Autologous bone marrow-derived mononuclear cell therapy prevents the damage of viable myocardium and improves rat heart function following acute anterior myocardial infarction.
BACKGROUND
We examined the effects of bone marrow-derived mononuclear cells (BMDMNCs) on preventing viable myocardium damage from myocardial infarction (MI) in a rat MI model.


RESULTS
Saline (group 1) or BMDMNCs (group 2) were implanted into the infarct area (IA) of 1-week-old anterior wall MI Sprague-Dawley (SD) rats. Twenty SD rats without MI served as the controls (group 3). The results demonstrated that in remote viable myocardium, the integrated area (microm2) of connexin43 spots was lower, whereas the number of apoptotic nuclei were higher in group 1 than in groups 2 and 3 on day 90 following BMDMNC implantation (all p<0.001). Additionally, the number of vessels and survival myocardium in the IA was lower in group 1 than in groups 2 and 3 (all p<0.005). Furthermore, the mRNA expressions of nitric oxide synthase, interleukin-8/Gro-alpha, interleukin-10 and matrix metalloproteinase-9 were higher in group 2 than in groups 1 and 3 in peri-IA (all p<0.05). On days 42 and 90, the left ventricular (LV) function was lower in group 1 than in groups 2 and 3 (p<0.001).


CONCLUSIONS
Autologous BMDMNC therapy improves LV function, and mitigates molecular and cellular perturbation following MI.
Yip
Hon-Kan
HK
Division of Cardiology, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Chang
Li-Teh
LT
Wu
Chiung-Jen
CJ
Sheu
Jiunn-Jye
JJ
Youssef
Ali A
AA
Pei
Sung-Nan
SN
Lee
Fan-Yen
FY
Sun
Cheuk-Kwan
CK
D000818:Animals; D017209:Apoptosis; D015153:Blotting, Western; D016026:Bone Marrow Transplantation; D002465:Cell Movement; D018031:Connexin 43 / Q000378:metabolism; D003331:Coronary Vessels / Q000503:physiopathology; D004195:Disease Models, Animal; D004452:Echocardiography; D005434:Flow Cytometry; D005455:Fluorescent Antibody Technique; D016753:Interleukin-10 / Q000235:genetics / Q000378:metabolism; D016209:Interleukin-8 / Q000235:genetics / Q000378:metabolism; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000235:genetics / Q000378:metabolism; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology / Q000601:surgery*; D009206:Myocardium / Q000201:enzymology / Q000473:pathology*; D018919:Neovascularization, Physiologic; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D014022:Tissue Survival; D014182:Transplantation, Autologous; D015854:Up-Regulation; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling
D018031:Connexin 43; D016209:Interleukin-8; D012333:RNA, Messenger; D016753:Interleukin-10; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat; D020780:Matrix Metalloproteinase 9