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| Autores principales: | , , , |
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| Formato: | Artículo científico |
| Lenguaje: | en |
| Publicado: |
Cellular and molecular life sciences : CMLS
2025
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| Materias: | |
| Acceso en línea: | https://pubmed.ncbi.nlm.nih.gov/40074973/ |
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| _version_ | 1868266232026759168 |
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| author | Yang, Shuaiqi Zhang, Xiangmin Li, Xianpeng Li, Hongyan |
| author_facet | Yang, Shuaiqi Zhang, Xiangmin Li, Xianpeng Li, Hongyan Yang, Shuaiqi Zhang, Xiangmin Li, Xianpeng Li, Hongyan |
| collection | PubMed - marine biology |
| contents | Crip2 affects vascular development by fine-tuning endothelial cell aggregation and proliferation. Yang, Shuaiqi Zhang, Xiangmin Li, Xianpeng Li, Hongyan Humans Cell Proliferation Human Umbilical Vein Endothelial Cells Animals Zebrafish Signal Transduction Cell Movement LIM Domain Proteins Cell Aggregation Vascular Endothelial Growth Factor A Cell Adhesion Zebrafish Proteins Neovascularization, Physiologic Vimentin Endothelial Cells cdc42 GTP-Binding Protein Cytoskeleton Endothelial cell adhesion and migration are crucial to various biological processes, including vascular development. The identification of factors that modulate vascular development through these cell functions has emerged as a prominent focus in cardiovascular research. Crip2 is known to play a crucial role in cardiac development, yet its involvement in vascular development and the underlying mechanism remains elusive. In this study, we revealed that Crip2 is expressed predominantly in the vascular system, particularly in the posterior cardinal vein and caudal vein plexus intersegmental vein. Upon Crip2 loss, the posterior cardinal vein plexus and caudal vein plexus are hypoplastic, and endothelial cells exhibit aberrant aggregation. In human umbilical vein endothelial cells (HUVECs), CRIP2 interacts with the cytoskeleton proteins KRT8 and VIM. The absence of CRIP2 negatively regulates their expression, thereby fine-tuning cytoskeleton formation, resulting in a hyperadhesive phenotype. Moreover, CRIP2 deficiency perturbs the VEGFA/CDC42 signaling pathway, which in turn diminishes the migrating capacity of HUVECs. Furthermore, the loss of CRIP2 impairs cell proliferation by affecting its interaction with SRF through PDE10A/cAMP and PDGF/JAK/STAT/SRF signaling. Collectively, our findings delineate a crucial role for CRIP2 in controlling the migration, adhesion and proliferation of endothelial cells, thereby contributing to vascular development in zebrafish. These insights may provide a deeper understanding of the etiology of cardiovascular disorders. |
| format | Artículo científico |
| id | pubmed_40074973 |
| institution | PubMed |
| language | en |
| publishDate | 2025 |
| publisher | Cellular and molecular life sciences : CMLS |
| record_format | pubmed |
| spellingShingle | Crip2 affects vascular development by fine-tuning endothelial cell aggregation and proliferation. Yang, Shuaiqi Zhang, Xiangmin Li, Xianpeng Li, Hongyan Humans Cell Proliferation Human Umbilical Vein Endothelial Cells Animals Zebrafish Signal Transduction Cell Movement LIM Domain Proteins Cell Aggregation Vascular Endothelial Growth Factor A Cell Adhesion Zebrafish Proteins Neovascularization, Physiologic Vimentin Endothelial Cells cdc42 GTP-Binding Protein Cytoskeleton Crip2 affects vascular development by fine-tuning endothelial cell aggregation and proliferation. Yang, Shuaiqi Zhang, Xiangmin Li, Xianpeng Li, Hongyan Humans Cell Proliferation Human Umbilical Vein Endothelial Cells Animals Zebrafish Signal Transduction Cell Movement LIM Domain Proteins Cell Aggregation Vascular Endothelial Growth Factor A Cell Adhesion Zebrafish Proteins Neovascularization, Physiologic Vimentin Endothelial Cells cdc42 GTP-Binding Protein Cytoskeleton Endothelial cell adhesion and migration are crucial to various biological processes, including vascular development. The identification of factors that modulate vascular development through these cell functions has emerged as a prominent focus in cardiovascular research. Crip2 is known to play a crucial role in cardiac development, yet its involvement in vascular development and the underlying mechanism remains elusive. In this study, we revealed that Crip2 is expressed predominantly in the vascular system, particularly in the posterior cardinal vein and caudal vein plexus intersegmental vein. Upon Crip2 loss, the posterior cardinal vein plexus and caudal vein plexus are hypoplastic, and endothelial cells exhibit aberrant aggregation. In human umbilical vein endothelial cells (HUVECs), CRIP2 interacts with the cytoskeleton proteins KRT8 and VIM. The absence of CRIP2 negatively regulates their expression, thereby fine-tuning cytoskeleton formation, resulting in a hyperadhesive phenotype. Moreover, CRIP2 deficiency perturbs the VEGFA/CDC42 signaling pathway, which in turn diminishes the migrating capacity of HUVECs. Furthermore, the loss of CRIP2 impairs cell proliferation by affecting its interaction with SRF through PDE10A/cAMP and PDGF/JAK/STAT/SRF signaling. Collectively, our findings delineate a crucial role for CRIP2 in controlling the migration, adhesion and proliferation of endothelial cells, thereby contributing to vascular development in zebrafish. These insights may provide a deeper understanding of the etiology of cardiovascular disorders. |
| title | Crip2 affects vascular development by fine-tuning endothelial cell aggregation and proliferation. |
| topic | Humans Cell Proliferation Human Umbilical Vein Endothelial Cells Animals Zebrafish Signal Transduction Cell Movement LIM Domain Proteins Cell Aggregation Vascular Endothelial Growth Factor A Cell Adhesion Zebrafish Proteins Neovascularization, Physiologic Vimentin Endothelial Cells cdc42 GTP-Binding Protein Cytoskeleton |
| url | https://pubmed.ncbi.nlm.nih.gov/40074973/ |