TY - JOUR
T1 - Effects of combined radiation and burn injury on the rennin-angiotensin system
AU - Jadhav, Sachin S.
AU - Sharma, Natasha
AU - Meeks, Christopher J.
AU - Mordwinkin, Nicholas M.
AU - Espinoza, Theresa B.
AU - Roda, Norma R.
AU - Dizerega, Gere S.
AU - Hill, Colin K.
AU - Louie, Stan G.
AU - Rodgers, Kathleen E.
PY - 2013/1
Y1 - 2013/1
N2 - The renin-angiotensin system (RAS) plays an important role in wound repair; however, little is known pertaining to RAS expression in response to thermal injury and the combination of radiation plus burn injury (CRBI). The purpose of this study was to test the hypothesis that thermal injury modifies expression of RAS components and CRBI delayed this up-regulation of RAS. Skin from uninjured mice was compared with mice receiving local thermal injury or CRBI (injury site). Skin was analyzed for gene and protein expression of RAS components. There was an initial increase in the expression of various components of RAS following thermal injury. However, in the higher CRBI group there is an initial decrease in AT1b (vasoconstriction, pro-proliferative), AT 2 (vasodilation, differentiation), and Mas (vasodilation, anti-inflammatory) gene expression. This corresponded with a delay and decrease in AT1, AT2, and MAS protein expression in fibroblasts and keratinocytes. The reduction in RAS receptor positive fibroblasts and keratinocytes correlated with a reduction in collagen deposition and keratinocyte infiltration into the wounded area resulting in a delay of reepithelialization following CRBI. These data support the hypothesis that delayed wound healing observed in subjects following radiation exposure may be in part due to decreased expression of RAS.
AB - The renin-angiotensin system (RAS) plays an important role in wound repair; however, little is known pertaining to RAS expression in response to thermal injury and the combination of radiation plus burn injury (CRBI). The purpose of this study was to test the hypothesis that thermal injury modifies expression of RAS components and CRBI delayed this up-regulation of RAS. Skin from uninjured mice was compared with mice receiving local thermal injury or CRBI (injury site). Skin was analyzed for gene and protein expression of RAS components. There was an initial increase in the expression of various components of RAS following thermal injury. However, in the higher CRBI group there is an initial decrease in AT1b (vasoconstriction, pro-proliferative), AT 2 (vasodilation, differentiation), and Mas (vasodilation, anti-inflammatory) gene expression. This corresponded with a delay and decrease in AT1, AT2, and MAS protein expression in fibroblasts and keratinocytes. The reduction in RAS receptor positive fibroblasts and keratinocytes correlated with a reduction in collagen deposition and keratinocyte infiltration into the wounded area resulting in a delay of reepithelialization following CRBI. These data support the hypothesis that delayed wound healing observed in subjects following radiation exposure may be in part due to decreased expression of RAS.
UR - http://www.scopus.com/inward/record.url?scp=84872102318&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84872102318&partnerID=8YFLogxK
U2 - 10.1111/j.1524-475X.2012.00867.x
DO - 10.1111/j.1524-475X.2012.00867.x
M3 - Article
C2 - 23231670
AN - SCOPUS:84872102318
SN - 1067-1927
VL - 21
SP - 131
EP - 140
JO - Wound Repair and Regeneration
JF - Wound Repair and Regeneration
IS - 1
ER -