title: uPARAP function in cutaneous wound repair.
abstract: Optimal skin wound healing relies on tight balance between collagen synthesis and degradation in new tissue formation and remodeling phases. The endocytic receptor uPARAP regulates collagen uptake and intracellular degradation. In this study we examined cutaneous wound repair response of uPARAP null (uPARAP-/-) mice. Full thickness wounds were created on dorsal surface of uPARAP-/- or their wildtype littermates. Wound healing evaluation was done by macroscopic observation, histology, gene transcription and biochemical analysis at specific intervals. We found that absence of uPARAP delayed re-epithelialization during wound closure, and altered stiffness of the scar tissue. Despite the absence of the uPARAP-mediated intracellular pathway for collagen degradation, there was no difference in total collagen content of the wounds in uPARAP-/- compared to wildtype mice. This suggests in the absence of uPARAP, a compensatory feedback mechanism functions to keep net collagen in balance.
authors.affiliation: Center for Lung Biology, Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Washington, Seattle, Washington, United States of America.
authors.forename: Maryam G
authors.initials: MG
authors.lastname: Rohani
authors.affiliation: Center for Lung Biology, Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Washington, Seattle, Washington, United States of America.
authors.forename: Yu-Hua
authors.initials: YH
authors.lastname: Chow
authors.affiliation: Department of Bioengineering, University of Washington, Seattle, Washington, United States of America.
authors.forename: Maria V
authors.initials: MV
authors.lastname: Razumova
authors.affiliation: Center for Lung Biology, Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Washington, Seattle, Washington, United States of America.
authors.forename: Samuel
authors.initials: S
authors.lastname: Ash
authors.affiliation: Center for Lung Biology, Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Washington, Seattle, Washington, United States of America.
authors.forename: Chi F
authors.initials: CF
authors.lastname: Hung
authors.affiliation: Center for Lung Biology, Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Washington, Seattle, Washington, United States of America.
authors.forename: Lynn M
authors.initials: LM
authors.lastname: Schnapp
mesh_terms: D000818:Animals; D001696:Biomechanical Phenomena; D003094:Collagen / Q000378:metabolism; D004847:Epithelial Cells / Q000166:cytology; D005786:Gene Expression Regulation; D008562:Membrane Glycoproteins / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D011956:Receptors, Cell Surface / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D012867:Skin / Q000166:cytology / Q000378:metabolism*; D012879:Skin Physiological Phenomena; D014945:Wound Healing
chemical_list: D008562:Membrane Glycoproteins; C474081:Mrc2 protein, mouse; D011956:Receptors, Cell Surface; D003094:Collagen