Proteins differentially expressed in the 18 months and 24 months versus 10-weeks old group

<p><b>Copyright information:</b></p><p>Taken from "Age-related subproteomic analysis of mouse liver and kidney peroxisomes"</p><p>http://www.proteomesci.com/content/5/1/19</p><p>Proteome Science 2007;5():19-19.</p><p>Published online 27 Nov 2007</p><p>PMCID:PMC2231346.</p><p></p> The ratios were calculated dividing the volume percentage per each spot from the 18 months or 24 months by the volume percentage per spot in the 10 weeks old group. The vertical axis corresponds to the average ratio of expression, above the 0 value for the up-regulated proteins and below the 0 value for the down-regulated ones. According to 18 months old group, in the horizontal axis the down-regulated proteins are organized with the lowest values on the left side and the up-regulated ones show the highest values on the right side. Color code: green for 18 months group and orange for the 24 months old group. Liver age-related proteins. Kidney age-related proteins. Differential spot detection in fold from the 8 proteins composing the common age-related PES to both tissues. The four groups correspond to 18 months liver, 24 months liver, 18 months kidney and 24 months kidney samples

Posttranscriptional Regulation in Adenovirus Infected Cells

A deeper understanding of how viruses reprogram their hosts for production of progeny is needed to combat infections. Most knowledge on the regulation of cellular gene expression during adenovirus infection is derived from mRNA studies. Here, we investigated the changes in protein expression during the late phase of adenovirus type 2 (Ad2) infection of the IMR-90 cell line by stable isotope labeling in cell culture with subsequent liquid chromatography–high resolution tandem mass spectrometric analysis. Two biological replicates of samples collected at 24 and 36 h post-infection (hpi) were investigated using swapped labeling. In total, 2648 and 2394 proteins were quantified at 24 and 36 hpi, respectively. Among them, 659 and 645 were deregulated >1.6-fold at the two time points. The protein expression was compared with RNA expression using cDNA sequencing data. The correlation was surprisingly low (<i>r</i> = 0.3), and several examples of posttranscriptional regulation were observed; e.g., proteins related to carbohydrate metabolism were up-regulated at the protein level but unchanged at the RNA level, whereas histone proteins were down-regulated at the protein level but up-regulated at the RNA level. The deregulation of cellular gene expression by adenovirus is mediated at multiple levels and more complex than hitherto believed

DataSheet_1_An insight into the different responses to salt stress in growth characteristics of two legume species during seedling growth.docx

Legumes play a crucial role in the restoration and utilization of salinized grassland. To explore the physiological response mechanism of Astragalus membranaceus and Medicago sativa seedlings to salt stress, salt stress culture experiments with five NaCl concentration treatments (0 mmol/L, 50 mmol/L, 100 mmol/L, 200 mmol/L, and 300 mmol/L) were conducted on these two legume seedlings. Morphological characteristics, physiological features, biomass, and the protective enzyme system were measured for both seedlings. Correlation analysis, principal component analysis (PCA), and membership function analysis (MFA) were conducted for each index. Structural equation modeling (SEM) was employed to analyze the salt stress pathways of plants. The results indicated that number of primary branches (PBN), ascorbate peroxidase (APX) activity in stems and leaves, catalase (CAT) activity in roots, etc. were identified as the primary indicators for evaluating the salt tolerance of A. membranaceus during its seedling growth period. And CAT and peroxidase (POD) activity in roots, POD and superoxide dismutase (SOD) activity in stems and leaves, etc. were identified as the primary indicators for evaluating the salt tolerance of M. sativa during its growth period. Plant morphological characteristics, physiological indexes, and underground biomass (UGB) were directly affected by salinity, while physiological indexes indirectly affected the degree of leaf succulence (LSD). Regarding the response of the protective enzyme system to salt stress, the activity of POD and APX increased in A. membranaceus, while the activity of CAT increased in M. sativa. Our findings suggest that salt stress directly affects the growth strategies of legumes. Furthermore, the response of the protective enzyme system and potential cell membrane damage to salinity were very different in the two legumes.</p

Simulated Digestion and Fermentation in Vitro by Human Gut Microbiota of Polysaccharides from Bee Collected Pollen of Chinese Wolfberry

Digestion and fermentation in vitro of polysaccharides from bee collected pollen of Chinese wolfberry (WBPPS) were investigated in the present study. It was found that WBPPS mainly consisted of mannose, ribose, rhamnose, galacturonic acid, glucose, galactose, xylose, and arabinose in a molar ratio of 0.38:0.09:0.17:0.64:0.22:0.67:0.08:1.03, respectively. WBPPS was not affected by human saliva. The fraction A (molecular weight 1340 kDa) of WBPPS was not broken down in simulated gastric and small intestinal juices, while the small fraction B (molecular weight 523 kDa) of WBPPS was degraded. Moreover, fermentation in vitro revealed that WBPPS could significantly enhance the production of short-chain fatty acids and modulate gut microbiota composition via increasing the relative abundances of genera <i>Prevotella</i>, <i>Dialister</i>, <i>Megamonas</i>, <i>Faecalibacterium</i>, and <i>Alloprevotella</i> and decreasing the numbers of genera <i>Bacteroides</i>, <i>Clostridium XlVa</i>, <i>Parabacteroides</i>, <i>Escherichia/Shigella</i>, <i>Phascolarctobacterium</i>, <i>Parasutterella</i>, <i>Clostridium sensu stricto</i>, and <i>Fusobacterium</i>

Table_2_Transcriptome-wide association study reveals cholesterol metabolism gene Lpl is a key regulator of cognitive dysfunction.xlsx

Cholesterol metabolism in the brain plays a crucial role in normal physiological function, and its aberrations are associated with cognitive dysfunction. The present study aimed to determine which cholesterol-related genes play a vital role in cognitive dysfunction and to dissect its underlying molecular mechanisms using a systems genetics approach in the BXD mice family. We first systematically analyzed the association of expression of 280 hippocampal genes related to cholesterol metabolism with cognition-related traits and identified lipoprotein lipase (Lpl) as a critical regulator. This was further confirmed by phenome-wide association studies that indicate Lpl associated with hippocampus volume residuals and anxiety-related traits. By performing expression quantitative trait locus mapping, we demonstrate that Lpl is strongly cis-regulated in the BXD hippocampus. We also identified ∼3,300 genes significantly (p < 0.05) correlated with the Lpl expression. Those genes are mainly involved in the regulation of neuron-related traits through the MAPK signaling pathway, axon guidance, synaptic vesicle cycle, and NF-kappa B signaling pathway. Furthermore, a protein–protein interaction network analysis identified several direct interactors of Lpl, including Rab3a, Akt1, Igf1, Crp, and Lrp1, which indicates that Lpl involves in the regulation of cognitive dysfunction through Rab3a-mediated synaptic vesicle cycle and Akt1/Igf1/Crp/Lrp1-mediated MAPK signaling pathway. Our findings demonstrate the importance of the Lpl, among the cholesterol-related genes, in regulating cognitive dysfunction and highlighting the potential signaling pathways, which may serve as novel therapeutic targets for the treatment of cognitive dysfunction.</p

Table_1_Transcriptome-wide association study reveals cholesterol metabolism gene Lpl is a key regulator of cognitive dysfunction.XLSX

Cholesterol metabolism in the brain plays a crucial role in normal physiological function, and its aberrations are associated with cognitive dysfunction. The present study aimed to determine which cholesterol-related genes play a vital role in cognitive dysfunction and to dissect its underlying molecular mechanisms using a systems genetics approach in the BXD mice family. We first systematically analyzed the association of expression of 280 hippocampal genes related to cholesterol metabolism with cognition-related traits and identified lipoprotein lipase (Lpl) as a critical regulator. This was further confirmed by phenome-wide association studies that indicate Lpl associated with hippocampus volume residuals and anxiety-related traits. By performing expression quantitative trait locus mapping, we demonstrate that Lpl is strongly cis-regulated in the BXD hippocampus. We also identified ∼3,300 genes significantly (p < 0.05) correlated with the Lpl expression. Those genes are mainly involved in the regulation of neuron-related traits through the MAPK signaling pathway, axon guidance, synaptic vesicle cycle, and NF-kappa B signaling pathway. Furthermore, a protein–protein interaction network analysis identified several direct interactors of Lpl, including Rab3a, Akt1, Igf1, Crp, and Lrp1, which indicates that Lpl involves in the regulation of cognitive dysfunction through Rab3a-mediated synaptic vesicle cycle and Akt1/Igf1/Crp/Lrp1-mediated MAPK signaling pathway. Our findings demonstrate the importance of the Lpl, among the cholesterol-related genes, in regulating cognitive dysfunction and highlighting the potential signaling pathways, which may serve as novel therapeutic targets for the treatment of cognitive dysfunction.</p

The Combination of Quantitative Proteomics and Systems Genetics Analysis Reveals that PTN Is Associated with Sleep-Loss-Induced Cognitive Impairment

Sleep loss is associated with cognitive dysfunction. However, the detailed mechanisms remain unclear. In this study, we established a para-chlorophenylalanine (PCPA)-induced insomniac mouse model with impaired cognitive function. Mass-spectrometry-based proteomics showed that the expression of 164 proteins was significantly altered in the hippocampus of the PCPA mice. To identify critical regulators among the potential markers, a transcriptome-wide association screening was performed in the BXD mice panel. Among the candidates, the expression of pleiotrophin (Ptn) was significantly associated with cognitive functions, indicating that Ptn-mediates sleep-loss-induced cognitive impairment. Gene co-expression analysis further revealed the potential mechanism by which Ptn mediates insomnia-induced cognitive impairment via the MAPK signaling pathway; that is, the decreased secretion of Ptn induced by insomnia leads to reduced binding to Ptprz1 on the postsynaptic membrane with the activation of the MAPK pathway via Fos and Nr4a1, further leading to the apoptosis of neurons. In addition, Ptn is genetically trans-regulated in the mouse hippocampus and implicated in neurodegenerative diseases in human genome-wide association studies. Our study provides a novel biomarker for insomnia-induced cognitive impairment and a new strategy for seeking neurological biomarkers by the integration of proteomics and systems genetics

The Combination of Quantitative Proteomics and Systems Genetics Analysis Reveals that PTN Is Associated with Sleep-Loss-Induced Cognitive Impairment

Sleep loss is associated with cognitive dysfunction. However, the detailed mechanisms remain unclear. In this study, we established a para-chlorophenylalanine (PCPA)-induced insomniac mouse model with impaired cognitive function. Mass-spectrometry-based proteomics showed that the expression of 164 proteins was significantly altered in the hippocampus of the PCPA mice. To identify critical regulators among the potential markers, a transcriptome-wide association screening was performed in the BXD mice panel. Among the candidates, the expression of pleiotrophin (Ptn) was significantly associated with cognitive functions, indicating that Ptn-mediates sleep-loss-induced cognitive impairment. Gene co-expression analysis further revealed the potential mechanism by which Ptn mediates insomnia-induced cognitive impairment via the MAPK signaling pathway; that is, the decreased secretion of Ptn induced by insomnia leads to reduced binding to Ptprz1 on the postsynaptic membrane with the activation of the MAPK pathway via Fos and Nr4a1, further leading to the apoptosis of neurons. In addition, Ptn is genetically trans-regulated in the mouse hippocampus and implicated in neurodegenerative diseases in human genome-wide association studies. Our study provides a novel biomarker for insomnia-induced cognitive impairment and a new strategy for seeking neurological biomarkers by the integration of proteomics and systems genetics

The Combination of Quantitative Proteomics and Systems Genetics Analysis Reveals that PTN Is Associated with Sleep-Loss-Induced Cognitive Impairment

Sleep loss is associated with cognitive dysfunction. However, the detailed mechanisms remain unclear. In this study, we established a para-chlorophenylalanine (PCPA)-induced insomniac mouse model with impaired cognitive function. Mass-spectrometry-based proteomics showed that the expression of 164 proteins was significantly altered in the hippocampus of the PCPA mice. To identify critical regulators among the potential markers, a transcriptome-wide association screening was performed in the BXD mice panel. Among the candidates, the expression of pleiotrophin (Ptn) was significantly associated with cognitive functions, indicating that Ptn-mediates sleep-loss-induced cognitive impairment. Gene co-expression analysis further revealed the potential mechanism by which Ptn mediates insomnia-induced cognitive impairment via the MAPK signaling pathway; that is, the decreased secretion of Ptn induced by insomnia leads to reduced binding to Ptprz1 on the postsynaptic membrane with the activation of the MAPK pathway via Fos and Nr4a1, further leading to the apoptosis of neurons. In addition, Ptn is genetically trans-regulated in the mouse hippocampus and implicated in neurodegenerative diseases in human genome-wide association studies. Our study provides a novel biomarker for insomnia-induced cognitive impairment and a new strategy for seeking neurological biomarkers by the integration of proteomics and systems genetics

The Combination of Quantitative Proteomics and Systems Genetics Analysis Reveals that PTN Is Associated with Sleep-Loss-Induced Cognitive Impairment

Sleep loss is associated with cognitive dysfunction. However, the detailed mechanisms remain unclear. In this study, we established a para-chlorophenylalanine (PCPA)-induced insomniac mouse model with impaired cognitive function. Mass-spectrometry-based proteomics showed that the expression of 164 proteins was significantly altered in the hippocampus of the PCPA mice. To identify critical regulators among the potential markers, a transcriptome-wide association screening was performed in the BXD mice panel. Among the candidates, the expression of pleiotrophin (Ptn) was significantly associated with cognitive functions, indicating that Ptn-mediates sleep-loss-induced cognitive impairment. Gene co-expression analysis further revealed the potential mechanism by which Ptn mediates insomnia-induced cognitive impairment via the MAPK signaling pathway; that is, the decreased secretion of Ptn induced by insomnia leads to reduced binding to Ptprz1 on the postsynaptic membrane with the activation of the MAPK pathway via Fos and Nr4a1, further leading to the apoptosis of neurons. In addition, Ptn is genetically trans-regulated in the mouse hippocampus and implicated in neurodegenerative diseases in human genome-wide association studies. Our study provides a novel biomarker for insomnia-induced cognitive impairment and a new strategy for seeking neurological biomarkers by the integration of proteomics and systems genetics