Foxc1 and Foxc2 deletion causes abnormal lymphangiogenesis and correlates with ERK hyperactivation.
Identifieur interne : 000901 ( PubMed/Checkpoint ); précédent : 000900; suivant : 000902Foxc1 and Foxc2 deletion causes abnormal lymphangiogenesis and correlates with ERK hyperactivation.
Auteurs : Anees Fatima ; Ying Wang ; Yutaka Uchida ; Pieter Norden ; Ting Liu ; Austin Culver ; William H. Dietz ; Ford Culver ; Meredith Millay ; Yoh-Suke Mukouyama ; Tsutomu KumeSource :
- The Journal of clinical investigation [ 1558-8238 ] ; 2016.
Abstract
The lymphatic vasculature is essential for maintaining interstitial fluid homeostasis, and dysfunctional lymphangiogenesis contributes to various pathological processes, including inflammatory disease and tumor metastasis. Mutations in FOXC2 are dominantly associated with late-onset lymphedema; however, the precise role of FOXC2 and a closely related factor, FOXC1, in the lymphatic system remains largely unknown. Here we identified a molecular cascade by which FOXC1 and FOXC2 regulate ERK signaling in lymphatic vessel growth. In mice, lymphatic endothelial cell-specific (LEC-specific) deletion of Foxc1, Foxc2, or both resulted in increased LEC proliferation, enlarged lymphatic vessels, and abnormal lymphatic vessel morphogenesis. Compared with LECs from control animals, LECs from mice lacking both Foxc1 and Foxc2 exhibited aberrant expression of Ras regulators, and embryos with LEC-specific deletion of Foxc1 and Foxc2, alone or in combination, exhibited ERK hyperactivation. Pharmacological ERK inhibition in utero abolished the abnormally enlarged lymphatic vessels in FOXC-deficient embryos. Together, these results identify FOXC1 and FOXC2 as essential regulators of lymphangiogenesis and indicate a new potential mechanistic basis for lymphatic-associated diseases.
DOI: 10.1172/JCI80465
PubMed: 27214551
Affiliations:
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pubmed:27214551Le document en format XML
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<front><div type="abstract" xml:lang="en">The lymphatic vasculature is essential for maintaining interstitial fluid homeostasis, and dysfunctional lymphangiogenesis contributes to various pathological processes, including inflammatory disease and tumor metastasis. Mutations in FOXC2 are dominantly associated with late-onset lymphedema; however, the precise role of FOXC2 and a closely related factor, FOXC1, in the lymphatic system remains largely unknown. Here we identified a molecular cascade by which FOXC1 and FOXC2 regulate ERK signaling in lymphatic vessel growth. In mice, lymphatic endothelial cell-specific (LEC-specific) deletion of Foxc1, Foxc2, or both resulted in increased LEC proliferation, enlarged lymphatic vessels, and abnormal lymphatic vessel morphogenesis. Compared with LECs from control animals, LECs from mice lacking both Foxc1 and Foxc2 exhibited aberrant expression of Ras regulators, and embryos with LEC-specific deletion of Foxc1 and Foxc2, alone or in combination, exhibited ERK hyperactivation. Pharmacological ERK inhibition in utero abolished the abnormally enlarged lymphatic vessels in FOXC-deficient embryos. Together, these results identify FOXC1 and FOXC2 as essential regulators of lymphangiogenesis and indicate a new potential mechanistic basis for lymphatic-associated diseases.</div>
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<Abstract><AbstractText>The lymphatic vasculature is essential for maintaining interstitial fluid homeostasis, and dysfunctional lymphangiogenesis contributes to various pathological processes, including inflammatory disease and tumor metastasis. Mutations in FOXC2 are dominantly associated with late-onset lymphedema; however, the precise role of FOXC2 and a closely related factor, FOXC1, in the lymphatic system remains largely unknown. Here we identified a molecular cascade by which FOXC1 and FOXC2 regulate ERK signaling in lymphatic vessel growth. In mice, lymphatic endothelial cell-specific (LEC-specific) deletion of Foxc1, Foxc2, or both resulted in increased LEC proliferation, enlarged lymphatic vessels, and abnormal lymphatic vessel morphogenesis. Compared with LECs from control animals, LECs from mice lacking both Foxc1 and Foxc2 exhibited aberrant expression of Ras regulators, and embryos with LEC-specific deletion of Foxc1 and Foxc2, alone or in combination, exhibited ERK hyperactivation. Pharmacological ERK inhibition in utero abolished the abnormally enlarged lymphatic vessels in FOXC-deficient embryos. Together, these results identify FOXC1 and FOXC2 as essential regulators of lymphangiogenesis and indicate a new potential mechanistic basis for lymphatic-associated diseases.</AbstractText>
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<affiliations><list></list>
<tree><noCountry><name sortKey="Culver, Austin" sort="Culver, Austin" uniqKey="Culver A" first="Austin" last="Culver">Austin Culver</name>
<name sortKey="Culver, Ford" sort="Culver, Ford" uniqKey="Culver F" first="Ford" last="Culver">Ford Culver</name>
<name sortKey="Dietz, William H" sort="Dietz, William H" uniqKey="Dietz W" first="William H" last="Dietz">William H. Dietz</name>
<name sortKey="Fatima, Anees" sort="Fatima, Anees" uniqKey="Fatima A" first="Anees" last="Fatima">Anees Fatima</name>
<name sortKey="Kume, Tsutomu" sort="Kume, Tsutomu" uniqKey="Kume T" first="Tsutomu" last="Kume">Tsutomu Kume</name>
<name sortKey="Liu, Ting" sort="Liu, Ting" uniqKey="Liu T" first="Ting" last="Liu">Ting Liu</name>
<name sortKey="Millay, Meredith" sort="Millay, Meredith" uniqKey="Millay M" first="Meredith" last="Millay">Meredith Millay</name>
<name sortKey="Mukouyama, Yoh Suke" sort="Mukouyama, Yoh Suke" uniqKey="Mukouyama Y" first="Yoh-Suke" last="Mukouyama">Yoh-Suke Mukouyama</name>
<name sortKey="Norden, Pieter" sort="Norden, Pieter" uniqKey="Norden P" first="Pieter" last="Norden">Pieter Norden</name>
<name sortKey="Uchida, Yutaka" sort="Uchida, Yutaka" uniqKey="Uchida Y" first="Yutaka" last="Uchida">Yutaka Uchida</name>
<name sortKey="Wang, Ying" sort="Wang, Ying" uniqKey="Wang Y" first="Ying" last="Wang">Ying Wang</name>
</noCountry>
</tree>
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