Literature DB >> 31285044

Protective effect of phosphatidylserine blockade in sepsis induced organ dysfunction.

Genna Beattie1, Caitlin Cohan2, Emily Miraflor2, William Brigode2, Gregory P Victorino2.   

Abstract

BACKGROUND: Phosphatidylserine is usually an intracellularly oriented cell membrane phospholipid. Externalized phosphatidylserine on activated cells is a signal for phagocytosis. In sepsis, persistent phosphatidylserine exposure is also a signal for activation of the coagulation and inflammatory cascades. As such, phosphatidylserine may be a key molecule in sepsis induced cellular and organ injury. We hypothesize that phosphatidylserine blockade provides a protective effect in sepsis induced organ dysfunction.
METHODS: Sepsis was induced in adult female rats using an endotoxin model. Diannexin, a homodimer of annexin A5, was administered for phosphatidylserine blockade. Rats were allocated to control (n = 5), sepsis (n = 6), or sepsis and phosphatidylserine blockade (n = 9) groups. Gut, pulmonary, renal, and hematologic dysfunctions were evaluated by mesenteric microvascular fluid leak, partial pressure of oxygen, serum creatinine, activated clotting time, and glomerular fibrin deposition, respectively.
RESULTS: Rats in the sepsis group demonstrated gut, renal, and hematologic dysfunction. Phosphatidylserine blockade reversed signs of gut dysfunction and mesenteric microvascular leak (P < .01). In addition, phosphatidylserine blockade corrected systemic coagulopathy, as measured by activated clotting time (P = .03) and glomerular fibrin deposition (P = .008). There was no difference in renal dysfunction (P = .1) or pulmonary dysfunction in any of the groups (P = .6).
CONCLUSION: In sepsis, phosphatidylserine blockade had a protective effect on gut dysfunction and coagulopathy. Increased phosphatidylserine exposure may be a key mediator of organ dysfunction and coagulopathy during sepsis. These data may provide insights into novel treatment options for septic patients.
Copyright © 2019 Elsevier Inc. All rights reserved.

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Year:  2019        PMID: 31285044      PMCID: PMC6802284          DOI: 10.1016/j.surg.2019.05.020

Source DB:  PubMed          Journal:  Surgery        ISSN: 0039-6060            Impact factor:   3.982


  34 in total

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Review 2.  Transbilayer movement of phospholipids in red cell and platelet membranes.

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Journal:  Biochim Biophys Acta       Date:  1991-11-13

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Authors:  Jessica L Slocum; Michael Heung; Subramaniam Pennathur
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Review 4.  Exposure of phosphatidylserine on the cell surface.

Authors:  S Nagata; J Suzuki; K Segawa; T Fujii
Journal:  Cell Death Differ       Date:  2016-02-19       Impact factor: 15.828

5.  Endotoxin-induced disseminated intravascular coagulation in nonpregnant rats. A new experimental model.

Authors:  T H Schoendorf; M Rosenberg; F K Beller
Journal:  Am J Pathol       Date:  1971-10       Impact factor: 4.307

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Review 7.  Annexin V, the regulator of phosphatidylserine-catalyzed inflammation and coagulation during apoptosis.

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8.  Interaction of an annexin V homodimer (Diannexin) with phosphatidylserine on cell surfaces and consequent antithrombotic activity.

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10.  Diannexin, a novel annexin V homodimer, protects rat liver transplants against cold ischemia-reperfusion injury.

Authors:  X-D Shen; B Ke; Y Zhai; S-I Tsuchihashi; F Gao; S Duarte; A Coito; R W Busuttil; A C Allison; J W Kupiec-Weglinski
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4.  Expression and role of ABIN1 in sepsis: In vitro and in vivo studies.

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5.  Recombinant Human Annexin A5 Alleviated Traumatic-Brain-Injury Induced Intestinal Injury by Regulating the Nrf2/HO-1/HMGB1 Pathway.

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  5 in total

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