Minocycline inhibits PDGF-BB-induced human aortic smooth muscle cell proliferation and migration by reversing miR-221- and -222-mediated RECK suppression

Cellular Signalling
Yusuke HigashiBysani Chandrasekar


Minocycline, a tetracycline antibiotic, is known to exert vasculoprotective effects independent of its anti-bacterial properties; however the underlying molecular mechanisms are not completely understood. Reversion Inducing Cysteine Rich Protein with Kazal Motifs (RECK) is a cell surface expressed, membrane anchored protein, and its overexpression inhibits cancer cell migration. We hypothesized that minocycline inhibits platelet-derived growth factor (PDGF)-induced human aortic smooth muscle cell (SMC) proliferation and migration via RECK upregulation. Our data show that the BB homodimer of recombinant PDGF (PDGF-BB) induced SMC migration and proliferation, effects significantly blunted by pre-treatment with minocycline. Further investigations revealed that PDGF-BB induced PI3K-dependent AKT activation, ERK activation, reactive oxygen species generation, Nuclear Factor-κB and Activator Protein-1 activation, microRNA (miR)-221 and miR-222 induction, RECK suppression, and matrix metalloproteinase (MMP2 and 9) activation, effects that were reversed by minocycline. Notably, minocycline induced RECK expression dose-dependently within the therapeutic dose of 1-100 μM, and silencing RECK partially reversed the inhibitory effects of mi...Continue Reading


Jan 1, 1989·Proceedings of the National Academy of Sciences of the United States of America·M NodaY Ikawa
Nov 1, 1993·Proceedings of the National Academy of Sciences of the United States of America·L M GravesE G Krebs
May 1, 1994·Arthritis and Rheumatism·M KloppenburgB A Dijkmans
Oct 28, 1998·Proceedings of the National Academy of Sciences of the United States of America·C TakahashiM Noda
Sep 15, 1999·Nature·J A Romashkova, S S Makarov
Oct 29, 2000·Drug Safety : an International Journal of Medical Toxicology and Drug Experience·R A LawrensonR D Farmer
Jan 15, 2002·Arteriosclerosis, Thrombosis, and Vascular Biology·Yumei ZhanHiroshi Iwao
Sep 26, 2003·Journal of Cardiovascular Pharmacology·Sean P PinneyLeRoy E Rabbani
Apr 13, 2004·Proceedings of the National Academy of Sciences of the United States of America·Andrew I SuJohn B Hogenesch
Jun 30, 2009·American Journal of Physiology. Heart and Circulatory Physiology·Balachandar VenkatesanBysani Chandrasekar
Sep 16, 2010·Physiological Genomics·Sebastian Albinsson, William C Sessa
Jul 2, 2011·Atherosclerosis·Khurrum ShahzadBerend Isermann
Sep 6, 2011·Genome Medicine·Maitri Y Shah, George A Calin
Nov 16, 2011·Current Molecular Medicine·M GarofaloG Condorelli
May 12, 2012·Journal of Molecular and Cellular Cardiology·Anthony J ValenteBysani Chandrasekar
Oct 23, 2012·Cellular Signalling·Balachandar VenkatesanBysani Chandrasekar
Nov 10, 2012·Biochimica Et Biophysica Acta·Po-Han ChenXiaolin He
Feb 12, 2013·American Journal of Physiology. Heart and Circulatory Physiology·Yuanyuan WeiChristian Weber
Oct 8, 2013·Journal of Molecular and Cellular Cardiology·Jalahalli M SiddeshaBysani Chandrasekar
Jan 23, 2014·Cellular Signalling·Jalahalli M SiddeshaBysani Chandrasekar
Feb 25, 2014·Free Radical Biology & Medicine·Anthony J ValenteBysani Chandrasekar
Sep 15, 2015·Medical Science Monitor : International Medical Journal of Experimental and Clinical Research·Wenneng LiuGuoxin Li
Mar 23, 2017·Journal of Hepatology·Thomas Jacob UrbanUNKNOWN International Serious Adverse Events Consortium (iSAEC)
Oct 4, 2017·American Journal of Physiology. Heart and Circulatory Physiology·Jaume PadillaBysani Chandrasekar
Feb 1, 2018·Oncotarget·Weiyang LouWeimin Fan

❮ Previous
Next ❯

Related Concepts

Related Feeds

Cell Migration

Cell migration is involved in a variety of physiological and pathological processes such as embryonic development, cancer metastasis, blood vessel formation and remoulding, tissue regeneration, immune surveillance and inflammation. Here is the latest research.