ArticlePloS one2015
p21WAF1 Is Required for Interleukin-16-Induced Migration and Invasion of Vascular Smooth Muscle Cells via the p38MAPK/Sp-1/MMP-9 Pathway.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Diagnostic biomarkers and aortic dissection: a systematic review and meta-analysis.BMC cardiovascular disorders · 2023Pooled it
- High-Salt Diet-Induced Endothelial Dysfunction Is Mediated by Cellular Senescence.Journal of the American Heart Association · 2026Article
- Cellular heterogeneity in hypertrophic burn scars in response to carbon dioxide laser therapy.Communications medicine · 2026Article
- Role of vascular smooth muscle cell pathobiology in sepsis‑induced vasoplegia (Review).International journal of molecular medicine · 2026Review
- CCR7 Promotes Neutrophil Recruitment and N2 Polarization Through Regulation of IL-16 in Head and Neck Squamous Cell Carcinoma.International dental journal · 2026Article
- Interleukin-16 upregulates tissue inhibitor of metalloproteinase 3 to promote atherosclerotic plaque stability.Journal of translational medicine · 2026Article
- Article
- Role of IL-16 in age-related skeletal muscle atrophy: an integrated study.BMC musculoskeletal disorders · 2025Observational
- Interleukin-16 is increased in dialysis patients but is not a cardiovascular risk factor.Scientific reports · 2024Article
- Role of Sp1 in atherosclerosis.Molecular biology reports · 2022Review
- A comprehensive profile of chemokines in the peripheral blood and vascular tissue of patients with Takayasu arteritis.Arthritis research & therapy · 2022Article
- Anti-Interleukin-16-Neutralizing Antibody Attenuates Cardiac Inflammation and Protects against Cardiac Injury in Doxorubicin-Treated Mice.Mediators of inflammation · 2021Article
- Association of functionalOncotarget · 2020Article
- Electronegative low-density lipoprotein of patients with metabolic syndrome induces pathogenesis of aorta through disruption of the stimulated by retinoic acid 6 cascade.Journal of diabetes investigation · 2020Article
- WNT7A Promotes EGF-Induced Migration of Oral Squamous Cell Carcinoma Cells by Activating β-Catenin/MMP9-Mediated Signaling.Frontiers in pharmacology · 2020Article
- Cellular and Molecular Effects of High-Molecular-Weight Heparin on Matrix Metalloproteinase 9 Expression.International journal of molecular sciences · 2019Article
- Interrogation of transcriptomic changes associated with drug-induced hepatic sinusoidal dilatation in colorectal cancer.PloS one · 2018Article
- Adipose differentiation‑related protein knockdown inhibits vascular smooth muscle cell proliferation and migration and attenuates neointima formation.Molecular medicine reports · 2017Article
- Leptin decreases the expression of low-density lipoprotein receptor via PCSK9 pathway: linking dyslipidemia with obesity.Journal of translational medicine · 2016Article
- Silence of bFGF enhances chemosensitivity of glioma cells to temozolomide through the MAPK signal pathway.Acta biochimica et biophysica Sinica · 2016Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-16 (IL-16) is a lymphocyte chemoattractant factor well known for its role in immune responses, but its role in vascular disease is unknown. Here, we explored the novel physiological function of IL-16 in vascular smooth muscle cells (VSMCs). The expression of IL-16 and its receptor CD4 was observed in VSMCs. Treatment with IL-16 enhanced the migration and invasion by VSMCs without altering the proliferative potential. IL-16 induced MMP-9 expression via the binding activity of transcription factors NF-κB, AP-1, and Sp-1 motifs in VSMCs. Among the relevant signaling pathways examined, only p38MAPK phosphorylation was significantly stimulated in IL-16-treated VSMCs. Treatment with p38MAPK inhibitor SB203580 prevented the IL-16-induced migration and invasion of VSMCs. SB203580 treatment inhibited the MMP-9 expression and activation of Sp-1 binding in IL-16-treated VSMCs, and siRNA knockdown of CD4 expression blocked the induction of migration, invasion, p38MAPK phosphorylation, MMP-9 expression, and Sp-1 binding activation stimulated by IL-16. The IL-16 induced cell-cycle-inhibitor p21WAF1 expression in VSMCs, but had no effect on the expression levels of other cell-cycle negative regulators. Finally, blockage of p21WAF1 function with specific siRNA abolished the IL-16-induced elevation of migration, invasion, p38MAPK phosphorylation, MMP-9 expression, and Sp-1 binding activation in VSMCs. Taken together, p21WAF1 was required for the induction of p38MAPK-mediated MMP-9 expression via activation of the Sp-1 binding motif, which led to migration and invasion of VSMCs interacting with IL-16/CD4. These results could provide that IL-16 is a new target in the treatment of vascular diseases such as atherosclerosis and re-stenosis.
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