title: 12/15-Lipoxygenase deficiency reduces densities of mesenchymal stem cells in the dermis of wounded and unwounded skin.
abstract: BACKGROUND
  Mesenchymal stem cells (MSCs) promote skin healing. 12/15-Lipoxgenase (LOX) is crucial in producing specific lipid mediators in wounded skin. The consequences of 12/15-LOX deficiency in MSC densities in skin are unknown.
  
  
  OBJECTIVE
  To determine the effect of 12/15-LOX deficiency in MSC densities in wounded and unwounded dermis.
  
  
  METHODS
  Full-thickness skin incisional wounds were made to 12/15-LOX-deficient (12/15-LOX(-/-) ) and wild-type (WT) C57BL/6 mice. Wounded skin was collected at 3, 8, or 14 days postwounding (dpw). MSCs were analysed in skin sections using histology. 12S- or 15S-hydroxy-eicosatetraenoic acid (HETE) was analysed using a reversed-phase Chiral liquid chromatography-ultraviolet-tandem mass spectrometer.
  
  
  RESULTS
  There were more stem cell antigen (Sca)1(+) CD29(+) MSCs (cells/field) at 3, 8, and 14 dpw, more Sca1(+) CD106(+) MSCs at 3 and 14 dpw in the wounded dermis, more MSCs in unwounded dermis of WT mice compared with 12/15-LOX(-/-) mice, and more MSCs in the wounded dermis than in the unwounded dermis. For 12/15-LOX(-/-) dermis, Sca1(+) CD106(+) MSCs peaked and Sca1(+) CD29(+) MSCs reached a flat level at 8 dpw. However, for the WT dermis, MSCs increased from 8 to 14 dpw. There were more Sca1(+) CD106(+) MSCs than Sca1(+) CD29(+) MSCs in the 12/15-LOX(-/-) wounded dermis at 8 dpw. However, there were more Sca1(+) CD29(+) MSCs in the 12/15-LOX(-/-) than Sca1(+) CD106(+) MSCs in the WT wounded dermis at 3 dpw, and Sca1(+) CD106(+) MSCs and Sca1(+) CD29(+) MSCs were at comparable levels in other conditions. 12/15-LOX deficiency suppressed levels of 12/15-LOX protein and their products, 12S-HETE and 15S-HETE, in wounds.
  
  
  CONCLUSIONS
  12/15-LOX deficiency reduces MSC densities in the dermis, which correlates with the suppressed 12/15-LOX pathways in wounded and unwounded skin.
authors.affiliation: Center of Neuroscience Excellence, Louisiana State University Health Science Center, New Orleans, LA 70112.
authors.forename: S
authors.initials: S
authors.lastname: Hong
authors.affiliation: Center of Neuroscience Excellence, Louisiana State University Health Science Center, New Orleans, LA 70112.
authors.forename: B V
authors.initials: BV
authors.lastname: Alapure
authors.affiliation: Center of Neuroscience Excellence, Louisiana State University Health Science Center, New Orleans, LA 70112.
authors.forename: Y
authors.initials: Y
authors.lastname: Lu
authors.affiliation: Center of Neuroscience Excellence, Louisiana State University Health Science Center, New Orleans, LA 70112.
authors.forename: H
authors.initials: H
authors.lastname: Tian
authors.affiliation: Center of Neuroscience Excellence, Louisiana State University Health Science Center, New Orleans, LA 70112.
authors.forename: Q
authors.initials: Q
authors.lastname: Wang
mesh_terms: D000818:Animals; D001092:Arachidonate 12-Lipoxygenase / Q000172:deficiency*; D001093:Arachidonate 15-Lipoxygenase / Q000172:deficiency*; D002452:Cell Count; D020405:Dermis / Q000166:cytology*; D059630:Mesenchymal Stem Cells / Q000201:enzymology*; D008810:Mice, Inbred C57BL; D012867:Skin / Q000293:injuries*; D014945:Wound Healing / Q000502:physiology
chemical_list: C475064:12-15-lipoxygenase; D001092:Arachidonate 12-Lipoxygenase; D001093:Arachidonate 15-Lipoxygenase