PMID- 23729446
OWN - NLM
STAT- MEDLINE
DCOM- 20130916
LR  - 20211021
IS  - 1550-6606 (Electronic)
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 191
IP  - 1
DP  - 2013 Jul 1
TI  - Myeloid hypoxia-inducible factor-1alpha is essential for skeletal muscle regeneration 
      in mice.
PG  - 407-14
LID - 10.4049/jimmunol.1103779 [doi]
AB  - The outstanding regeneration ability of skeletal muscle is based on stem cells 
      that become activated and develop to myoblasts after myotrauma. Proliferation and 
      growth of myoblasts result in self-renewal of skeletal muscle. In this article, 
      we show that myotrauma causes a hypoxic microenvironment leading to accumulation 
      of the transcription factor hypoxia-inducible factor-1 (HIF-1) in skeletal muscle 
      cells, as well as invading myeloid cells. To evaluate the impact of HIF-1 in 
      skeletal muscle injury and repair, we examined mice with a conditional HIF-1alpha 
      knockout targeted to skeletal muscle or myeloid cells in a model of soft tissue 
      trauma. No differences in acute trauma size were detected between control and 
      HIF-1alpha knockout mice. However, muscles of myeloid HIF-1alpha knockout mice showed a 
      significant delay in myoblast proliferation and growth of regenerating myofibers, 
      in association with decreased expression of cyclooxygenase-2 in HIF-1alpha-deficient 
      myeloid cells. Moreover, the removal of necrotic cell debris and the regeneration 
      of endothelial cell structure were impaired in myeloid HIF-1alpha knockout mice that 
      showed delayed invasion of macrophages to the injury site. Our findings for the 
      first time, to our knowledge, demonstrate that myeloid HIF-1alpha is required for 
      adequate skeletal muscle regeneration.
FAU - Scheerer, Nina
AU  - Scheerer N
AD  - Institut fur Physiologie, Universitat Duisburg-Essen, D-45122 Essen, Germany.
FAU - Dehne, Nathalie
AU  - Dehne N
FAU - Stockmann, Christian
AU  - Stockmann C
FAU - Swoboda, Sandra
AU  - Swoboda S
FAU - Baba, Hideo A
AU  - Baba HA
FAU - Neugebauer, Agnes
AU  - Neugebauer A
FAU - Johnson, Randall S
AU  - Johnson RS
FAU - Fandrey, Joachim
AU  - Fandrey J
LA  - eng
GR  - 092738/Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130531
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Hif1a protein, mouse)
RN  - 0 (Hypoxia-Inducible Factor 1, alpha Subunit)
SB  - IM
MH  - Animals
MH  - Down-Regulation/genetics/*immunology
MH  - Hindlimb
MH  - Hypoxia-Inducible Factor 1, alpha Subunit/deficiency/genetics/*physiology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Mice, Transgenic
MH  - Muscle, Skeletal/cytology/*immunology
MH  - Myeloid Cells/*immunology/metabolism/pathology
MH  - Myoblasts, Skeletal/immunology/metabolism/pathology
MH  - Regeneration/genetics/*immunology
MH  - Up-Regulation/genetics/*immunology
MH  - Wound Healing/genetics/immunology
PMC - PMC6614040
MID - EMS83459
COIS- Disclosures The authors have no financial conflicts of interest.
EDAT- 2013/06/05 06:00
MHDA- 2013/09/17 06:00
PMCR- 2019/07/08
CRDT- 2013/06/05 06:00
PHST- 2013/06/05 06:00 [entrez]
PHST- 2013/06/05 06:00 [pubmed]
PHST- 2013/09/17 06:00 [medline]
PHST- 2019/07/08 00:00 [pmc-release]
AID - jimmunol.1103779 [pii]
AID - 10.4049/jimmunol.1103779 [doi]
PST - ppublish
SO  - J Immunol. 2013 Jul 1;191(1):407-14. doi: 10.4049/jimmunol.1103779. Epub 2013 May 
      31.