[Effects of in vivo transfer of human chemokine-like factor 1 gene on cardiac function after acute myocardial infarction in rats].
OBJECTIVE
To study the effects of chemokine-like factor 1(CKLF1)-plasmid transfer on cardiac function in a rat acute myocardial infarction (AMI) model.


METHODS
Thirty male SD rats were randomly devided into 3 groups. One hundred micrograms of CKLF1-plasmid, empty plasmid or saline were injected intramuscularly with in vivo electroporation, respectively. Rats were subjected to left coronary artery ligation on the 6th day after gene transfer. Ultrasonic cardiography and hemodynamics were conducted and evaluated on the 22nd day after gene transfer. Then, the animals were sacrificed for determination of percentage of myocardial infarcion.


RESULTS
The left ventricular ejection fraction in CKLF1 group (67.02% +/- 12.24%) was significantly higher than that in the saline group (43.64% +/- 7.82%) and empty plasmid group (47.56% +/- 4.10%), P<0.05. Fractional shortening of left ventricle in CKLF1 group (33.83% +/- 10.15%) was higher than that in saline group (18.49% +/- 3.96%) and empty plasmid group (20.85% +/- 2.24%), P<0.05. The maximal velocity of left ventricular pressure ascensus was higher in CKLF1 group [(5 720.01 +/- 826.32) mmHg/s, 1 mmHg=0.133 kPa] than in saline group [(3 955.69 +/- 685.91) mmHg/s] and in empty plasmid group [(4 412.03 +/- 500.74) mmHg/s)], P<0.05. And the maximal velosity of left ventricular pressure descensus was higher in CKLF1 group [(4 636.23 +/- 407.17) mmHg/s] than in saline group [(2 984.82 +/- 615.24) mmHg/s] and in empty plasmid group [(2 963.87 +/- 419.36) mmHg/s], P<0.05. While the percentage of myocardial infarction in CKLF1 group (29.63% +/- 3.93%) was smaller than that in saline group (38.01% +/- 5.48%) and in empty plasmid group (37.50% +/- 6.33%), P<0.05.


CONCLUSIONS
CKLF1 gene transfer can limit the mass of myocardial infarction and improve post-infarction cardiac function.
Yang
Bo
B
Department of Cardiology, Peking University First Hospital, Beijing 100034, China.
Hong
Tao
T
Liu
Qian-zhu
QZ
Feng
Xue-ru
XR
Gong
Yan-jun
YJ
Bu
Ding-fang
DF
Li
Xue-mei
XM
Xue
Lin
L
Zhao
Chun-yu
CY
Huo
Yong
Y
D000818:Animals; D018925:Chemokines / Q000235:genetics*; D018274:Electroporation; D018014:Gene Transfer Techniques; D015316:Genetic Therapy / Q000379:methods*; D006801:Humans; D062792:MARVEL Domain-Containing Proteins; D008297:Male; D009203:Myocardial Infarction / Q000235:genetics / Q000503:physiopathology / Q000628:therapy*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function; D016277:Ventricular Function, Left / Q000502:physiology*
C432676:CKLF protein, human; D018925:Chemokines; D062792:MARVEL Domain-Containing Proteins