Adipose tissue drives response to ischemia-reperfusion injury in a murine pressure sore model

Madeleine J. Gust; Seok Jong Hong; Robert C. Fang; Steven T. Lanier; Donald W. Buck; Jennifer M. Nuñez; Shengxian Jia; Eugene D. Park; Robert D. Galiano; Thomas A. Mustoe

doi:10.1097/PRS.0000000000003271

Adipose tissue drives response to ischemia-reperfusion injury in a murine pressure sore model

Madeleine J. Gust, Seok Jong Hong, Robert C. Fang, Steven T. Lanier, Donald W. Buck, Jennifer M. Nuñez, Shengxian Jia, Eugene D. Park, Robert D. Galiano, Thomas A. Mustoe

Department of Surgery

Research output: Contribution to journal › Article › peer-review

10 Scopus citations

Abstract

Background: Ischemia-reperfusion injury contributes significantly to the pathogenesis of chronic wounds such as pressure sores and diabetic foot ulcers. The authors' laboratory has previously developed a cyclical murine ischemia-reperfusion injury model. The authors here use this model to determine factors underlying tissue response to ischemia-reperfusion injury. Methods: C57BL/6 mice were subjected to cycles of ischemia-reperfusion that varied in number (one to four cycles) and duration of ischemia (1 to 2 hours). For each ischemia-reperfusion condition, the following variables were analyzed: (1) digital photographs for area of necrosis; (2) hematoxylin and eosin staining and immunohistochemistry for inflammatory infiltrate; and (3) expression of inflammatory markers by quantitative polymerase chain reaction. In addition, human adipocytes and fibroblasts were cultured in vitro under conditions of hypoxia and reoxygenation, and expression of inflammatory markers was analyzed by quantitative polymerase chain reaction. Results: Increases in both ischemia-reperfusion cycle number and ischemia duration correlated with increased areas of epithelial necrosis both grossly and histologically, and with an increase in cellularity and neutrophil density. This increased inflammatory infiltrate and a significant increase in the expression of proinflammatory markers (Hmox1, interleukin-6, interleukin-1, and monocyte chemoattractant protein-1) was observed in adipose tissue subjected to ischemia-reperfusion injury, but not in dermis. These results were mirrored in human adipose tissue. Conclusions: The authors further characterize a novel, reproducible murine model of ischemia-reperfusion injury. The results of their study indicate that adipose tissue is less tolerant of ischemia-reperfusion than dermal tissue. Rather than being an "innocent bystander," adipose tissue plays an active role in driving the inflammatory response to ischemia-reperfusion injury.

Original language	English
Pages (from-to)	1128e-1138e
Journal	Plastic and reconstructive surgery
Volume	139
Issue number	5
DOIs	https://doi.org/10.1097/PRS.0000000000003271
State	Published - May 1 2017

Access to Document

10.1097/PRS.0000000000003271

Cite this

@article{a3ff356d2328457c8c6d22196eb99919,

title = "Adipose tissue drives response to ischemia-reperfusion injury in a murine pressure sore model",

abstract = "Background: Ischemia-reperfusion injury contributes significantly to the pathogenesis of chronic wounds such as pressure sores and diabetic foot ulcers. The authors' laboratory has previously developed a cyclical murine ischemia-reperfusion injury model. The authors here use this model to determine factors underlying tissue response to ischemia-reperfusion injury. Methods: C57BL/6 mice were subjected to cycles of ischemia-reperfusion that varied in number (one to four cycles) and duration of ischemia (1 to 2 hours). For each ischemia-reperfusion condition, the following variables were analyzed: (1) digital photographs for area of necrosis; (2) hematoxylin and eosin staining and immunohistochemistry for inflammatory infiltrate; and (3) expression of inflammatory markers by quantitative polymerase chain reaction. In addition, human adipocytes and fibroblasts were cultured in vitro under conditions of hypoxia and reoxygenation, and expression of inflammatory markers was analyzed by quantitative polymerase chain reaction. Results: Increases in both ischemia-reperfusion cycle number and ischemia duration correlated with increased areas of epithelial necrosis both grossly and histologically, and with an increase in cellularity and neutrophil density. This increased inflammatory infiltrate and a significant increase in the expression of proinflammatory markers (Hmox1, interleukin-6, interleukin-1, and monocyte chemoattractant protein-1) was observed in adipose tissue subjected to ischemia-reperfusion injury, but not in dermis. These results were mirrored in human adipose tissue. Conclusions: The authors further characterize a novel, reproducible murine model of ischemia-reperfusion injury. The results of their study indicate that adipose tissue is less tolerant of ischemia-reperfusion than dermal tissue. Rather than being an {"}innocent bystander,{"} adipose tissue plays an active role in driving the inflammatory response to ischemia-reperfusion injury.",

author = "Gust, {Madeleine J.} and Hong, {Seok Jong} and Fang, {Robert C.} and Lanier, {Steven T.} and Buck, {Donald W.} and Nu{\~n}ez, {Jennifer M.} and Shengxian Jia and Park, {Eugene D.} and Galiano, {Robert D.} and Mustoe, {Thomas A.}",

note = "Publisher Copyright: Copyright {\textcopyright} 2017 by the American Society of Plastic Surgeons.",

year = "2017",

month = may,

day = "1",

doi = "10.1097/PRS.0000000000003271",

language = "English",

volume = "139",

pages = "1128e--1138e",

journal = "Plastic and reconstructive surgery",

issn = "0032-1052",

number = "5",

}

TY - JOUR

T1 - Adipose tissue drives response to ischemia-reperfusion injury in a murine pressure sore model

AU - Gust, Madeleine J.

AU - Hong, Seok Jong

AU - Fang, Robert C.

AU - Lanier, Steven T.

AU - Buck, Donald W.

AU - Nuñez, Jennifer M.

AU - Jia, Shengxian

AU - Park, Eugene D.

AU - Galiano, Robert D.

AU - Mustoe, Thomas A.

PY - 2017/5/1

Y1 - 2017/5/1

N2 - Background: Ischemia-reperfusion injury contributes significantly to the pathogenesis of chronic wounds such as pressure sores and diabetic foot ulcers. The authors' laboratory has previously developed a cyclical murine ischemia-reperfusion injury model. The authors here use this model to determine factors underlying tissue response to ischemia-reperfusion injury. Methods: C57BL/6 mice were subjected to cycles of ischemia-reperfusion that varied in number (one to four cycles) and duration of ischemia (1 to 2 hours). For each ischemia-reperfusion condition, the following variables were analyzed: (1) digital photographs for area of necrosis; (2) hematoxylin and eosin staining and immunohistochemistry for inflammatory infiltrate; and (3) expression of inflammatory markers by quantitative polymerase chain reaction. In addition, human adipocytes and fibroblasts were cultured in vitro under conditions of hypoxia and reoxygenation, and expression of inflammatory markers was analyzed by quantitative polymerase chain reaction. Results: Increases in both ischemia-reperfusion cycle number and ischemia duration correlated with increased areas of epithelial necrosis both grossly and histologically, and with an increase in cellularity and neutrophil density. This increased inflammatory infiltrate and a significant increase in the expression of proinflammatory markers (Hmox1, interleukin-6, interleukin-1, and monocyte chemoattractant protein-1) was observed in adipose tissue subjected to ischemia-reperfusion injury, but not in dermis. These results were mirrored in human adipose tissue. Conclusions: The authors further characterize a novel, reproducible murine model of ischemia-reperfusion injury. The results of their study indicate that adipose tissue is less tolerant of ischemia-reperfusion than dermal tissue. Rather than being an "innocent bystander," adipose tissue plays an active role in driving the inflammatory response to ischemia-reperfusion injury.

AB - Background: Ischemia-reperfusion injury contributes significantly to the pathogenesis of chronic wounds such as pressure sores and diabetic foot ulcers. The authors' laboratory has previously developed a cyclical murine ischemia-reperfusion injury model. The authors here use this model to determine factors underlying tissue response to ischemia-reperfusion injury. Methods: C57BL/6 mice were subjected to cycles of ischemia-reperfusion that varied in number (one to four cycles) and duration of ischemia (1 to 2 hours). For each ischemia-reperfusion condition, the following variables were analyzed: (1) digital photographs for area of necrosis; (2) hematoxylin and eosin staining and immunohistochemistry for inflammatory infiltrate; and (3) expression of inflammatory markers by quantitative polymerase chain reaction. In addition, human adipocytes and fibroblasts were cultured in vitro under conditions of hypoxia and reoxygenation, and expression of inflammatory markers was analyzed by quantitative polymerase chain reaction. Results: Increases in both ischemia-reperfusion cycle number and ischemia duration correlated with increased areas of epithelial necrosis both grossly and histologically, and with an increase in cellularity and neutrophil density. This increased inflammatory infiltrate and a significant increase in the expression of proinflammatory markers (Hmox1, interleukin-6, interleukin-1, and monocyte chemoattractant protein-1) was observed in adipose tissue subjected to ischemia-reperfusion injury, but not in dermis. These results were mirrored in human adipose tissue. Conclusions: The authors further characterize a novel, reproducible murine model of ischemia-reperfusion injury. The results of their study indicate that adipose tissue is less tolerant of ischemia-reperfusion than dermal tissue. Rather than being an "innocent bystander," adipose tissue plays an active role in driving the inflammatory response to ischemia-reperfusion injury.

UR - http://www.scopus.com/inward/record.url?scp=85020259513&partnerID=8YFLogxK

U2 - 10.1097/PRS.0000000000003271

DO - 10.1097/PRS.0000000000003271

M3 - Article

C2 - 28445367

AN - SCOPUS:85020259513

SN - 0032-1052

VL - 139

SP - 1128e-1138e

JO - Plastic and reconstructive surgery

JF - Plastic and reconstructive surgery

IS - 5

ER -

Adipose tissue drives response to ischemia-reperfusion injury in a murine pressure sore model

Abstract

Access to Document

Other files and links

Fingerprint

Cite this