A micro RNA‐146a polymorphism is associated with coronary restenosis

The association of the miRNA‐146a polymorphism rs2910164 with atherosclerosis and restenosis was investigated. We found no association with atherosclerosis; however, we found a negative association for the G/C (P = 0.007) and a positive association for the C/C genotype with the risk of restenosis, which is the main drawback for cardiac surgery.

[1]  Y. Suh,et al.  A common variant in pre-miR-146 is associated with coronary artery disease risk and its mature miRNA expression. , 2014, Mutation research.

[2]  D. Moodley,et al.  miR-146a Polymorphism Influences Levels of miR-146a, IRAK-1, and TRAF-6 in Young Patients with Coronary Artery Disease , 2013, Cell Biochemistry and Biophysics.

[3]  F. Gourronc,et al.  Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis , 2012 .

[4]  K. Moore,et al.  CD36 ligands promote sterile inflammation through assembly of a Toll-like receptor 4 and 6 heterodimer , 2009, Nature Immunology.

[5]  K. Jażdżewski,et al.  Polymorphic mature microRNAs from passenger strand of pre-miR-146a contribute to thyroid cancer , 2009, Proceedings of the National Academy of Sciences.

[6]  Shuang Chen,et al.  Chlamydia pneumoniae-Induced Foam Cell Formation Requires MyD88-Dependent and -Independent Signaling and Is Reciprocally Modulated by Liver X Receptor Activation1 , 2008, The Journal of Immunology.

[7]  P. Tornvall,et al.  Serum C-reactive protein response to percutaneous coronary intervention in patients with unstable or stable angina pectoris is associated with the risk of clinical restenosis. , 2007, Atherosclerosis.

[8]  A. Bowie,et al.  The family of five: TIR-domain-containing adaptors in Toll-like receptor signalling , 2007, Nature Reviews Immunology.

[9]  D. Baltimore,et al.  NF-κB-dependent induction of microRNA miR-146, an inhibitor targeted to signaling proteins of innate immune responses , 2006, Proceedings of the National Academy of Sciences.

[10]  I. Kubota,et al.  Central role of endogenous Toll-like receptor-2 activation in regulating inflammation, reactive oxygen species production, and subsequent neointimal formation after vascular injury. , 2006, Biochemical and biophysical research communications.

[11]  K. Michelsen,et al.  Toll-like receptor signaling and atherosclerosis , 2006, Current opinion in hematology.

[12]  S. Anker,et al.  A frequent toll-like receptor (TLR)-2 polymorphism is a risk factor for coronary restenosis , 2005, Journal of Molecular Medicine.

[13]  L. Hansson,et al.  Stent implantation, but not pathogen burden, is associated with plasma C-reactive protein and interleukin-6 levels after percutaneous coronary intervention in patients with stable angina pectoris. , 2005, American heart journal.

[14]  L. Hansson,et al.  A novel common single nucleotide polymorphism in the promoter region of the C-reactive protein gene associated with the plasma concentration of C-reactive protein. , 2005, Atherosclerosis.

[15]  C. Held,et al.  Genetic predisposition of the interleukin-6 response to inflammation: implications for a variety of major diseases? , 2004, Clinical chemistry.

[16]  D. Bartel.  MicroRNAs Genomics, Biogenesis, Mechanism, and Function , 2004, Cell.

[17]  F. Crea,et al.  Immunosuppressive Therapy for the Prevention of Restenosis after Coronary Artery Stent Implantation (IMPRESS Study). , 2002, Journal of the American College of Cardiology.

[18]  D. Waters,et al.  Coronary angioplasty induces a systemic inflammatory response. , 1997, The American journal of cardiology.