Evidence map›Paper›PMID 33539284›Full record

ArticleBlood transfusion = Trasfusione del sangue2021

Fibrinogen inhibits microRNA-19b, a novel mechanism for repair of haemorrhagic shock-induced endothelial cell dysfunction.

Amanda M Chipman, Feng Wu, Rosemary A Kozar

Open access · greenAbstract read
In one paragraph

Article in Blood transfusion = Trasfusione del sangue, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.1field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 17 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Amanda M ChipmanDepartment of Surgery, University of Maryland School of Medicine, Baltimore, MD, United States of America.
Feng WuShock Trauma Center, University of Maryland School of Medicine, Baltimore, MD, United States of America.
Rosemary A KozarShock Trauma Center, University of Maryland School of Medicine, Baltimore, MD, United States of America.
University of Maryland, Baltimore · US

Funding

Vascular Biology Training ProgramT32HL007698 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI Rosemary A Kozar, Dudley K. Strickland · 1991 to 2026
$8.7M
Endothelial injury and repair following hemorrhagic shockR01GM129533 · NIGMS · UNIVERSITY OF MARYLAND BALTIMORE · PI KOZAR, ROSEMARY A · 2018 to 2021
$1.4M
Syndecan shedding after trauma and hemorrhagic shockR01GM107482 · NIGMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI KOZAR, ROSEMARY A · 2013 to 2016
$1.2M
NHLBI NIH HHS T32 HL007698NIGMS NIH HHS R01 GM107482NIGMS NIH HHS R01 GM129533
6 · The paper itself

Abstract

backgroundThe benefits of plasma as an adjunct to the treatment of haemorrhagic shock are well established; however, the mechanism by which plasma modulates the endotheliopathy of trauma remains unclear. Our recent data demonstrated a novel role of microRNA-19b in post-haemorrhagic shock endothelial dysfunction via targeting of syndecan-1. Additionally, fibrinogen, as a key component of plasma or an isolated haemostatic protein, protects the endothelium by stabilizing syndecan-1. We therefore hypothesized that fibrinogen would inhibit microRNA-19b to mitigate the endotheliopathy of trauma in a murine model of haemorrhagic shock. MATERIALS AND

methodsC57BL/6J mice were subjected to haemorrhagic shock (mean arterial pressure 35±5 mmHg for 90 minutes) followed by resuscitation with lactated Ringer's, fresh frozen plasma, fibrinogen or no resuscitation. MicroRNA-19b and syndecan-1 mRNA were measured in lung tissue by qRT-PCR. Lungs were stained for histopathologic injury, and broncheoalveolar lavage was collected for protein as a permeability indicator.

resultsPulmonary microRNA-19b was increased after haemorrhagic shock and lactated Ringers, but reduced to sham levels by plasma and fibrinogen. Conversely, pulmonary syndecan-1 mRNA was downregulated by haemorrhagic shock and lactated Ringers, but returned to sham levels by plasma and fibrinogen. Plasma and fibrinogen-based resuscitation reduced lung injury compared to haemorrhagic shock and lactated Ringers while fibrinogen also reduced broncheoalveolar lavage protein. DISCUSSION: We have demonstrated a novel mechanism by which fibrinogen, a key component of plasma and haemostatic agent, inhibits miR-19b, possibly by mitigating the endotheliopathy of trauma. Complete demonstration of the mechanism of fibrinogen inhibition of endotheliopathy via microRNA, however, remains to be elucidated. These findings support the early and empiric use of fibrinogen in post-haemorrhagic shock resuscitation.

Indexed as

HemostaticsMicroRNAsShock, HemorrhagicAnimalsDisease Models, AnimalEndothelial CellsFibrinogenHumansIsotonic SolutionsMiceMice, Inbred C57BLResuscitationFibrinogenHemostaticsIsotonic SolutionsMicroRNAsMIRN19 microRNA, mouse

Identifiers

PMID33539284
PMCPMC8486605
OpenAlexW3128273369

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.