Autologous transplantation of endothelial progenitor cells attenuates acute lung injury in rabbits

Chen Fuh Lam, Yen-Chin Liu, Jen Kuo Hsu, Pei An Yeh, Ting Ya Su, Chien Chi Huang, Ming Wei Lin, Ping-Ching Wu, Pei Jung Chang, Yu-Chuan Tsai

研究成果: Article

69 引文 (Scopus)

摘要

BACKGROUND: Acute lung injury (ALI) and end-stage acute respiratory distress syndrome (ARDS) are among the most common causes of death in intensive care units. Activation and damage of pulmonary endothelium is the hallmark of ALI/ARDS. Recent studies have demonstrated the importance of circulating endothelial progenitor cells (EPCs) in maintaining normal endothelial function as well as endothelial repairing after vascular injury. Here, the authors present the first study demonstrating the therapeutic potential of EPCs in a rabbit model of ALI/ARDS. METHODS: Circulating EPCs were obtained from rabbits using Ficoll centrifugation. One week after culturing, ALI was induced in rabbits by oleic acid (75 mg/kg, intravenous), and autologous EPCs were transplanted intravenously. Vasomotor function of isolated pulmonary artery and degrees of lung injury were assessed 2 days later. RESULTS: Endothelial dysfunction in the pulmonary artery was significantly attenuated in rabbits treated with EPCs, whereas the endothelium-independent relaxation responses were not different. Expression of inducible nitric oxide synthase was suppressed in the pulmonary artery of EPC-treated animals. Infiltration of leukocytes in the lung parenchyma was significantly reduced after EPC transplantation. EPCs also decreased water content, hyaline membrane formation, and hemorrhage in lungs. CONCLUSION: The authors demonstrated that autologous transplantation of EPCs preserves pulmonary endothelial function and maintains the integrity of pulmonary alveolar-capillary barrier. Transplantation of EPCs can be a novel cell-based, endothelium-targeted therapeutic strategy for prevention and treatment of ALI/ARDS.

原文English
頁(從 - 到)392-401
頁數10
期刊Anesthesiology
108
發行號3
DOIs
出版狀態Published - 2008 一月 1

指紋

Autologous Transplantation
Acute Lung Injury
Rabbits
Adult Respiratory Distress Syndrome
Lung
Pulmonary Artery
Endothelium
Endothelial Progenitor Cells
Ficoll
Hyalin
Vascular System Injuries
Cell Transplantation
Lung Injury
Nitric Oxide Synthase Type II
Oleic Acid
Centrifugation
Intensive Care Units
Cause of Death
Leukocytes
Therapeutics

All Science Journal Classification (ASJC) codes

  • Anesthesiology and Pain Medicine

引用此文

Lam, Chen Fuh ; Liu, Yen-Chin ; Hsu, Jen Kuo ; Yeh, Pei An ; Su, Ting Ya ; Huang, Chien Chi ; Lin, Ming Wei ; Wu, Ping-Ching ; Chang, Pei Jung ; Tsai, Yu-Chuan. / Autologous transplantation of endothelial progenitor cells attenuates acute lung injury in rabbits. 於: Anesthesiology. 2008 ; 卷 108, 編號 3. 頁 392-401.
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title = "Autologous transplantation of endothelial progenitor cells attenuates acute lung injury in rabbits",
abstract = "BACKGROUND: Acute lung injury (ALI) and end-stage acute respiratory distress syndrome (ARDS) are among the most common causes of death in intensive care units. Activation and damage of pulmonary endothelium is the hallmark of ALI/ARDS. Recent studies have demonstrated the importance of circulating endothelial progenitor cells (EPCs) in maintaining normal endothelial function as well as endothelial repairing after vascular injury. Here, the authors present the first study demonstrating the therapeutic potential of EPCs in a rabbit model of ALI/ARDS. METHODS: Circulating EPCs were obtained from rabbits using Ficoll centrifugation. One week after culturing, ALI was induced in rabbits by oleic acid (75 mg/kg, intravenous), and autologous EPCs were transplanted intravenously. Vasomotor function of isolated pulmonary artery and degrees of lung injury were assessed 2 days later. RESULTS: Endothelial dysfunction in the pulmonary artery was significantly attenuated in rabbits treated with EPCs, whereas the endothelium-independent relaxation responses were not different. Expression of inducible nitric oxide synthase was suppressed in the pulmonary artery of EPC-treated animals. Infiltration of leukocytes in the lung parenchyma was significantly reduced after EPC transplantation. EPCs also decreased water content, hyaline membrane formation, and hemorrhage in lungs. CONCLUSION: The authors demonstrated that autologous transplantation of EPCs preserves pulmonary endothelial function and maintains the integrity of pulmonary alveolar-capillary barrier. Transplantation of EPCs can be a novel cell-based, endothelium-targeted therapeutic strategy for prevention and treatment of ALI/ARDS.",
author = "Lam, {Chen Fuh} and Yen-Chin Liu and Hsu, {Jen Kuo} and Yeh, {Pei An} and Su, {Ting Ya} and Huang, {Chien Chi} and Lin, {Ming Wei} and Ping-Ching Wu and Chang, {Pei Jung} and Yu-Chuan Tsai",
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Lam, CF, Liu, Y-C, Hsu, JK, Yeh, PA, Su, TY, Huang, CC, Lin, MW, Wu, P-C, Chang, PJ & Tsai, Y-C 2008, 'Autologous transplantation of endothelial progenitor cells attenuates acute lung injury in rabbits', Anesthesiology, 卷 108, 編號 3, 頁 392-401. https://doi.org/10.1097/ALN.0b013e318164ca64

Autologous transplantation of endothelial progenitor cells attenuates acute lung injury in rabbits. / Lam, Chen Fuh; Liu, Yen-Chin; Hsu, Jen Kuo; Yeh, Pei An; Su, Ting Ya; Huang, Chien Chi; Lin, Ming Wei; Wu, Ping-Ching; Chang, Pei Jung; Tsai, Yu-Chuan.

於: Anesthesiology, 卷 108, 編號 3, 01.01.2008, p. 392-401.

研究成果: Article

TY - JOUR

T1 - Autologous transplantation of endothelial progenitor cells attenuates acute lung injury in rabbits

AU - Lam, Chen Fuh

AU - Liu, Yen-Chin

AU - Hsu, Jen Kuo

AU - Yeh, Pei An

AU - Su, Ting Ya

AU - Huang, Chien Chi

AU - Lin, Ming Wei

AU - Wu, Ping-Ching

AU - Chang, Pei Jung

AU - Tsai, Yu-Chuan

PY - 2008/1/1

Y1 - 2008/1/1

N2 - BACKGROUND: Acute lung injury (ALI) and end-stage acute respiratory distress syndrome (ARDS) are among the most common causes of death in intensive care units. Activation and damage of pulmonary endothelium is the hallmark of ALI/ARDS. Recent studies have demonstrated the importance of circulating endothelial progenitor cells (EPCs) in maintaining normal endothelial function as well as endothelial repairing after vascular injury. Here, the authors present the first study demonstrating the therapeutic potential of EPCs in a rabbit model of ALI/ARDS. METHODS: Circulating EPCs were obtained from rabbits using Ficoll centrifugation. One week after culturing, ALI was induced in rabbits by oleic acid (75 mg/kg, intravenous), and autologous EPCs were transplanted intravenously. Vasomotor function of isolated pulmonary artery and degrees of lung injury were assessed 2 days later. RESULTS: Endothelial dysfunction in the pulmonary artery was significantly attenuated in rabbits treated with EPCs, whereas the endothelium-independent relaxation responses were not different. Expression of inducible nitric oxide synthase was suppressed in the pulmonary artery of EPC-treated animals. Infiltration of leukocytes in the lung parenchyma was significantly reduced after EPC transplantation. EPCs also decreased water content, hyaline membrane formation, and hemorrhage in lungs. CONCLUSION: The authors demonstrated that autologous transplantation of EPCs preserves pulmonary endothelial function and maintains the integrity of pulmonary alveolar-capillary barrier. Transplantation of EPCs can be a novel cell-based, endothelium-targeted therapeutic strategy for prevention and treatment of ALI/ARDS.

AB - BACKGROUND: Acute lung injury (ALI) and end-stage acute respiratory distress syndrome (ARDS) are among the most common causes of death in intensive care units. Activation and damage of pulmonary endothelium is the hallmark of ALI/ARDS. Recent studies have demonstrated the importance of circulating endothelial progenitor cells (EPCs) in maintaining normal endothelial function as well as endothelial repairing after vascular injury. Here, the authors present the first study demonstrating the therapeutic potential of EPCs in a rabbit model of ALI/ARDS. METHODS: Circulating EPCs were obtained from rabbits using Ficoll centrifugation. One week after culturing, ALI was induced in rabbits by oleic acid (75 mg/kg, intravenous), and autologous EPCs were transplanted intravenously. Vasomotor function of isolated pulmonary artery and degrees of lung injury were assessed 2 days later. RESULTS: Endothelial dysfunction in the pulmonary artery was significantly attenuated in rabbits treated with EPCs, whereas the endothelium-independent relaxation responses were not different. Expression of inducible nitric oxide synthase was suppressed in the pulmonary artery of EPC-treated animals. Infiltration of leukocytes in the lung parenchyma was significantly reduced after EPC transplantation. EPCs also decreased water content, hyaline membrane formation, and hemorrhage in lungs. CONCLUSION: The authors demonstrated that autologous transplantation of EPCs preserves pulmonary endothelial function and maintains the integrity of pulmonary alveolar-capillary barrier. Transplantation of EPCs can be a novel cell-based, endothelium-targeted therapeutic strategy for prevention and treatment of ALI/ARDS.

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