PMID- 19603100
OWN - NLM
STAT- MEDLINE
DCOM- 20091231
LR  - 20211020
IS  - 1528-3658 (Electronic)
IS  - 1076-1551 (Print)
IS  - 1076-1551 (Linking)
VI  - 15
IP  - 9-10
DP  - 2009 Sep-Oct
TI  - CD151 gene delivery after myocardial infarction promotes functional 
      neovascularization and activates FAK signaling.
PG  - 307-15
LID - 10.2119/molmed.2009.00025 [doi]
AB  - Our previous studies showed that tetraspanin CD151 promotes neovascularization in 
      rat hindlimb and myocardial ischemia models. This study is to assess whether 
      CD151 induces arteriogenesis and promotes functional neovascularization in a pig 
      myocardial infarction model, and to determine the signaling pathways involved. 
      CD151 cDNA and antiCD151 sequence were constructed into a recombinant 
      adeno-associated virus (rAAV) vector. All 26 pigs used either were subjected to 
      coronary artery ligation or did not undergo surgery. Eight wks after viral 
      administration, the expression of CD151 protein was measured by Western blot. The 
      densities of capillaries and arterioles were determined using 
      immunohistochemistry. Regional myocardial perfusion and other myocardial 
      functions were evaluated by (13)N-labeled NH(3) positron emission computed 
      tomography ((13)N-NH(3) PET) and echocardiography. Western blot was performed for 
      assessing the signaling mechanisms. Overexpression of CD151 markedly increased 
      the densities of capillaries and arterioles, significantly enhanced the regional 
      myocardial perfusion, reduced myocardial ischemia, and improved the myocardial 
      contraction, wall motion, and wall thickness. Conversely, antiCD151 gene delivery 
      reversed the above changes. In addition, CD151 activated focal adhesion kinase 
      (FAK), extracellular signal-regulated kinase (ERK), c-Jun N-teminal kinase (JNK), 
      phosphatidylinositol-3 kinase (PI3K), protein kinase B (Akt), and endothelial 
      nitric-oxide synthase (eNOS), and increased nitric oxide (NO) level. These 
      findings demonstrate a robust role of CD151 in inducing and/or upregulating 
      neovascularization. CD151-dependent neovascularization correlates with the 
      activations of FAK, mitogen activated protein kinases (MAPKs), and PI3K 
      signaling, suggesting that CD151 may promote neovascularization via MAPKs and 
      PI3K pathways.
FAU - Zuo, Houjuan
AU  - Zuo H
AD  - Department of Cardiology of Tongji Hospital, Tongji Medical College, Huazhong 
      University of Science and Technology, Wuhan, China.
FAU - Liu, Zhengxiang
AU  - Liu Z
FAU - Liu, Xiaochun
AU  - Liu X
FAU - Yang, Jun
AU  - Yang J
FAU - Liu, Tao
AU  - Liu T
FAU - Wen, Sha
AU  - Wen S
FAU - Zhang, Xin A
AU  - Zhang XA
FAU - Cianflone, Katherine
AU  - Cianflone K
FAU - Wang, Daowen
AU  - Wang D
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090618
PL  - England
TA  - Mol Med
JT  - Molecular medicine (Cambridge, Mass.)
JID - 9501023
RN  - 0 (Antigens, CD)
RN  - 0 (Cd151 protein, rat)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tetraspanin 24)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - EC 2.7.10.2 (Focal Adhesion Kinase 1)
RN  - EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases)
SB  - IM
MH  - Analysis of Variance
MH  - Animals
MH  - Antigens, CD/*genetics/metabolism
MH  - Dependovirus/genetics
MH  - Enzyme Activation
MH  - Focal Adhesion Kinase 1/*metabolism
MH  - Gene Transfer Techniques
MH  - Genetic Therapy/*methods
MH  - Heart/physiology
MH  - Male
MH  - Mitogen-Activated Protein Kinase Kinases/metabolism
MH  - Myocardial Infarction/*therapy
MH  - Neovascularization, Pathologic/genetics/therapy
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Recombinant Proteins/genetics/metabolism
MH  - Signal Transduction
MH  - Swine
MH  - Tetraspanin 24
PMC - PMC2710288
EDAT- 2009/07/16 09:00
MHDA- 2010/01/01 06:00
PMCR- 2009/09/01
CRDT- 2009/07/16 09:00
PHST- 2009/05/30 00:00 [received]
PHST- 2009/06/04 00:00 [accepted]
PHST- 2009/07/16 09:00 [entrez]
PHST- 2009/07/16 09:00 [pubmed]
PHST- 2010/01/01 06:00 [medline]
PHST- 2009/09/01 00:00 [pmc-release]
AID - 09_25_zuo [pii]
AID - 10.2119/molmed.2009.00025 [doi]
PST - ppublish
SO  - Mol Med. 2009 Sep-Oct;15(9-10):307-15. doi: 10.2119/molmed.2009.00025. Epub 2009 
      Jun 18.