scholarly journals Proteomic analysis of machine perfusion solution from brain dead donor kidneys reveals that elevated complement, cytoskeleton and lipid metabolism proteins are associated with 1‐year outcome

2021 ◽  
Vol 34 (9) ◽  
pp. 1618-1629
Author(s):  
L. Leonie Leeuwen ◽  
Nora A. Spraakman ◽  
Aukje Brat ◽  
Honglei Huang ◽  
Adam M. Thorne ◽  
...  
Biomolecules ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 1164
Author(s):  
Siying Song ◽  
Linlin Guo ◽  
Di Wu ◽  
Jingfei Shi ◽  
Yunxia Duan ◽  
...  

Background: Animal and clinical studies have shown that remote ischemic conditioning (RIC) has protective effects for cerebral vascular diseases, with induced humoral factor changes in the peripheral blood. However, many findings are heterogeneous, perhaps due to differences in the RIC intervention schemes, enrolled populations, and sample times. This study aimed to examine the RIC-induced changes in the plasma proteome using rhesus monkey models of strokes. Methods: Two adult rhesus monkeys with autologous blood clot-induced middle cerebral artery (MCA) occlusion underwent RIC interventions twice a week for five consecutive weeks. Each RIC treatment included five cycles of five minutes of ischemia alternating with five minutes of reperfusion of the forearm. The blood samples were taken from the median cubital vein of the monkeys at baseline and immediately after each week’s RIC stimulus. The plasma samples were isolated for a proteomic analysis using mass spectrometry (MS). Results: Several proteins related to lipid metabolism (Apolipoprotein A-II and Apolipoprotein C-II), coagulation (Fibrinogen alpha chain and serpin), immunoinflammatory responses (complement C3 and C1), and endovascular hemostasis (basement membrane-specific heparan sulfate proteoglycan) were significantly modulated after the RIC intervention. Many of these induced changes, such as in the lipid metabolism regulation and anticoagulation responses, starting as early as two weeks following the RIC intervention. The complementary activation and protection of the endovascular cells occurred more than three weeks postintervention. Conclusions: Multiple protective effects were induced by RIC and involved lipid metabolism regulation (anti-atherogenesis), anticoagulation (antithrombosis), complement activation, and endovascular homeostasis (anti-inflammation). In conclusion, this study indicates that RIC results in significant modulations of the plasma proteome. It also provides ideas for future research and screening targets.


2013 ◽  
Vol 29 (3) ◽  
pp. 544-549 ◽  
Author(s):  
S. Hoeger ◽  
J. Fontana ◽  
J. Jarczyk ◽  
J. Selhorst ◽  
R. Waldherr ◽  
...  

2005 ◽  
Vol 37 (1) ◽  
pp. 387-388 ◽  
Author(s):  
O. Kuecuek ◽  
L. Mantouvalou ◽  
R. Klemz ◽  
K. Kotsch ◽  
H.D. Volk ◽  
...  

2008 ◽  
Vol 86 (Supplement) ◽  
pp. 377
Author(s):  
B Yard ◽  
S Hoeger ◽  
K Petrov ◽  
A Reisenbuechler ◽  
R Waldherr ◽  
...  

2021 ◽  
Author(s):  
Yaqin Yan ◽  
Jintian Tang ◽  
Qinfeng Yuan ◽  
Liping Liu ◽  
Hao Liu ◽  
...  

Colletotrichum higginsianum is an important hemibiotrophic fungal pathogen that causes anthracnose disease on various cruciferous plants. Discovery of new virulence factors could lead to strategies for effectively controlling anthracnose. Acyl-CoA binding proteins (ACBPs) are mainly involved in binding and trafficking acyl-CoA esters in eukaryotic cells. However, the functions of this important class of proteins in plant fungal pathogens remain unclear. In this study, we performed an iTRAQ-based quantitative proteomic analysis to identify differentially expressed proteins (DEPs) between a nonpathogenic mutant ΔCh-MEL1 and the wild-type. Based on iTRAQ data, DEPs in the ΔCh-MEL1 mutant were mainly associated with melanin biosynthesis, carbohydrate and energy metabolism, lipid metabolism, redox processes, and amino acid metabolism. Proteomic analysis revealed that many DEPs might be involved in growth and pathogenesis of C. higginsianum. Among them, an acyl-CoA binding protein, ChAcb1, was selected for further functional studies. Deletion of ChAcb1 caused defects in vegetative growth and conidiation. ChAcb1 is also required for response to hyperosmotic and oxidative stresses, and maintenance of cell wall integrity. Importantly, the ΔChAcb1 mutant exhibited reduced virulence, and microscopic examination revealed that it was defective in appressorial penetration and infectious growth. Furthermore, the ΔChAcb1 mutant was impaired in fatty acid and lipid metabolism. Taken together, ChAcb1 was identified as a new virulence gene in this plant pathogenic fungus.


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