ArticleDisease models & mechanisms2013
Deletion of integrin-linked kinase from neural crest cells in mice results in aortic aneurysms and embryonic lethality.
Article in Disease models & mechanisms, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Fibronectin-induced overactivation of αNature communications · 2026Article
- Focal adhesion proteins confer smooth muscle anoikis resistance and protection against aortic aneurysm and dissection.JCI insight · 2026Article
- Microenvironmental stiffness directs microtubule perturbation in chondrocyte mitosis via ILK-refilinB/Smad3 axis.Bone research · 2026Article
- ELMO2 is an essential regulator of carotid artery development.Nature communications · 2025Article
- Downregulation of RhoA/ROCK1/YAP/F-actin causing decreased aortic smooth muscle cell stiffness promotes aortic dissection formation.Life metabolism · 2024Article
- The synergistic mechanism of fibroblast growth factor 18 and integrin β1 in rat abdominal aortic aneurysm repair.BMC cardiovascular disorders · 2022Article
- Crk and Crkl have shared functions in neural crest cells for cardiac outflow tract septation and vascular smooth muscle differentiation.Human molecular genetics · 2022Article
- Roles of mTOR in thoracic aortopathy understood by complex intracellular signaling interactions.PLoS computational biology · 2021Article
- Elastic fibers and biomechanics of the aorta: Insights from mouse studies.Matrix biology : journal of the International Society for Matrix Biology · 2020Review
- Molecular Regulation of Arterial Aneurysms: Role of Actin Dynamics and microRNAs in Vascular Smooth Muscle.Frontiers in physiology · 2017Review
- Neural crest cell-autonomous roles of fibronectin in cardiovascular development.Development (Cambridge, England) · 2016Article
- Review of molecular and mechanical interactions in the aortic valve and aorta: implications for the shared pathogenesis of aortic valve disease and aortopathy.Journal of cardiovascular translational research · 2014Review
- High-throughput phenotypic assessment of cardiac physiology in four commonly used inbred mouse strains.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
Neural crest cells (NCCs) participate in the remodeling of the cardiac outflow tract and pharyngeal arch arteries during cardiovascular development. Integrin-linked kinase (ILK) is a serine/threonine kinase and a major regulator of integrin signaling. It links integrins to the actin cytoskeleton and recruits other adaptor molecules into a large complex to regulate actin dynamics and integrin function. Using the Cre-lox system, we deleted Ilk from NCCs of mice to investigate its role in NCC morphogenesis. The resulting mutants developed a severe aneurysmal arterial trunk that resulted in embryonic lethality during late gestation. Ilk mutants showed normal cardiac NCC migration but reduced differentiation into smooth muscle within the aortic arch arteries and the outflow tract. Within the conotruncal cushions, Ilk-deficient NCCs exhibited disorganization of F-actin stress fibers and a significantly rounder morphology, with shorter cellular projections. Additionally, absence of ILK resulted in reduced in vivo phosphorylation of Smad3 in NCCs, which correlated with reduced αSMA levels. Our findings resemble those seen in Pinch1 and β1 integrin conditional mutant mice, and therefore support that, in neural crest-derived cells, ILK and Pinch1 act as cytoplasmic effectors of β1 integrin in a pathway that protects against aneurysms. In addition, our conditional Ilk mutant mice might prove useful as a model to study aortic aneurysms caused by reduced Smad3 signaling, as occurs in the newly described aneurysms-osteoarthritis syndrome, for example.
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