ArticleArteriosclerosis, thrombosis, and vascular biology2017
Janus Kinase 3, a Novel Regulator for Smooth Muscle Proliferation and Vascular Remodeling.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 34 citations in OpenAlex.
- From Atherosclerotic Plaque to Myocardial Infarction-The Leading Cause of Coronary Artery Occlusion.International journal of molecular sciences · 2024Review
- Broader Perspective on Atherosclerosis-Selected Risk Factors, Biomarkers, and Therapeutic Approach.International journal of molecular sciences · 2024Review
- BMPRIINeural regeneration research · 2024Article
- Gene-repressing epigenetic reader EED unexpectedly enhances cyclinD1 gene activation.Molecular therapy. Nucleic acids · 2023Article
- A 9‑gene expression signature to predict stage development in resectable stomach adenocarcinoma.BMC gastroenterology · 2022Article
- Radiation-induced C-reactive protein triggers apoptosis of vascular smooth muscle cells through ROS interfering with the STAT3/Ref-1 complex.Journal of cellular and molecular medicine · 2022Article
- Janus Kinase 3 Deficiency Promotes Vascular Reendothelialization-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- Endothelial Jak3 expression enhances pro-hematopoietic angiocrine function in mice.Communications biology · 2021Article
- 17β-Estradiol Inhibits Proliferation and Oxidative Stress in Vascular Smooth Muscle Cells by Upregulating BHLHE40 Expression.Frontiers in cardiovascular medicine · 2021Article
- JANEX-1 improves acute pulmonary embolism through VEGF and FAK in pulmonary artery smooth muscle cells.Experimental biology and medicine (Maywood, N.J.) · 2020Article
- Smooth Muscle Cells in Vascular Remodeling.Arteriosclerosis, thrombosis, and vascular biology · 2019Review
- Interleukin-21 receptor gene polymorphism is associated with hepatitis B virus-related hepatocellular carcinoma in Chinese patients.Journal of clinical laboratory analysis · 2019Article
- Contribution of p62/SQSTM1 to PDGF-BB-induced myofibroblast-like phenotypic transition in vascular smooth muscle cells lacking Smpd1 gene.Cell death & disease · 2018Article
- Reporting Sex and Sex Differences in Preclinical Studies.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectiveVascular remodeling because of smooth muscle cell (SMC) proliferation is a common process occurring in several vascular diseases, such as atherosclerosis, aortic aneurysm, post-transplant vasculopathy, restenosis after angioplasty, etc. The molecular mechanism underlying SMC proliferation, however, is not completely understood. The objective of this study is to determine the role and mechanism of Janus kinase 3 (JAK3) in vascular remodeling and SMC proliferation. APPROACH AND
resultsPlatelet-derived growth factor-BB, an SMC mitogen, induces JAK3 expression and phosphorylation while stimulating SMC proliferation. Janex-1, a specific inhibitor of JAK3, or knockdown of JAK3 by short hairpin RNA, inhibits the SMC proliferation. Conversely, ectopic expression of JAK3 promotes SMC proliferation. Mechanistically, JAK3 promotes the phosphorylation of signal transducer and activator of transcription 3 and c-Jun N-terminal kinase in SMC, 2 signaling pathways known to be critical for SMC proliferation and vascular remodeling. Blockade of these 2 signaling pathways by their inhibitors impeded the JAK3-mediated SMC proliferation. In vivo, knockdown of JAK3 attenuates injury-induced neointima formation with attenuated neointimal SMC proliferation. Knockdown of JAK3 also induces neointimal SMC apoptosis in rat carotid artery balloon injury model.
conclusionsOur results demonstrate that JAK3 mediates SMC proliferation and survival during injury-induced vascular remodeling, which provides a potential therapeutic target for preventing neointimal hyperplasia in proliferative vascular diseases.
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