ArticleMolecular biology of the cell2016
Lamin-B1 contributes to the proper timing of epicardial cell migration and function during embryonic heart development.
Article in Molecular biology of the cell, 2016. 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, 15 citations in OpenAlex.
- Circadian regulation of cardiovascular function: from physiology to clinical implications.Genome medicine · 2026Review
- Review
- Viscoelasticity of the Heart: An Overview of Viscoelastic Measurements at Different Scales.Annual review of biomedical engineering · 2026Review
- Epicardium and Coronary Vessels.Advances in experimental medicine and biology · 2024Review
- Hypoxia promotes a perinatal-like progenitor state in the adult murine epicardium.Scientific reports · 2022Article
- Nuclear lamin isoforms differentially contribute to LINC complex-dependent nucleocytoskeletal coupling and whole-cell mechanics.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Nuclear lamins: Structure and function in mechanobiology.APL bioengineering · 2022Review
- Regulation of diverse nuclear shapes: pathways working independently, together.Communicative & integrative biology · 2021Review
- Increased Lamin B1 Levels Promote Cell Migration by Altering Perinuclear Actin Organization.Cells · 2020Article
- Organelle size scaling over embryonic development.Wiley interdisciplinary reviews. Developmental biology · 2020Review
- Epicardium in Heart Development.Cold Spring Harbor perspectives in biology · 2020Review
- Covering and Re-Covering the Heart: Development and Regeneration of the Epicardium.Journal of cardiovascular development and disease · 2018Review
- Studying Electrotaxis in Microfluidic Devices.Sensors (Basel, Switzerland) · 2017Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
Lamin proteins form a meshwork beneath the nuclear envelope and contribute to many different cellular processes. Mutations in lamins cause defective organogenesis in mouse models and human diseases that affect adipose tissue, brain, skeletal muscle, and the heart. In vitro cell culture studies have shown that lamins help maintain nuclear shape and facilitate cell migration. However, whether these defects contribute to improper tissue building in vivo requires further clarification. By studying the heart epicardium during embryogenesis, we show that Lb1-null epicardial cells exhibit in vivo and in vitro migratory delay. Transcriptome analyses of these cells suggest that Lb1 influences the expression of cell adhesion genes, which could affect cell migration during epicardium development. These epicardial defects are consistent with incomplete development of both vascular smooth muscle and compact myocardium at later developmental stages in Lb1-null embryos. Further, we found that Lb1-null epicardial cells have a delayed nuclear morphology change in vivo, suggesting that Lb1 facilitates morphological changes associated with migration. These findings suggest that Lb1 contributes to nuclear shape maintenance and migration of epicardial cells and highlights the use of these cells for in vitro and in vivo study of these classic cell biological phenomena.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.