ArticleProceedings of the National Academy of Sciences of the United States of America2016
Nuclear envelope proteins modulate proliferation of vascular smooth muscle cells during cyclic stretch application.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 84 citations in OpenAlex.
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- Hydrogel soft tissue expander for gingiva-periosteal expansion: a narrative literature review.Maxillofacial plastic and reconstructive surgery · 2026Review
- Vascular mechanical forces and vascular diseases.Journal of advanced research · 2026Review
- IFFO1 inhibits breast cancer by coordinating mitochondrial fission and fatty acid synthesis via the LaminA/C-PGC1α axis.Oncogenesis · 2026Article
- Antioxidation is a Common Defense Strategy for Different Species Under Mechanical Stress.Advanced genetics (Hoboken, N.J.) · 2026Article
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- A Bibliometric Analysis of P2X7R in Cardiovascular Diseases from 2005 to 2024.Current cardiology reviews · 2026Review
- Endothelial Nuclear and Cytoskeletal Responses to Mechanical Stresses.Advances in experimental medicine and biology · 2026Article
- PGC1α regulates the mitochondrial metabolism response to cyclic stretch, which inhibits neointimal hyperplasia.Cellular and molecular life sciences : CMLS · 2025Article
- Emerin is an effector of oncogenic KRAS-driven nuclear dynamics in pancreatic cancer.JCI insight · 2025Article
- Mechanical Stress Induced NOX2 Promotes Endothelial Dysfunction in Ventilator-Induced Lung Injury: Potential Treatment with Quercetin.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Downregulation of Nesprin1 by Runx2 deficiency is critical for the development of skeletal laminopathy-like pathology.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mechanical Activation of cPLA2 Impedes Fatty Acid β-Oxidation in Vein Grafts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Injury and cyclic stretch induce vein graft failure: effective treatment with zinc oxide-loaded electrospun polycaprolactone external stent.Regenerative biomaterials · 2025Article
- Cardiovascular diseases in the elderly: possibilities for modulating autophagy using non-coding RNAs.Frontiers in cell and developmental biology · 2025Review
- Molecular Force Sensors for Biological Application.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
Cyclic stretch is an important inducer of vascular smooth muscle cell (VSMC) proliferation, which is crucial in vascular remodeling during hypertension. However, the molecular mechanism remains unclear. We studied the effects of emerin and lamin A/C, two important nuclear envelope proteins, on VSMC proliferation in hypertension and the underlying mechano-mechanisms. In common carotid artery of hypertensive rats in vivo and in cultured cells subjected to high (15%) cyclic stretch in vitro, VSMC proliferation was increased significantly, and the expression of emerin and lamin A/C was repressed compared with normotensive or normal (5%) cyclic stretch controls. Using targeted siRNA to mimic the repressed expression of emerin or lamin A/C induced by 15% stretch, we found that VSMC proliferation was enhanced under static and 5%-stretch conditions. Overexpression of emerin or lamin A/C reversed VSMC proliferation induced by 15% stretch. Hence, emerin and lamin A/C play critical roles in suppressing VSMC hyperproliferation induced by hyperstretch. ChIP-on-chip and MOTIF analyses showed that the DNAs binding with emerin contain three transcription factor motifs: CCNGGA, CCMGCC, and ABTTCCG; DNAs binding with lamin A/C contain the motifs CVGGAA, GCCGCYGC, and DAAGAAA. Protein/DNA array proved that altered emerin or lamin A/C expression modulated the activation of various transcription factors. Furthermore, accelerating local expression of emerin or lamin A/C reversed cell proliferation in the carotid artery of hypertensive rats in vivo. Our findings establish the pathogenetic role of emerin and lamin A/C repression in stretch-induced VSMC proliferation and suggest mechanobiological mechanism underlying this process that involves the sequence-specific binding of emerin and lamin A/C to specific transcription factor motifs.
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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.