specific pattern [ 15 ], and with tumor cell growth [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

Proliferative and Invasive Effects of Progesterone-Induced Blocking Factor in Human Glioblastoma Cells

Gutiérrez-Rodríguez

Hansberg-Pastor

2017

BioMed Research International

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Progesterone-induced blocking factor (PIBF) is a progesterone (P4) regulated protein expressed in different types of high proliferative cells including astrocytomas, the most frequent and aggressive brain tumors. It has been shown that PIBF increases the number of human astrocytoma cells. In this work, we evaluated PIBF regulation by P4 and the effects of PIBF on proliferation, migration, and invasion of U87 and U251 cells, both derived from human glioblastomas. PIBF mRNA expression was upregulated by P4 (10 nM) from 12 to 24 h. Glioblastoma cells expressed two PIBF isoforms, 90 and 57 kDa. The content of the shorter isoform was increased by P4 at 24 h, while progesterone receptor antagonist RU486 (10 μM) blocked this effect. PIBF (100 ng/mL) increased the number of U87 cells on days 4 and 5 of treatment and induced cell proliferation on day 4. Wound-healing assays showed that PIBF increased the migration of U87 (12–48 h) and U251 (24 and 48 h) cells. Transwell invasion assays showed that PIBF augmented the number of invasive cells in both cell lines at 24 h. These data suggest that PIBF promotes proliferation, migration, and invasion of human glioblastoma cells.

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“…However, we and others have shown in the BALB/c mouse model that pregnancy increases lung inflammation and expression of stress-induced prostaglandins (PGs) and cyclooxygenase-2 (COX-2) prior to infection and that IAV infection enhances immunopathology in the lungs of pregnant mice relative to non-pregnant mice ( 86 – 88 ). Oxidative stress interferes with lipid raft clustering and has been shown to inhibit the ability of PIBF to bind its transmembrane receptor and IL-4R to induce the STAT6 signaling pathway; this interference reduces the sensitivity of cells to PIBF ( 96 , 97 ). Thus, influenza viral infection and subsequent oxidative stress may interfere with the unique lung and mucosal physiology tightly regulated by sex hormones toward successful pregnancy and fetal development.…”

Section: Introductionmentioning

confidence: 99%

Hormonal Regulation of Physiology, Innate Immunity and Antibody Response to H1N1 Influenza Virus Infection During Pregnancy

Littauer

Skountzou

2018

Front. Immunol.

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In 2009, the H1N1 swine flu pandemic highlighted the vulnerability of pregnant women to influenza viral infection. Pregnant women infected with influenza A virus were at increased risk of hospitalization and severe acute respiratory distress syndrome (ARDS), which is associated with high mortality, while their newborns had an increased risk of pre-term birth or low birth weight. Pregnant women have a unique immunological profile modulated by the sex hormones required to maintain pregnancy, namely progesterone and estrogens. The role of these hormones in coordinating maternal immunotolerance in uterine tissue and cellular subsets has been well researched; however, these hormones have wide-ranging effects outside the uterus in modulating the immune response to disease. In this review, we compile research findings in the clinic and in animal models that elaborate on the unique features of H1N1 influenza A viral pathogenesis during pregnancy, the crosstalk between innate immune signaling and hormonal regulation during pregnancy, and the role of pregnancy hormones in modulating cellular responses to influenza A viral infection at mid-gestation. We highlight the ways in which lung architecture and function is stressed by pregnancy, increasing baseline inflammation prior to infection. We demonstrate that infection disrupts progesterone production and upregulates inflammatory mediators, such as cyclooxygenase-2 (COX-2) and prostaglandins, resulting in pre-term labor and spontaneous abortions. Lastly, we profile the ways in which pregnancy alters innate and adaptive cellular immune responses to H1N1 influenza viral infection, and the ways in which these protect fetal development at the expense of effective long-term immune memory. Thus, we highlight advancements in the field of reproductive immunology in response to viral infection and illustrate how that knowledge might be used to develop more effective post-infection therapies and vaccination strategies.

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Oxidative stress effect on progesterone-induced blocking factor (PIBF) binding to PIBF-receptor in lymphocytes

Cited by 7 publications

References 69 publications

Progesterone-Related Immune Modulation of Pregnancy and Labor

Progesterone-Related Immune Modulation of Pregnancy and Labor

Proliferative and Invasive Effects of Progesterone-Induced Blocking Factor in Human Glioblastoma Cells

Hormonal Regulation of Physiology, Innate Immunity and Antibody Response to H1N1 Influenza Virus Infection During Pregnancy

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