Increased oxygen tension attenuates acute ultraviolet-B-induced skin angiogenesis and wrinkle formation.
Acute ultraviolet (UV)-B irradiation causes skin wrinkle formation associated with hyperplasia of cutaneous blood vessels. This study reports that increased dermal oxygen tension attenuates acute UVB-induced angiogenesis and wrinkle formation. Twenty-four hairless mice (HOS:HR-1) were assigned to 3 groups: 1) control group, 2) UVB-irradiated (UVB) group, and 3) UVB-irradiated and hyperoxia-exposed (UVB+HO) group. The backs of the mice were exposed to UVB irradiation 3 times per week for a 5-wk period. To increase dermal oxygen tension, the mice were exposed to hyperoxia (90% oxygen) for 2 h immediately after each UVB irradiation. Hyperoxic exposure increased dermal oxygen tension by about 10 times compared with the control level. Degree of wrinkle formation and epidermal thickness increased significantly after a 5-wk UVB-irradiation period, whereas hyperoxic exposure attenuated these increases. Tissue adenosine triphosphate concentration and angiogenesis increased significantly only in the UVB group compared with the control group. Although the expression of hypoxia inducible factor-1alpha mRNA, a key molecule for angiogenesis, increased significantly in the UVB and UVB+HO groups compared with the control group, the protein level increased significantly only in the UVB group. The activity of matrix metalloproteinase-2 and -9, critical molecules for angiogenesis, did not increase in the UVB and UVB+HO groups compared with the control group. Active type 1 collagenase activity and soluble collagen content in all of the groups were roughly similar. These results suggest that increased dermal oxygen tension attenuates angiogenesis and wrinkle formation following acute UVB irradiation.
Kawada
Shigeo
S
Laboratory of Tissue Plasticity Science, Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, Tokyo, Japan. kawada@idaten.c.u-tokyo.ac.jp
Ohtani
Masaru
M
Ishii
Naokata
N
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003094:Collagen / Q000378:metabolism; D004195:Disease Models, Animal; D005786:Gene Expression Regulation / Q000528:radiation effects; D018496:Hyperoxia / Q000378:metabolism* / Q000503:physiopathology; D006965:Hyperplasia; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000235:genetics; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D051379:Mice; D008812:Mice, Hairless; D009389:Neovascularization, Pathologic / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D010100:Oxygen / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D012867:Skin / Q000098:blood supply / Q000378:metabolism / Q000473:pathology / Q000528:radiation effects*; D015595:Skin Aging / Q000473:pathology / Q000528:radiation effects*; D014466:Ultraviolet Rays; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
C497443:Hif1a protein, mouse; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D012333:RNA, Messenger; D042461:Vascular Endothelial Growth Factor A; C467480:vascular endothelial growth factor A, mouse; D000255:Adenosine Triphosphate; D003094:Collagen; D020778:Matrix Metalloproteinase 2; C522362:Mmp2 protein, mouse; D020780:Matrix Metalloproteinase 9; C501830:Mmp9 protein, mouse; D010100:Oxygen