PMID- 17174868
OWN - NLM
STAT- MEDLINE
DCOM- 20070315
LR  - 20141120
IS  - 1553-8389 (Print)
IS  - 1878-0938 (Linking)
VI  - 7
IP  - 4
DP  - 2006 Oct-Dec
TI  - Bone marrow-derived stem cell interactions with adult cardiomyocytes and skeletal 
      myoblasts in vitro.
PG  - 222-30
AB  - BACKGROUND AND OBJECTIVES: Secreted growth factors and cell-to-cell contact are 
      both required to elicit cellular functions. We tested the hypothesis that 
      bone-marrow-derived growth factors, together with cell-to-cell contact between 
      bone-marrow-derived stem cells and cardiomyocytes or myoblasts, promote the 
      proliferation of cardiomyocytes and myoblasts. METHODS: Human cardiomyocytes or 
      skeletal myoblasts were cultured for 4 days in the presence of low and high 
      concentrations of bone-marrow-derived mononuclear cell conditioned medium 
      (MNC-CM) or marrow stromal cell conditioned medium (MSC-CM). The concentrations 
      of vascular endothelial growth factor (VEGF), monocyte chemoattractant protein-1 
      (MCP-1), hepatocyte growth factor (HGF), and insulin-like growth factor-1 in 
      their respective conditioned media were assayed by enzyme-linked immunosorbent 
      assay. Stem cells were mixed with cardiomyocytes or skeletal myoblasts at a 1:1 
      ratio and cultured for 7 days to assess the proliferation of these cells. In 
      parallel experiments, equal numbers of various cell types were cultured alone. 
      RESULTS: The concentrations of VEGF, MCP-1, and HGF increased in MNC-CM and 
      MSC-CM. MNC-CM showed no effect on cardiomyocyte proliferation. A low 
      concentration of MSC-CM increased cardiomyocyte proliferation by 60% (P<.05). Low 
      concentrations of MNC-CM or MSC-CM showed a trend toward an increased 
      proliferation of myoblasts. A high concentration of either conditioned medium 
      showed a toxic effect. In contact coculture, the proliferation of cardiomyocytes 
      and MNC showed no synergistic effect; instead, there was some evidence of 
      inhibition. The proliferation of cardiomyocytes and stromal cells showed an 
      additive effect. Myoblasts in contact coculture with MNC or MSC showed no 
      synergistic effect. CONCLUSION: These in vitro results suggest that paracrine 
      effects may be the mechanism by which stromal cells become beneficial in cardiac 
      therapy. MNC do not induce the proliferation of cardiomyocytes. 
      Stem-cell-secreted growth factors induce the proliferation of myoblasts, which is 
      not influenced by cell-to-cell contact.
FAU - Baffour, Richard
AU  - Baffour R
AD  - Division of Cardiology, Washington Hospital Center, Washington, DC 20010, USA.
FAU - Pakala, Rajbabu
AU  - Pakala R
FAU - Hellinga, David
AU  - Hellinga D
FAU - Joner, Michael
AU  - Joner M
FAU - Okubagzi, Petros
AU  - Okubagzi P
FAU - Epstein, Stephen E
AU  - Epstein SE
FAU - Waksman, Ron
AU  - Waksman R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cardiovasc Revasc Med
JT  - Cardiovascular revascularization medicine : including molecular interventions
JID - 101238551
RN  - 0 (Chemokine CCL2)
RN  - 0 (IGFBP1 protein, human)
RN  - 0 (Insulin-Like Growth Factor Binding Protein 1)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 67256-21-7 (Hepatocyte Growth Factor)
SB  - IM
MH  - Analysis of Variance
MH  - Bone Marrow Cells/*metabolism
MH  - Cells, Cultured
MH  - Chemokine CCL2/metabolism
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Hepatocyte Growth Factor/metabolism
MH  - Humans
MH  - In Vitro Techniques
MH  - Insulin-Like Growth Factor Binding Protein 1/metabolism
MH  - Myoblasts, Skeletal/metabolism/*physiology
MH  - Myocytes, Cardiac/metabolism/*physiology
MH  - Stem Cells/*metabolism
MH  - Vascular Endothelial Growth Factor A/metabolism
EDAT- 2006/12/19 09:00
MHDA- 2007/03/16 09:00
CRDT- 2006/12/19 09:00
PHST- 2006/06/28 00:00 [received]
PHST- 2006/06/28 00:00 [accepted]
PHST- 2006/12/19 09:00 [pubmed]
PHST- 2007/03/16 09:00 [medline]
PHST- 2006/12/19 09:00 [entrez]
AID - S1553-8389(06)00181-3 [pii]
AID - 10.1016/j.carrev.2006.06.005 [doi]
PST - ppublish
SO  - Cardiovasc Revasc Med. 2006 Oct-Dec;7(4):222-30. doi: 
      10.1016/j.carrev.2006.06.005.