Prospective plasma proteome changes in preterm infants with different gestational ages

Abstract Background Chorioamnionitis (CA) is a risk factor for preterm birth and is associated with neurodevelopmental delay and cognitive disorders. Prenatal inflammation-induced brain injury may resolve during the immediate postnatal period, which is a time of rapid metabolic and brain remodeling. Cerebrospinal fluid (CSF) collected at birth may be a critical source of predictive biomarkers. Using pigs as a model of preterm infants exposed to CA, we hypothesized that prenatal lipopolysaccharide (LPS) exposure induces proteome changes in the CSF and brain both at birth and later. Methods Fetal piglets (103 days gestation of the full-term 117 days) were administered intra-amniotic (IA) lipopolysaccharide (LPS) 3 days before preterm delivery by caesarian section. CSF and brain tissue were collected on postnatal Days 1 and 5 (P1 and P5). CSF and hippocampal proteins were profiled by LC–MS-based quantitative proteomics. Neuroinflammatory responses in the cerebral cortex, periventricular white matter and hippocampus were evaluated by immunohistochemistry, and gene expression was evaluated by qPCR. Results Pigs exposed to LPS in utero showed changes in CSF protein levels at birth but not at P5. Complement protein C3, hemopexin, vasointestinal peptide, carboxypeptidase N subunit 2, ITIH1 and plasminogen expression was upregulated in the CSF, while the expression of proteins associated with axon growth and synaptic functions (FGFR1, BASP1, HSPD1, UBER2N, and RCN2), adhesion (Talin1), and neuronal survival (Atox1) was downregulated. Microglia, but not astrocytes, were activated by LPS at P5 in the hippocampus but not in other brain regions. At this time, marginal increases in complement protein C3, LBP, Hif1a, Basp1, Minpp1 and FGFR1 transcription indicated hippocampal proinflammatory responses. Conclusion A brief period of prenatal endotoxin exposure induces proteome changes in the CSF and brain at birth, but most changes resolve a few days later. The developing hippocampus has high neuronal plasticity in response to perinatal inflammation. Changes in CSF protein expression at birth may help to predict later structural brain damage in preterm infants exposed to variable types and durations of CA-related inflammation in utero.

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Characteristics of blood plasma proteome changes associated with the hemorrhagic purpura of cosmonauts on the first day after long-term space missions

Life Sciences in Space Research ◽

10.1016/j.lssr.2022.01.001 ◽

2022 ◽

Author(s):

LKh Pastushkova ◽

IN Goncharov ◽

MI Koloteva ◽

AG Goncharova ◽

DN Kashirina ◽

...

Keyword(s):

Blood Plasma ◽

Space Missions ◽

Plasma Proteome ◽

Proteome Changes

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Plasma proteome changes associated with refractory cytopenia with multilineage dysplasia

Proteome Science ◽

10.1186/1477-5956-9-64 ◽

2011 ◽

Vol 9 (1) ◽

pp. 64 ◽

Cited By ~ 12

Author(s):

Pavel Májek ◽

Zuzana Reicheltová ◽

Jiří Suttnar ◽

Jaroslav Čermák ◽

Jan E Dyr

Keyword(s):

Plasma Proteome ◽

Multilineage Dysplasia ◽

Proteome Changes

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Abstract 182: Quantitative Proteomics Reveals Dynamic Changes of Plasma Proteome in APOE-Deficient Mice at Four Phases of Atherosclerosis

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.33.suppl_1.a182 ◽

2013 ◽

Vol 33 (suppl_1) ◽

Author(s):

Linhong Jing ◽

Zhu-qiu Jin ◽

Wei Xie ◽

Shuaipeng J Zhang

Keyword(s):

High Fat Diet ◽

Plasma Proteins ◽

Immune Modulation ◽

Complement C3 ◽

Plasma Proteome ◽

High Fat ◽

Dynamic Changes ◽

Proteome Changes ◽

Disease Stages ◽

Deficient Mice

Introduction To understand the mechanism for atherosclerotic disease at molecular level, we analyzed the dynamic changes of plasma proteome in mice at four different disease stages vs. control based on hypothesis that a panel of plasma proteins might associate with the progression of atherosclerosis. Methods Male APOE knockout (-/-) mice were fed with high fat diet and euthanized at 8, 12, 18 or 24 weeks of age, representing the early, intermediate, moderate and later stages of disease. Age-matched male wild type mice fed with high fat diet served as controls. At the time of euthanasia, aorta and plasma were collected. A mass spectrometry-based proteomics approach was employed to simultaneously quantify proteins in eight pooled samples. Results Image analysis of lesions in aortas (stained with Sudan IV) from 40 APOE -/- mice (10 mice at each time point) demonstrated the development of four different phases of disease (Fig.). No lesion was observed in the control mice. We have identified 57 dysregulated proteins (e.g., fibrinogen beta and gamma chains, complement C3, C4B, C9, apolipoproteins, etc.) at four disease stages. These protein’s expression levels, biological functions (e.g. immune modulation and inflammation), and pathways (e.g., complement and cogulation cascades) provide a better understanding of the basic molecular processes in atherosclerosis. Conclusions 1) Proteomics analysis of plasma proteome changes at different stages of APOE-deficient mice facilitated the mechanistic studies of atherosclerosis. 2) A panel of plasma proteins was identified as potential “signatures” of atherosclerosis which may help early diagnosis and therapeutic intervention.

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