Document Detail


Impact of pre-existing elastic matrix on TGFβ1 and HA oligomer-induced regenerative elastin repair by rat aortic smooth muscle cells.
MedLine Citation:
PMID:  20653044     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Regenerating elastic matrices lost to disease (e.g. in aneurysms) is vital to re-establishing vascular homeostasis but is challenged by the poor elastogenicity of post-neonatal cells. We previously showed that exogenous hyaluronan oligomers (HA-o) and TGFβ1 synergistically enhance tropo- and matrix elastin deposition by healthy adult rat aortic SMCs (RASMCs). Towards treating aortic aneurysms (AAs), which exhibit cause- and site-specific heterogeneity in matrix content/structure and contain proteolytically-injured SMCs, we investigated the impact of pre-existing elastic matrix degeneration on elastogenic induction of injured RASMCs. Elastin-rich RASMC layers at 21 days of culture were treated with 0.15 U/ml (PPE15) and 0.75 U/ml (PPE75) porcine pancreatic elastase to degrade the elastic matrix variably, or left uninjured (control). One set of cultures was harvested at 21 days, before and after injury, to quantify viable cell count, matrix elastin loss. Other injured cell layers were cultured to 42 days with or without factors (0.2 µg/ml HA oligomers, 1 ng/ml TGFβ1). We showed that: (a) the ability of cultures to self-repair and regenerate elastic matrices following proteolysis is limited when elastolysis is severe; (b) HA oligomers and TGFβ1 elastogenically stimulate RASMCs in mildly-injured (i.e. PPE15) cultures to restore both elastic matrix amounts and elastic fibre deposition to levels in healthy cultures; and (c) in severely injured (i.e. PPE75) cultures, the factors stimulate matrix elastin synthesis and crosslinking, although not to control levels. The outcomes underscore the need to enhance elastogenic factor doses based on the severity of elastin loss. This study will help in customizing therapies for elastin regeneration within AAs, based on cause and location.
Authors:
Carmen E Gacchina; Anand Ramamurthi
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Journal of tissue engineering and regenerative medicine     Volume:  5     ISSN:  1932-7005     ISO Abbreviation:  J Tissue Eng Regen Med     Publication Date:  2011 Feb 
Date Detail:
Created Date:  2011-01-26     Completed Date:  2011-04-25     Revised Date:  2013-03-11    
Medline Journal Info:
Nlm Unique ID:  101308490     Medline TA:  J Tissue Eng Regen Med     Country:  England    
Other Details:
Languages:  eng     Pagination:  85-96     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 John Wiley & Sons, Ltd.
Affiliation:
Department of Bioengineering, Clemson University, 173 Ashley Avenue, Clemson, SC 29425, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Aorta / cytology*,  metabolism
Aortic Aneurysm / metabolism,  therapy
Cells, Cultured
Elasticity
Elastin*
Extracellular Matrix*
Hyaluronic Acid*
Myocytes, Smooth Muscle / cytology*,  metabolism
Pancreatic Elastase / pharmacology
Rats
Rats, Sprague-Dawley
Regeneration*
Swine
Tissue Engineering / methods
Transforming Growth Factor beta1 / pharmacology*
Grant Support
ID/Acronym/Agency:
C06 RR018823-01/RR/NCRR NIH HHS; C06RR018823/RR/NCRR NIH HHS; EB006078-01A1/EB/NIBIB NIH HHS; HL007260/HL/NHLBI NIH HHS; P20 RR016461-04/RR/NCRR NIH HHS; P20RR016461/RR/NCRR NIH HHS; R01 HL092051-01A1/HL/NHLBI NIH HHS; R01 HL092051-04/HL/NHLBI NIH HHS; R01 HL092051-05/HL/NHLBI NIH HHS; R21 EB006078-01A1/EB/NIBIB NIH HHS; T32 HL007260/HL/NHLBI NIH HHS; T32 HL007260-33/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Transforming Growth Factor beta1; 9004-61-9/Hyaluronic Acid; 9007-58-3/Elastin; EC 3.4.21.36/Pancreatic Elastase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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