In:
PLOS ONE, Public Library of Science (PLoS), Vol. 17, No. 6 ( 2022-6-8), p. e0268986-
Abstract:
Tyrosine-protein kinase receptor Tie2, also known as Tunica interna Endothelial cell Kinase or TEK plays a prominent role in endothelial responses to angiogenic and inflammatory stimuli. Here we generated a novel inducible Tie2 knockout mouse model, which targets mature (micro)vascular endothelium, enabling the study of the organ-specific contribution of Tie2 to these responses. Mice with floxed Tie2 exon 9 alleles ( Tie2 floxed/floxed ) were crossed with end-SCL-Cre-ER T transgenic mice, generating offspring in which Tie2 exon 9 is deleted in the endothelial compartment upon tamoxifen-induced activation of Cre-recombinase ( Tie2 ΔE9 ). Successful deletion of Tie2 exon 9 in kidney, lung, heart, aorta, and liver, was accompanied by a heterogeneous, organ-dependent reduction in Tie2 mRNA and protein expression. Microvascular compartment-specific reduction in Tie2 mRNA and protein occurred in arterioles of all studied organs, in renal glomeruli, and in lung capillaries. In kidney, lung, and heart, reduced Tie2 expression was accompanied by a reduction in Tie1 mRNA expression. The heterogeneous, organ- and microvascular compartment-dependent knockout pattern of Tie2 in the Tie2 floxed/floxed ;end-SCL-Cre-ER T mouse model suggests that future studies using similar knockout strategies should include a meticulous analysis of the knockout extent of the gene of interest, prior to studying its role in pathological conditions, so that proper conclusions can be drawn.
Type of Medium:
Online Resource
ISSN:
1932-6203
DOI:
10.1371/journal.pone.0268986
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10.1371/journal.pone.0268986.g001
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10.1371/journal.pone.0268986.g002
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10.1371/journal.pone.0268986.g003
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10.1371/journal.pone.0268986.g004
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10.1371/journal.pone.0268986.g005
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10.1371/journal.pone.0268986.t001
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10.1371/journal.pone.0268986.s020
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10.1371/journal.pone.0268986.r001
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10.1371/journal.pone.0268986.r002
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10.1371/journal.pone.0268986.r003
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10.1371/journal.pone.0268986.r006
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10.1371/journal.pone.0268986.r007
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10.1371/journal.pone.0268986.r008
Language:
English
Publisher:
Public Library of Science (PLoS)
Publication Date:
2022
detail.hit.zdb_id:
2267670-3
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