In vivo evidence for an endothelium-dependent mechanism in radiation-induced normal tissue injury View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-10-29

AUTHORS

Emilie Rannou, Agnès François, Aurore Toullec, Olivier Guipaud, Valérie Buard, Georges Tarlet, Elodie Mintet, Cyprien Jaillet, Maria Luisa Iruela-Arispe, Marc Benderitter, Jean-Christophe Sabourin, Fabien Milliat

ABSTRACT

The pathophysiological mechanism involved in side effects of radiation therapy and especially the role of the endothelium remains unclear. Previous results showed that plasminogen activator inhibitor-type 1 (PAI-1) contributes to radiation-induced intestinal injury and suggested that this role could be driven by an endothelium-dependent mechanism. We investigated whether endothelial-specific PAI-1 deletion could affect radiation-induced intestinal injury. We created a mouse model with a specific deletion of PAI-1 in the endothelium (PAI-1KOendo) by a Cre-LoxP system. In a model of radiation enteropathy, survival and intestinal radiation injury were followed as well as intestinal gene transcriptional profile and inflammatory cells intestinal infiltration. Irradiated PAI-1KOendo mice exhibited increased survival, reduced acute enteritis severity and attenuated late fibrosis compared with irradiated PAI-1flx/flx mice. Double E-cadherin/TUNEL labeling confirmed a reduced epithelial cell apoptosis in irradiated PAI-1KOendo. High-throughput gene expression combined with bioinformatic analyses revealed a putative involvement of macrophages. We observed a decrease in CD68+cells in irradiated intestinal tissues from PAI-1KOendo mice as well as modifications associated with M1/M2 polarization. This work shows that PAI-1 plays a role in radiation-induced intestinal injury by an endothelium-dependent mechanism and demonstrates in vivo that the endothelium is directly involved in the progression of radiation-induced enteritis. More... »

PAGES

15738

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/srep15738

DOI

http://dx.doi.org/10.1038/srep15738

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1045655172

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/26510580


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23 schema:description The pathophysiological mechanism involved in side effects of radiation therapy and especially the role of the endothelium remains unclear. Previous results showed that plasminogen activator inhibitor-type 1 (PAI-1) contributes to radiation-induced intestinal injury and suggested that this role could be driven by an endothelium-dependent mechanism. We investigated whether endothelial-specific PAI-1 deletion could affect radiation-induced intestinal injury. We created a mouse model with a specific deletion of PAI-1 in the endothelium (PAI-1KOendo) by a Cre-LoxP system. In a model of radiation enteropathy, survival and intestinal radiation injury were followed as well as intestinal gene transcriptional profile and inflammatory cells intestinal infiltration. Irradiated PAI-1KOendo mice exhibited increased survival, reduced acute enteritis severity and attenuated late fibrosis compared with irradiated PAI-1flx/flx mice. Double E-cadherin/TUNEL labeling confirmed a reduced epithelial cell apoptosis in irradiated PAI-1KOendo. High-throughput gene expression combined with bioinformatic analyses revealed a putative involvement of macrophages. We observed a decrease in CD68+cells in irradiated intestinal tissues from PAI-1KOendo mice as well as modifications associated with M1/M2 polarization. This work shows that PAI-1 plays a role in radiation-induced intestinal injury by an endothelium-dependent mechanism and demonstrates in vivo that the endothelium is directly involved in the progression of radiation-induced enteritis.
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29 schema:keywords Cre-loxP system
30 M1/M2 polarization
31 M2 polarization
32 PAI-1
33 TUNEL labeling
34 activator
35 analysis
36 apoptosis
37 bioinformatics analysis
38 cell apoptosis
39 decrease
40 deletion
41 effect
42 endothelium
43 endothelium-dependent mechanism
44 enteritis
45 enteropathy
46 epithelial cell apoptosis
47 evidence
48 expression
49 fibrosis
50 gene expression
51 gene transcriptional profiles
52 high-throughput gene expression
53 infiltration
54 injury
55 intestinal infiltration
56 intestinal injury
57 intestinal radiation injury
58 intestinal tissue
59 involvement
60 labeling
61 late fibrosis
62 macrophages
63 mechanism
64 mice
65 model
66 modification
67 mouse model
68 normal tissue injury
69 pathophysiological mechanisms
70 plasminogen activator
71 polarization
72 previous results
73 profile
74 progression
75 putative involvement
76 radiation enteropathy
77 radiation injury
78 radiation therapy
79 radiation-induced enteritis
80 radiation-induced intestinal injury
81 radiation-induced normal tissue injury
82 results
83 role
84 severity
85 side effects
86 specific deletion
87 survival
88 system
89 therapy
90 tissue
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92 transcriptional profiles
93 vivo
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