PMID- 25799225
OWN - NLM
STAT- MEDLINE
DCOM- 20151221
LR  - 20181113
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 10
IP  - 3
DP  - 2015
TI  - Brain derived neurotrophic factor contributes to the cardiogenic potential of 
      adult resident progenitor cells in failing murine heart.
PG  - e0120360
LID - 10.1371/journal.pone.0120360 [doi]
LID - e0120360
AB  - AIMS: Resident cardiac progenitor cells show homing properties when injected into 
      the injured but not to the healthy myocardium. The molecular background behind 
      this difference in behavior needs to be studied to elucidate how adult progenitor 
      cells can restore cardiac function of the damaged myocardium. Since the brain 
      derived neurotrophic factor (BDNF) moderates cardioprotection in injured hearts, 
      we focused on delineating its regulatory role in the damaged myocardium. METHODS 
      AND RESULTS: Comparative gene expression profiling of freshly isolated 
      undifferentiated Sca-1 progenitor cells derived either from heart failure 
      transgenic alphaMHC-CyclinT1/Galphaq overexpressing mice or wildtype littermates revealed 
      transcriptional variations. Bdnf expression was up regulated 5-fold during heart 
      failure which was verified by qRT-PCR and confirmed at protein level. The 
      migratory capacity of Sca-1 cells from transgenic hearts was improved by 15% in 
      the presence of 25 ng/ml BDNF. Furthermore, BDNF-mediated effects on Sca-1 cells 
      were studied via pulsed Stable Isotope Labeling of Amino acids in Cell Culture 
      (pSILAC) proteomics approach. After BDNF treatment significant differences 
      between newly synthesized proteins in Sca-1 cells from control and transgenic 
      hearts were observed for CDK1, SRRT, HDGF, and MAP2K3 which are known to regulate 
      cell cycle, survival and differentiation. Moreover BDNF repressed the 
      proliferation of Sca-1 cells from transgenic hearts. CONCLUSION: Comparative 
      profiling of resident Sca-1 cells revealed elevated BDNF levels in the failing 
      heart. Exogenous BDNF (i) stimulated migration, which might improve the homing 
      ability of Sca-1 cells derived from the failing heart and (ii) repressed the cell 
      cycle progression suggesting its potency to ameliorate heart failure.
FAU - Samal, Rasmita
AU  - Samal R
AD  - Department of Internal Medicine B, University Medicine Greifswald, Greifswald, 
      Germany; Interfaculty Institute for Genetics and Functional Genomics, University 
      Medicine Greifswald, Greifswald, Germany.
FAU - Ameling, Sabine
AU  - Ameling S
AD  - Interfaculty Institute for Genetics and Functional Genomics, University Medicine 
      Greifswald, Greifswald, Germany.
FAU - Dhople, Vishnu
AU  - Dhople V
AD  - Interfaculty Institute for Genetics and Functional Genomics, University Medicine 
      Greifswald, Greifswald, Germany.
FAU - Sappa, Praveen Kumar
AU  - Sappa PK
AD  - Interfaculty Institute for Genetics and Functional Genomics, University Medicine 
      Greifswald, Greifswald, Germany.
FAU - Wenzel, Kristin
AU  - Wenzel K
AD  - Department of Internal Medicine B, University Medicine Greifswald, Greifswald, 
      Germany; DZHK (German Center for Cardiovascular Research) partner site, 
      Greifswald, Germany.
FAU - Volker, Uwe
AU  - Volker U
AD  - Interfaculty Institute for Genetics and Functional Genomics, University Medicine 
      Greifswald, Greifswald, Germany; DZHK (German Center for Cardiovascular Research) 
      partner site, Greifswald, Germany.
FAU - Felix, Stephan B
AU  - Felix SB
AD  - Department of Internal Medicine B, University Medicine Greifswald, Greifswald, 
      Germany; DZHK (German Center for Cardiovascular Research) partner site, 
      Greifswald, Germany.
FAU - Hammer, Elke
AU  - Hammer E
AD  - Interfaculty Institute for Genetics and Functional Genomics, University Medicine 
      Greifswald, Greifswald, Germany; DZHK (German Center for Cardiovascular Research) 
      partner site, Greifswald, Germany.
FAU - Konemann, Stephanie
AU  - Konemann S
AD  - Department of Internal Medicine B, University Medicine Greifswald, Greifswald, 
      Germany; DZHK (German Center for Cardiovascular Research) partner site, 
      Greifswald, Germany.
LA  - eng
SI  - GEO/GSE58577
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150323
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Antigens, Ly)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Ly6a protein, mouse)
RN  - 0 (Membrane Proteins)
SB  - IM
MH  - Adult Stem Cells/cytology/*metabolism/physiology
MH  - Animals
MH  - Antigens, Ly/genetics/metabolism
MH  - Brain-Derived Neurotrophic Factor/genetics/*metabolism
MH  - *Cell Differentiation
MH  - Cell Movement
MH  - Cell Proliferation
MH  - Cells, Cultured
MH  - Heart Failure/*metabolism
MH  - Human Umbilical Vein Endothelial Cells/metabolism
MH  - Humans
MH  - Membrane Proteins/genetics/metabolism
MH  - Mice
MH  - Myocytes, Cardiac/cytology/metabolism/physiology
PMC - PMC4370398
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2015/03/24 06:00
MHDA- 2015/12/22 06:00
PMCR- 2015/03/23
CRDT- 2015/03/24 06:00
PHST- 2014/11/18 00:00 [received]
PHST- 2015/02/05 00:00 [accepted]
PHST- 2015/03/24 06:00 [entrez]
PHST- 2015/03/24 06:00 [pubmed]
PHST- 2015/12/22 06:00 [medline]
PHST- 2015/03/23 00:00 [pmc-release]
AID - PONE-D-14-51149 [pii]
AID - 10.1371/journal.pone.0120360 [doi]
PST - epublish
SO  - PLoS One. 2015 Mar 23;10(3):e0120360. doi: 10.1371/journal.pone.0120360. 
      eCollection 2015.