PMID- 21602472
OWN - NLM
STAT- MEDLINE
DCOM- 20110930
LR  - 20211020
IS  - 1522-1539 (Electronic)
IS  - 0363-6135 (Print)
IS  - 0363-6135 (Linking)
VI  - 301
IP  - 2
DP  - 2011 Aug
TI  - SPARC mediates early extracellular matrix remodeling following myocardial 
      infarction.
PG  - H497-505
LID - 10.1152/ajpheart.01070.2010 [doi]
AB  - Secreted protein, acidic, and rich in cysteine (SPARC) is a matricellular protein 
      that functions in the extracellular processing of newly synthesized collagen. 
      Collagen deposition to form a scar is a key event following a myocardial 
      infarction (MI). Because the roles of SPARC in the early post-MI setting have not 
      been defined, we examined age-matched wild-type (WT; n=22) and SPARC-deficient 
      (null; n=25) mice at day 3 post-MI. Day 0 WT (n=28) and null (n=20) mice served 
      as controls. Infarct size was 52 +/- 2% for WT and 47 +/- 2% for SPARC null (P=NS), 
      indicating that the MI injury was comparable in the two groups. By 
      echocardiography, WT mice increased end-diastolic volumes from 45 +/- 2 to 83 +/- 5 
      mul (P < 0.05). SPARC null mice also increased end-diastolic volumes but to a 
      lesser extent than WT (39 +/- 3 to 63 +/- 5 mul; P < 0.05 vs. day 0 controls and vs. 
      WT day 3 MI). Ejection fraction fell post-MI in WT mice from 57 +/- 2 to 19 +/- 1%. 
      The decrease in ejection fraction was attenuated in the absence of SPARC (65 +/- 2 
      to 28 +/- 2%). Fibroblasts isolated from SPARC null left ventricle (LV) showed 
      differences in the expression of 22 genes encoding extracellular matrix and 
      adhesion molecule genes, including fibronectin, connective tissue growth factor 
      (CTGF; CCN2), matrix metalloproteinase-3 (MMP-3), and tissue inhibitor of 
      metalloproteinase-2 (TIMP-2). The change in fibroblast gene expression levels was 
      mirrored in tissue protein extracts for fibronectin, CTGF, and MMP-3 but not 
      TIMP-2. Combined, the results of this study indicate that SPARC deletion 
      preserves LV function at day 3 post-MI but may be detrimental for the long-term 
      response due to impaired fibroblast activation.
FAU - McCurdy, Sarah M
AU  - McCurdy SM
AD  - Cardiology Division, Department of Medicine, University of Texas Health Science 
      Center at San Antonio, San Antonio, TX 78229-3900, USA.
FAU - Dai, Qiuxia
AU  - Dai Q
FAU - Zhang, Jianhua
AU  - Zhang J
FAU - Zamilpa, Rogelio
AU  - Zamilpa R
FAU - Ramirez, Trevi A
AU  - Ramirez TA
FAU - Dayah, Tariq
AU  - Dayah T
FAU - Nguyen, Nguyen
AU  - Nguyen N
FAU - Jin, Yu-Fang
AU  - Jin YF
FAU - Bradshaw, Amy D
AU  - Bradshaw AD
FAU - Lindsey, Merry L
AU  - Lindsey ML
LA  - eng
GR  - SC2 HL101430/HL/NHLBI NIH HHS/United States
GR  - SC2 HL101430-02/HL/NHLBI NIH HHS/United States
GR  - R03 EB009496-01A2/EB/NIBIB NIH HHS/United States
GR  - R03 EB009496/EB/NIBIB NIH HHS/United States
GR  - R01 HL075360/HL/NHLBI NIH HHS/United States
GR  - 2P01-HL-48788/HL/NHLBI NIH HHS/United States
GR  - SC2-HL-101430/HL/NHLBI NIH HHS/United States
GR  - R01-HL-75360/HL/NHLBI NIH HHS/United States
GR  - 1R03-EB-009496/EB/NIBIB NIH HHS/United States
GR  - HL-094517/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20110520
PL  - United States
TA  - Am J Physiol Heart Circ Physiol
JT  - American journal of physiology. Heart and circulatory physiology
JID - 100901228
RN  - 0 (Extracellular Matrix Proteins)
RN  - 0 (Osteonectin)
SB  - IM
MH  - Analysis of Variance
MH  - Animals
MH  - Blotting, Western
MH  - Disease Models, Animal
MH  - Extracellular Matrix Proteins/genetics/*metabolism
MH  - Female
MH  - Fibroblasts/metabolism
MH  - Gene Expression Profiling/methods
MH  - Gene Expression Regulation
MH  - Heart Rupture, Post-Infarction/metabolism/pathology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Myocardial Contraction
MH  - Myocardial Infarction/diagnostic imaging/genetics/*metabolism/physiopathology
MH  - Myocardium/*metabolism/pathology
MH  - Oligonucleotide Array Sequence Analysis
MH  - Osteonectin/deficiency/genetics/*metabolism
MH  - Stroke Volume
MH  - Time Factors
MH  - Ultrasonography
MH  - *Ventricular Function, Left
MH  - *Ventricular Remodeling/genetics
PMC - PMC3154667
EDAT- 2011/05/24 06:00
MHDA- 2011/10/01 06:00
PMCR- 2012/08/01
CRDT- 2011/05/24 06:00
PHST- 2011/05/24 06:00 [entrez]
PHST- 2011/05/24 06:00 [pubmed]
PHST- 2011/10/01 06:00 [medline]
PHST- 2012/08/01 00:00 [pmc-release]
AID - ajpheart.01070.2010 [pii]
AID - H-01070-2010 [pii]
AID - 10.1152/ajpheart.01070.2010 [doi]
PST - ppublish
SO  - Am J Physiol Heart Circ Physiol. 2011 Aug;301(2):H497-505. doi: 
      10.1152/ajpheart.01070.2010. Epub 2011 May 20.