Role of urinary trypsin inhibitor in the maintenance of pregnancy in mice

Kaga, Nobuhiko; Katsuki, Yukio; Futamura, Yoshihiro; Obata, Masaomi; Shibutani, Yasunori

doi:10.1016/0029-7844(96)00268-2

Cited by 37 publications

(20 citation statements)

References 19 publications

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“…Although information is not available on the neuroprotective properties of the blood plasma derived IAIP complex (Lim, 2013), the light chain of IAIP exhibits neuroprotective properties and blocks production of inflammatory cytokines after ischemic injury in somatic organs (Cao, et al, 2000, El Maradny, et al, 1996, Kaga, et al, 1996, Kakinuma, et al, 1997, Koga, et al, 2010, Nakahama, et al, 1996, Shu, et al, 2011, Wang, et al, 2013, Yano, et al, 2003). Therefore, findings of the present study are the first to demonstrate that the blood plasma derived complex form of IAIP exhibits important neuroprotective properties.…”

Section: Discussionmentioning

confidence: 99%

Effects of inter-alpha inhibitor proteins on neonatal brain injury: Age, task and treatment dependent neurobehavioral outcomes

Threlkeld

Gaudet

Rue

et al. 2014

Experimental Neurology

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Hypoxic-ischemic (HI) brain injury is frequently associated with premature and/or full term birth related complications. HI injury often results in learning and processing deficits that reflect widespread damage to an extensive range of cortical and sub-cortical brain structures. Further, inflammation has been implicated in the long-term progression and severity of HI injury. Recently, Inter-alpha Inhibitor Proteins (IAIPs) have been shown to attenuate inflammation in models of systemic infection. Importantly, preclinical studies of neonatal HI injury and neuroprotection often focus on single time windows of assessment or single behavioral domains. This approach limits translational validity, given evidence for a diverse spectrum of neurobehavioral deficits that may change across developmental windows following neonatal brain injury. Therefore, the aims of this research were to assess the effects of human IAIPs on early neocortical cell death (72 hours post insult), adult regional brain volume measurements (cerebral cortex, hippocampus, striatum, corpus callosum) and long-term behavioral outcomes in juvenile (P38-50) and adult (P80+) periods across two independent learning domains (spatial and non-spatial learning), after postnatal day 7 HI injury in rats. Here, for the first time, we show that IAIPs reduce acute neocortical neuronal cell death and improve brain weight outcome 72 hours following HI injury in the neonatal rat. Further, these longitudinal studies are the first to show age, task and treatment dependent improvements in behavioral outcome for both spatial and non-spatial learning following systemic administration of IAIPs in neonatal HI injured rats. Finally, results also show sparing of brain regions critical for spatial and non-spatial learning in adult animals treated with IAIPs at the time of injury onset. These data support the proposal that Inter-alpha Inhibitor Proteins may serve as novel therapeutics for brain injury associated with premature birth and/or neonatal brain injury and highlight the importance of assessing multiple ages, brain regions and behavioral domains when investigating experimental treatment efficacy.

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Section: Discussionmentioning

confidence: 99%

Effects of inter-alpha inhibitor proteins on neonatal brain injury: Age, task and treatment dependent neurobehavioral outcomes

Threlkeld

Gaudet

Rue

et al. 2014

Experimental Neurology

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“…Additionally, bikunin has a significant anti-inflammatory function by blocking systemic cytokine induction in response to endotoxin challenge in vivo [34] Finally, bikunin inhibits entotoxin-induced preterm labor in mice, [35] inhibits prostaglandin expression from amnion cells [36] suppresses uterine contractions [37] by reducing calcium influx in myometrial cells [38] and suppresses premature cervical ripening [39] which are all key pathogenetic processes necessary for preterm birth. The observed upregulation in bikunin levels may reflect an endogenous compensatory mechanism aimed to prolong pregnancy and downplay inflammatory processes.…”

Section: Discussionmentioning

confidence: 99%

Multidimensional Proteomics Analysis of Amniotic Fluid to Provide Insight into the Mechanisms of Idiopathic Preterm Birth

et al. 2008

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BackgroundThough recent advancement in proteomics has provided a novel perspective on several distinct pathogenetic mechanisms leading to preterm birth (inflammation, bleeding), the etiology of most preterm births still remains elusive. We conducted a multidimensional proteomic analysis of the amniotic fluid to identify pathways related to preterm birth in the absence of inflammation or bleeding.Methodology/Principal FindingsA proteomic fingerprint was generated from fresh amniotic fluid using surface-enhanced laser desorbtion ionization time of flight (SELDI-TOF) mass spectrometry in a total of 286 consecutive samples retrieved from women who presented with signs or symptoms of preterm labor or preterm premature rupture of the membranes. Inflammation and/or bleeding proteomic patterns were detected in 32% (92/286) of the SELDI tracings. In the remaining tracings, a hierarchical algorithm was applied based on descriptors quantifying similarity/dissimilarity among proteomic fingerprints. This allowed identification of a novel profile (Q-profile) based on the presence of 5 SELDI peaks in the 10–12.5 kDa mass area. Women displaying the Q-profile (mean±SD, gestational age: 25±4 weeks, n = 40) were more likely to deliver preterm despite expectant management in the context of intact membranes and normal amniotic fluid clinical results. Utilizing identification-centered proteomics techniques (fluorescence two-dimensional differential gel electrophoresis, robotic tryptic digestion and mass spectrometry) coupled with Protein ANalysis THrough Evolutionary Relationships (PANTHER) ontological classifications, we determined that in amniotic fluids with Q-profile the differentially expressed proteins are primarily involved in non-inflammatory biological processes such as protein metabolism, signal transduction and transport.Conclusion/SignificanceProteomic profiling of amniotic fluid coupled with non-hierarchical bioinformatics algorithms identified a subgroup of patients at risk for preterm birth in the absence of intra-amniotic inflammation or bleeding, suggesting a novel pathogenetic pathway leading to preterm birth. The altered proteins may offer opportunities for therapeutical intervention and future drug development to prevent prematurity.

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“…cytokines into the amniotic fluid (11), and also by inhibiting the expression of cyclooxygenase-2, which is required for contraction of the uterus (12). In intrauterine infection, UTI administration prevents preterm delivery by inhibiting cervical ripening (13,14).…”

Section: Tablementioning

confidence: 99%

Impaired Fertility in Female Mice Lacking Urinary Trypsin Inhibitor

Sato

Kajikawa

Kuroda

et al. 2001

Biochemical and Biophysical Research Communications

100

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Role of urinary trypsin inhibitor in the maintenance of pregnancy in mice

Abstract: Urinary trypsin inhibitor prevents the pathogenicity of preterm delivery through the suppression of cytokine production.

Cited by 37 publications

References 19 publications

Effects of inter-alpha inhibitor proteins on neonatal brain injury: Age, task and treatment dependent neurobehavioral outcomes

Effects of inter-alpha inhibitor proteins on neonatal brain injury: Age, task and treatment dependent neurobehavioral outcomes

Multidimensional Proteomics Analysis of Amniotic Fluid to Provide Insight into the Mechanisms of Idiopathic Preterm Birth

Impaired Fertility in Female Mice Lacking Urinary Trypsin Inhibitor

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