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October 30, 2021SHILAP Revista de lepidopterologíaOpen Access

FXa upregulated CCL2 (>3-fold) and IL6 (>4-fold) gene expression at 4 hours in human cardiac fibroblasts, an effect that was prevented by PAR-1 gene knockdown.

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Why the study?

The effect of coagulation factor Xa on cardiac fibroblasts and the contribution of protease-activated receptors in factor Xa-induced cellular signalling had not been fully characterised.

Population

Human and rat cardiac fibroblasts

Comparison

FXa or TRAP-14 incubation with or without PAR silencing or SCH79797

Design

In vitro preclinical study

Follow-up

Up to 24 h

Authors

EDElisa D’AlessandroBSBilly ScafCMChantal Munts

Discussion

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Overview

Hypothesis-generating for FXa-PAR-1 inflammation in fibroblasts; in vivo studies needed before clinical relevance.

Structured PICO

P
Population
Human and rat cardiac fibroblasts (CFs)
I
Intervention
Incubation with Coagulation factor Xa (FXa) or TRAP-14 (PAR-1 agonist), with or without gene silencing of F2R (PAR-1) and F2RL1 (PAR-2) or PAR-1 antagonist SCH79797
C
Comparator
Control conditions (without FXa, or FXa with PAR-1 knockdown/antagonism)
O
Outcome
Gene expression of pro-fibrotic and proinflammatory markers (CCL2/MCP-1, IL-6) at 4 and 24 hourssurrogate

Coagulation factor Xa induces overexpression of proinflammatory genes in human cardiac fibroblasts via PAR-1 activation, highlighting a potential mechanism linking coagulation and cardiac inflammation/fibrosis.

Cite This Study

D’Alessandro et al. (2021) studied this question.

synapsesocial.com/papers/69db22c70d8d6ef495a3cf11https://doi.org/10.3390/cells10112958
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