Role of Hyaluronic Acid Treatment in the Prevention of Keloid Scarring.

Andrea Hoffmann, Jessica Lynn Hoing, Mackenzie Newman, Richard Simman
Author Information
  1. Andrea Hoffmann: Department of Pharmacology and Toxicology, Boonshoft School of Medicine, Wright State University, Dayton, OH, USA ; Department of Surgery, Division of Plastic Surgery, Boonshoft School of Medicine, Wright State University, Dayton, OH, USA.
  2. Jessica Lynn Hoing: Department of Pharmacology and Toxicology, Boonshoft School of Medicine, Wright State University, Dayton, OH, USA.
  3. Mackenzie Newman: Department of Pharmacology and Toxicology, Boonshoft School of Medicine, Wright State University, Dayton, OH, USA.
  4. Richard Simman: Department of Pharmacology and Toxicology, Boonshoft School of Medicine, Wright State University, Dayton, OH, USA ; Department of Surgery, Division of Plastic Surgery, Boonshoft School of Medicine, Wright State University, Dayton, OH, USA.

Abstract

BACKGROUND: Keloids are benign dermal scars characterized by enhanced growth factor signaling, hyperproliferation activity and reduced extracellular matrix (ECM) deposition of Hyaluronic Acid. Our hypothesis is that high molecular weight HA can be used to replenish HA deposition in Keloids thereby normalizing the keloid fibroblast phenotype.
METHODS: One normal (NF1) fibroblast culture and five keloid (KF1, KF2, KF3, KF4, KF5) fibroblast cultures were analyzed for changes in hyperproliferation, growth factor production and extracellular matrix deposition following 72 hour treatment with or without 10 μg/ml HA.
RESULTS: Proliferation activity decreased significantly in KF3 following HA treatment. Pro-collagen I expression in KF2 was decreased following HA treatment in association with changes in fiber arrangement to more parallel collagen bundles. In addition, HA demonstrated a downregulation on TGF-b1 growth factor expression in KF3 and KF4 and a decrease in active TGF-b1 release in KF2 and KF5 using ELISA.
CONCLUSION: Our data demonstrates that HA has the potential to normalize keloid fibroblast characteristic features such as hyperproliferation, growth factor production and ECM deposition depending on the specific genotype of the keloid fibroblast cell line. This study suggests that high molecular weight HA can be used to replenish HA deposition in keloid fibroblasts thereby decreasing fibrosis and ultimately decreasing keloid manifestation.

Keywords

References

  1. Proc Natl Acad Sci U S A. 1985 Sep;82(17):5935-9 [PMID: 3862108]
  2. Mol Med Today. 1998 Jan;4(1):19-24 [PMID: 9494966]
  3. Wound Repair Regen. 1999 Nov-Dec;7(6):511-7 [PMID: 10633011]
  4. Biotechnol Bioeng. 2003 Jun 5;82(5):578-89 [PMID: 12652481]
  5. Biomaterials. 2004 Aug;25(17):3689-98 [PMID: 15020144]
  6. J Invest Dermatol. 1995 Jan;104(1):128-33 [PMID: 7798630]
  7. J Pediatr Surg. 2000 Jun;35(6):874-9 [PMID: 10873029]
  8. J Mater Sci Mater Med. 2002 Sep;13(9):861-5 [PMID: 15348551]
  9. Dermatol Surg. 2009 Feb;35(2):171-81 [PMID: 19215252]
  10. Tissue Cell. 2003 Feb;35(1):37-45 [PMID: 12589728]
  11. Eur J Histochem. 2003;47(1):63-73 [PMID: 12685559]
  12. Prof Nurse. 2001 Dec;17(4):232-5 [PMID: 12030177]
  13. J Invest Dermatol. 1985 May;84(5):384-90 [PMID: 3998489]
  14. J Biol Chem. 2004 Apr 23;279(17):17079-84 [PMID: 14764599]
  15. J Burn Care Rehabil. 1996 Jul-Aug;17(4):302-4 [PMID: 8844349]
  16. Cell Biophys. 1980 Jun;2(2):165-75 [PMID: 6159090]
  17. Matrix. 1989 Jun;9(3):224-31 [PMID: 2779482]
  18. Plast Reconstr Surg. 2003 May;111(6):1969-79 [PMID: 12711959]
  19. Cell Death Differ. 2000 Feb;7(2):166-76 [PMID: 10713731]
  20. Exp Dermatol. 2008 Jul;17(7):610-3 [PMID: 18445023]
  21. Ann Plast Surg. 1994 Aug;33(2):152-4 [PMID: 7979046]
  22. Lancet. 1999 Jan 2;353(9146):35-6 [PMID: 10023951]
  23. Bioconjug Chem. 2001 Nov-Dec;12(6):1085-8 [PMID: 11716704]
  24. Oral Oncol. 2004 Mar;40(3):257-63 [PMID: 14747056]
  25. Am J Clin Dermatol. 2003;4(4):235-43 [PMID: 12680802]
  26. Anal Biochem. 1976 May 7;72:248-54 [PMID: 942051]
  27. Arch Dermatol. 1998 Aug;134(8):963-7 [PMID: 9722726]
  28. J Invest Dermatol. 2008 Apr;128(4):855-66 [PMID: 17943180]
  29. Plast Reconstr Surg. 2001 Aug;108(2):423-9 [PMID: 11496185]
  30. J Biomed Mater Res B Appl Biomater. 2003 Oct 15;67(1):586-92 [PMID: 14528455]
  31. Wound Repair Regen. 1999 Mar-Apr;7(2):79-89 [PMID: 10231509]
  32. Br J Dermatol. 2003 Nov;149 Suppl 66:62-5 [PMID: 14616355]
  33. J Invest Dermatol. 2000 May;114(5):953-9 [PMID: 10771477]
  34. J Refract Surg. 1995 Jan-Feb;11(1):42-4 [PMID: 7641048]
  35. Genes Dev. 2000 Jan 15;14(2):163-76 [PMID: 10652271]
  36. J Immunol. 2000 Aug 15;165(4):1863-70 [PMID: 10925265]
  37. J Pediatr Surg. 1995 Jul;30(7):949-52 [PMID: 7472951]
  38. Mol Cell Biol. 1989 Apr;9(4):1642-50 [PMID: 2524650]
  39. Cell Tissue Res. 1995 Aug;281(2):317-24 [PMID: 7648625]
  40. Dermatol Surg. 1996 Feb;22(2):126-30 [PMID: 8608373]
  41. Matrix. 1990 Jul;10(3):172-8 [PMID: 2215357]
  42. Br Med J (Clin Res Ed). 1985 Aug 17;291(6493):448-9 [PMID: 3926234]
  43. Am J Pathol. 1996 Nov;149(5):1441-7 [PMID: 8909233]
  44. Virchows Arch A Pathol Anat Histol. 1979 Mar 23;381(3):353-61 [PMID: 155931]
  45. Exp Dermatol. 2013 May;22(5):377-9 [PMID: 23614752]
  46. Ann Plast Surg. 2003 Jan;50(1):71-6 [PMID: 12545112]
  47. J Cell Physiol. 1979 Feb;98(2):341-6 [PMID: 422662]
  48. Am J Pathol. 2000 Sep;157(3):957-65 [PMID: 10980134]
  49. J Burn Care Rehabil. 1997 Nov-Dec;18(6):552 [PMID: 9404991]
  50. Med Sci Monit. 2003 Mar;9(3):BR97-108 [PMID: 12640331]
  51. Genes Dev. 2001 Apr 15;15(8):968-80 [PMID: 11316791]
  52. Ann Surg. 1992 Jan;215(1):3-7 [PMID: 1731647]
  53. Ann Plast Surg. 1994 Aug;33(2):148-51 [PMID: 7979045]
  54. J Eur Acad Dermatol Venereol. 2012 Feb;26(2):141-52 [PMID: 21838832]
  55. West J Med. 1993 Sep;159(3):350-5 [PMID: 8236977]
  56. Trends Immunol. 2003 Mar;24(3):112-4 [PMID: 12615203]
  57. Zhonghua Zheng Xing Shao Shang Wai Ke Za Zhi. 1999 Jul;15(4):283-5 [PMID: 11593607]
  58. Br J Dermatol. 2004 Mar;150(3):401-13 [PMID: 15030321]

Word Cloud

Created with Highcharts 10.0.0HAkeloiddepositionfibroblastgrowthfactorhyperproliferationKF2KF3followingtreatmentactivityextracellularmatrixECMacidhighmolecularweightcanusedreplenishtherebyKF4KF5changesproductiondecreasedexpressionTGF-b1decreasingHyaluronicScarringBACKGROUND:KeloidsbenigndermalscarscharacterizedenhancedsignalingreducedhyaluronichypothesiskeloidsnormalizingphenotypeMETHODS:OnenormalNF1culturefiveKF1culturesanalyzed72 hourwithout10 μg/mlRESULTS:ProliferationsignificantlyPro-collagenassociationfiberarrangementparallelcollagenbundlesadditiondemonstrateddownregulationdecreaseactivereleaseusingELISACONCLUSION:datademonstratespotentialnormalizecharacteristicfeaturesdependingspecificgenotypecelllinestudysuggestsfibroblastsfibrosisultimatelymanifestationRoleAcidTreatmentPreventionof KeloidKeloid

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