Fibrin glue alone and skeletal myoblasts in a fibrin scaffold preserve cardiac function after myocardial infarction

被引:297
作者
Christman, KL
Fok, HH
Sievers, RE
Fang, QH
Lee, RJ
机构
[1] Univ Calif Berkeley, Berkeley, CA 94720 USA
[2] Univ Calif San Francisco, San Francisco Joint Bioengn Grad Grp, San Francisco, CA USA
[3] Univ Calif San Francisco, Dept Med, San Francisco, CA USA
[4] Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA USA
来源
TISSUE ENGINEERING | 2004年 / 10卷 / 3-4期
关键词
D O I
10.1089/107632704323061762
中图分类号
Q813 [细胞工程];
学科分类号
摘要
Current efforts in cardiac tissue engineering center around the use of scaffolds that deliver cells to the epicardial surface. In this study, we examined the effects of fibrin glue as an injectable scaffold and wall support in ischemic myocardium. The left coronary artery of rats was occluded for 17 min, followed by reperfusion. Echocardiography was performed 8 days after infarction. One to 2 days later, either 0.5% bovine serum albumin (BSA) in phosphate-buffered saline, fibrin glue alone, skeletal myoblasts alone, or skeletal myoblasts in fibrin glue were injected into the ischemic left ventricle. Echocardiography was again performed 5 weeks after injection. The animals were then sacrificed and the hearts were fresh frozen and sectioned for histology and immunohistochemistry. Both the fractional shortening (FS) and infarct wall thickness of the BSA group decreased significantly after 5 weeks (p = 0.0005 and 0.02, respectively). In contrast, both measurements for the fibrin glue group, cells group, and cells in fibrin glue group did not change significantly (FS: p = 0.18, 0.89, and 0.19, respectively; wall thickness: p = 0.40, 0.44, 0.43, respectively). Fibrin glue is capable of preserving infarct wall thickness and cardiac function after a myocardial infarction in rats and may be useful as a biomaterial scaffold for myocardial cell transplantation.
引用
收藏
页码:403 / 409
页数:7
相关论文
共 37 条
[1]   Plasmid gene delivery to human keratinocytes through a fibrin-mediated transfection system [J].
Andree, C ;
Voigt, M ;
Wenger, A ;
Erichsen, T ;
Bittner, K ;
Schaefer, D ;
Walgenbach, KJ ;
Borges, J ;
Horch, RE ;
Eriksson, E ;
Stark, B .
TISSUE ENGINEERING, 2001, 7 (06) :757-766
[2]  
Chawla PS, 1999, INT ANGIOL, V18, P185
[3]  
CHRISTMAN KL, 2003, 7 ANN HILT HEAD WORK
[4]   REGULATION OF COLLAGEN DEGRADATION IN THE RAT MYOCARDIUM AFTER INFARCTION [J].
CLEUTJENS, JPM ;
KANDALA, JC ;
GUARDA, E ;
GUNTAKA, RV ;
WEBER, KT .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1995, 27 (06) :1281-1292
[5]   Measurement of cardiac function in conscious rats [J].
Doursout, MF ;
Wouters, P ;
Kashimoto, S ;
Hartley, CJ ;
Rabinovitz, R ;
Chelly, JE .
ULTRASOUND IN MEDICINE AND BIOLOGY, 2001, 27 (02) :195-202
[6]   EARLY DILATION OF THE INFARCTED SEGMENT IN ACUTE TRANSMURAL MYOCARDIAL-INFARCTION - ROLE OF INFARCT EXPANSION IN ACUTE LEFT-VENTRICULAR ENLARGEMENT [J].
ERLEBACHER, JA ;
WEISS, JL ;
WEISFELDT, ML ;
BULKLEY, BH .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1984, 4 (02) :201-208
[7]  
FISHBEIN MC, 1978, AM J PATHOL, V90, P57
[8]   Long-term efficacy of myoblast transplantation on regional structure and function after myocardial infarction [J].
Ghostine, S ;
Carrion, C ;
Souza, LCG ;
Richard, P ;
Bruneval, P ;
Vilquin, JT ;
Pouzet, B ;
Schwartz, K ;
Menasché, P ;
Hagège, AA .
CIRCULATION, 2002, 106 (13) :I131-I136
[9]   Transplantation of genetically marked cardiac muscle cells [J].
Gojo, S ;
Kitamura, S ;
Hatano, O ;
Takakusu, A ;
Hashimoto, K ;
Kanegae, Y ;
Saito, I .
JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY, 1997, 113 (01) :10-18
[10]   MUSCLE-FIBER TYPING IN ROUTINELY PROCESSED SKELETAL-MUSCLE WITH MONOCLONAL-ANTIBODIES [J].
HAVENITH, MG ;
VISSER, R ;
SCHRIJVERSVANSCHENDEL, JMC ;
BOSMAN, FT .
HISTOCHEMISTRY, 1990, 93 (05) :497-499