The effects of the plasminogen pathway on scar tissue formation.
OBJECTIVE
The authors sought to determine the role of the plasminogen pathway in wound healing. They hypothesized that decreased fibrin degradation may lead to increased collagen deposition. Presuming that the degree of histopathological abnormality correlates with the aesthetic appearance of the scar, we conducted a study that attempted to determine the histopathological appearance of scar tissue in mice with and without impaired function of the plasminogen pathway.


METHODS
Mice with and without deficiencies in the plasminogen pathway underwent surgery. The role of the plasminogen pathway in wound healing was studied by analysis of scar tissue formation using the methods described.


METHODS
A 2-cm incision was made on the dorsum of mice with and without specified genetic deficiencies in the plasminogen pathway. After the animals were killed, the tissue was harvested, fixed, and prepared using hematoxylin and eosin as well as trichrome stains. Histopathological analysis and scoring were performed by two separate investigators in a blinded manner. Student's t test was used to determine statistical significance between groups.


RESULTS
A statistically significant difference in collagen orientation was noted between mice with impaired plasminogen pathway function and the wild-type (control) group (P =.0163). A statistical trend toward improved wound healing for plasminogen-deficient mice was found for overall histomorphological score (P =.0706).


CONCLUSIONS
The role of the plasminogen pathway in wound healing is one that should be noted and may lead to the development of new therapies that reduce scar tissue formation. Hence, the role of other thrombolytic and anti-thrombolytic agents in wound healing should be further investigated to precisely identify agents that play the most significant role in scar tissue formation.
Samara
Ghassan J
GJ
Division of Otolaryngology-Head and Neck Surgery, Department of Surgery, University Hospital and Medical Center, School of Medicine, State University of NewYork at Stony Brook, 11794-8191, USA. samara@notes.cc.sunysb.edu
Schaffner
Adam D
AD
Eisenstat
Jonathan
J
Nguyen
Hoang-Lan T
HL
D000818:Animals; D002921:Cicatrix / Q000378:metabolism*; D003094:Collagen / Q000378:metabolism; D005337:Fibrin / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010959:Tissue Plasminogen Activator / Q000502:physiology*; D014945:Wound Healing / Q000502:physiology*
D005337:Fibrin; D003094:Collagen; D010959:Tissue Plasminogen Activator