MicroRNAs Involved in Asthma After Mesenchymal Stem Cells Treatment.

Item request has been placed! ×
Item request cannot be made. ×
loading   Processing Request
  • Additional Information
    • Source:
      Publisher: Mary Ann Liebert, Inc Country of Publication: United States NLM ID: 101197107 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1557-8534 (Electronic) Linking ISSN: 15473287 NLM ISO Abbreviation: Stem Cells Dev Subsets: MEDLINE
    • Publication Information:
      Original Publication: Larchmont, NY : Mary Ann Liebert, Inc., c2004-
    • Subject Terms:
    • Abstract:
      Administration of human bone marrow-derived mesenchymal stem cells (BM-MSCs) significantly alleviates allergic airway inflammation. There are no studies that refer to the role of microRNAs (miRNAs) after the BM-MSCs treatment in airway allergic inflammation. We induced a mouse model of asthma and performed the transplantation of BM-MSCs. We analyzed aberrant miRNAs and key immune regulators using both miRNA and messenger RNA (mRNA) polymerase chain reaction (PCR) arrays. We identified that 296 miRNAs were differently expressed after the induction of asthma and/or the treatment of BM-MSCs, in which 14 miRNAs presented the reverse variation tendency between asthma induction and BM-MSCs transplantation. Mmu-miR-21a-3p, mmu-miR-449c-5p, and mmu-miR-496a-3p were further confirmed to be differently expressed with additional samples and quantitative real-time PCR. With an mRNA PCR array, we identified 19 genes to be involved in the allergy induction and the administration of BM-MSCs. Further target genes analysis revealed that mmu-miR-21a-3p was significantly correlated with the immune regulator activin A receptor, Type IIA (Acvr2a). Mmu-miR-21a-3p had opposite expression with Acvr2a after asthma and BM-MSCs treatment. Acvr2a had binding sites for miR-21a for both mice and human, suggesting that miR-21/Acvr2a axis is conserved between human and mice. Dual-luciferase reporter assay showed that mmu-miR-21a-3p negatively regulated the transcript of Acvr2a. In addition, has-miR-21a inhibitor significantly increased the expression of Acvr2a mRNA in BEAS-2B cells under lipopolysaccharide stimulation. Our results suggest that there were different miRNA and mRNA profiles after asthma induction and BM-MSCs treatment, and the miR-21/Acvr2a axis is an important mechanism for the induction of asthmatic inflammation.
    • References:
      J Allergy Clin Immunol. 2008 Feb;121(2):309-19. (PMID: 18269923)
      Nat Rev Genet. 2004 Jul;5(7):522-31. (PMID: 15211354)
      Int J Clin Exp Med. 2014 May 15;7(5):1307-12. (PMID: 24995087)
      Iran J Allergy Asthma Immunol. 2014 Dec;13(6):412-9. (PMID: 25148799)
      PLoS One. 2013 Aug 13;8(8):e71342. (PMID: 23967196)
      Annu Rev Immunol. 1999;17:255-81. (PMID: 10358759)
      Immunity. 2000 Oct;13(4):573-83. (PMID: 11070175)
      J Exp Med. 2009 Aug 3;206(8):1769-85. (PMID: 19620629)
      Nature. 2014 Jun 5;510(7503):115-20. (PMID: 24899310)
      J Allergy Clin Immunol. 2011 Jul;128(1):160-167.e4. (PMID: 21571357)
      Mediators Inflamm. 2014;2014:436476. (PMID: 25246732)
      N Engl J Med. 2006 Nov 23;355(21):2226-35. (PMID: 17124020)
      Allergy. 2003 Aug;58(8):748-53. (PMID: 12859553)
      Curr Allergy Asthma Rep. 2005 Mar;5(2):155-60. (PMID: 15683617)
      J Allergy Clin Immunol. 2009 Sep;124(3):454-62. (PMID: 19733294)
      Nat Immunol. 2001 Jan;2(1):45-50. (PMID: 11135577)
      N Engl J Med. 2009 Mar 5;360(10):973-84. (PMID: 19264686)
      Cell Death Dis. 2014 Feb 27;5:e1095. (PMID: 24577093)
      Stem Cells. 2011 Jul;29(7):1137-48. (PMID: 21544902)
      J Immunol. 2009 Apr 15;182(8):4994-5002. (PMID: 19342679)
      Stem Cells Int. 2015;2015:583984. (PMID: 26064137)
      Proc Natl Acad Sci U S A. 2009 Nov 3;106(44):18704-9. (PMID: 19843690)
      Allergy. 2011 Apr;66(4):523-31. (PMID: 21091718)
      Clin Exp Allergy. 2015 Oct;45(10):1510-22. (PMID: 25962695)
      Allergy. 2012 Oct;67(10):1215-22. (PMID: 22882409)
      J Invest Dermatol. 2011 Mar;131(3):762-8. (PMID: 21085192)
      Nat Med. 2003 Aug;9(8):1047-54. (PMID: 12847520)
      Thorax. 2013 Jan;68(1):9-18. (PMID: 23051972)
      Cell. 2004 Jan 23;116(2):281-97. (PMID: 14744438)
      Am J Respir Crit Care Med. 2012 Nov 15;186(10):965-74. (PMID: 22955319)
      Genet Mol Biol. 2012 Jul;35(3):567-74. (PMID: 23055793)
      Allergy. 2002 Feb;57(2):180-1. (PMID: 11929427)
      Allergy. 2008 Apr;63 Suppl 86:8-160. (PMID: 18331513)
      Stem Cells. 2012 Dec;30(12):2692-9. (PMID: 22987325)
      Science. 2007 Apr 27;316(5824):608-11. (PMID: 17463290)
      J Allergy Clin Immunol. 2011 Nov;128(5):1077-85.e1-10. (PMID: 21616524)
      J Biol Chem. 2010 Sep 24;285(39):30139-49. (PMID: 20630862)
      Anesthesiology. 2014 Nov;121(5):1099-121. (PMID: 25211170)
      Immunol Rev. 2011 Jul;242(1):258-71. (PMID: 21682751)
      J Immunol. 1999 May 15;162(10):6178-83. (PMID: 10229862)
      Exp Lung Res. 2011 Oct;37(8):500-8. (PMID: 21892915)
      Am J Physiol Lung Cell Mol Physiol. 2010 Dec;299(6):L760-70. (PMID: 20817776)
      Nat Cell Biol. 2011 Jun;13(6):693-9. (PMID: 21602795)
      Trends Mol Med. 2010 May;16(5):203-9. (PMID: 20335067)
      Am J Respir Cell Mol Biol. 1995 Jul;13(1):54-9. (PMID: 7598937)
      Allergy. 2005 Aug;60(8):986-95. (PMID: 15969678)
    • Accession Number:
      0 (Cytokines)
      0 (Immunoglobulins)
      0 (Inflammation Mediators)
      0 (MicroRNAs)
      0 (RNA, Messenger)
      9006-59-1 (Ovalbumin)
      EC 2.7.11.30 (Activin Receptors, Type II)
      EC 2.7.11.30 (activin receptor type II-A)
    • Publication Date:
      Date Created: 20160424 Date Completed: 20170911 Latest Revision: 20181202
    • Publication Date:
      20240104
    • Accession Number:
      PMC4928133
    • Accession Number:
      10.1089/scd.2015.0339
    • Accession Number:
      27106170