ArticlePloS one2014
Tetraspanin CD9 regulates cell contraction and actin arrangement via RhoA in human vascular smooth muscle cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Junctions, Transporters, and Interactions of Endothelial Cells: Regulation by Ethanol.International journal of molecular sciences · 2026Review
- Article
- Prognostic value and multifaceted roles of tetraspanin CD9 in cancer.Frontiers in oncology · 2023Review
- Electric field promotes dermal fibroblast transdifferentiation through activation of RhoA/ROCK1 pathway.International journal of medical sciences · 2023Article
- Migrasome and Tetraspanins in Vascular Homeostasis: Concept, Present, and Future.Frontiers in cell and developmental biology · 2020Review
- Visualizing Coronavirus Entry into Cells.Methods in molecular biology (Clifton, N.J.) · 2020Article
- Tetraspanin-enriched microdomains regulate digitation junctions.Cellular and molecular life sciences : CMLS · 2018Article
- oxLDL induces endothelial cell proliferation via Rho/ROCK/Akt/p27American journal of physiology. Cell physiology · 2017Article
- Selective expression of TSPAN2 in vascular smooth muscle is independently regulated by TGF-β1/SMAD and myocardin/serum response factor.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Tetraspanins Function as Regulators of Cellular Signaling.Frontiers in cell and developmental biology · 2017Review
- Rho kinase activity governs arteriolar myogenic depolarization.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The most prevalent cardiovascular diseases arise from alterations in vascular smooth muscle cell (VSMC) morphology and function. Tetraspanin CD9 has been previously implicated in regulating vascular pathologies; however, insight into how CD9 may regulate adverse VSMC phenotypes has not been provided. We utilized a human model of aortic smooth muscle cells to understand the consequences of CD9 deficiency on VSMC phenotypes. Upon knocking down CD9, the cells developed an abnormally small and rounded morphology. We determined that this morphological change was due to a lack of typical parallel actin arrangement. We also found similar total RhoA but decreased GTP-bound (active) RhoA levels in CD9 deficient cells. As a result, cells lacking a full complement of CD9 were less contractile than their control treated counterparts. Upon restoration of RhoA activity in the CD9 deficient cells, the phenotype was reversed and cell contraction was restored. Conversely, inhibition of RhoA activity in the control cells mimicked the CD9-deficient cell phenotype. Thus, alteration in CD9 expression was sufficient to profoundly disrupt cellular actin arrangement and endogenous cell contraction by interfering with RhoA signaling. This study provides insight into how CD9 may regulate previously described vascular smooth muscle cell pathophysiology.
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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.