Human mesenchymal stem cells attenuate hyperoxia-induced lung injury through inhibition of the renin-angiotensin system in newborn rats

研究成果: 雜誌貢獻文章

摘要

Hyperoxia induces activation of the renin-angiotensin system (RAS) in newborn rat lungs. This study investigated the therapeutic effects of human mesenchymal stem cells (MSCs) on lung development and RAS expression in neonatal rats exposed to hyperoxia. Sprague-Dawley rat pups were exposed to either room air (RA) or oxygen-enriched atmosphere (O2) treatment from postnatal days 1 to 14. Human MSCs (1 × 105 cells) in 0.03 mL of normal saline (NS) were administered intratracheally on postnatal day 5, and four study groups were obtained: RA + NS, RA + MSCs, O2 + NS, and O2 + MSCs. The lungs were excised for cytokine, expression of RAS components, and histological analyses on postnatal day 14. Body and lung weights were significantly lower in rats reared in hyperoxia than in those reared in RA. The rats reared in hyperoxia and treated with NS exhibited significantly higher tumor necrosis factor (TNF)-α and interleukin (IL)-6 levels, mean linear intercept (MLI), and expression of angiotensin II, angiotensin II type 1 receptor, and angiotensin-converting enzyme than those reared in RA and treated with NS or MSCs did. Administering MSC to hyperoxia-exposed rats reduced TNF-α and IL-6 levels, improved MLI, and decreased expression of angiotensin II, angiotensin II type 1 receptor, and angiotensin-converting enzyme to normoxic levels. Thus, human MSCs attenuated hyperoxia-induced lung injury through inhibition of the RAS in newborn rats.
原文英語
文章編號AJTR0072975
頁(從 - 到)2628-2635
頁數8
期刊American Journal of Translational Research
10
發行號8
出版狀態已發佈 - 一月 1 2018

指紋

Hyperoxia
Angiotensins
Lung Injury
Renin-Angiotensin System
Stem cells
Mesenchymal Stromal Cells
Renin
Rats
Air
Lung
Angiotensin Type 1 Receptor
Peptidyl-Dipeptidase A
Angiotensin II
Interleukin-6
Tumor Necrosis Factor-alpha
Therapeutic Uses
Atmosphere
Sprague Dawley Rats
Chemical activation
Body Weight

Keywords

  • Angiotensin
  • Angiotensin-converting enzyme
  • Bronchopulmonary dysplasia
  • Cytokine
  • Mean linear intercept

ASJC Scopus subject areas

  • Molecular Medicine
  • Clinical Biochemistry
  • Cancer Research

引用此文

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abstract = "Hyperoxia induces activation of the renin-angiotensin system (RAS) in newborn rat lungs. This study investigated the therapeutic effects of human mesenchymal stem cells (MSCs) on lung development and RAS expression in neonatal rats exposed to hyperoxia. Sprague-Dawley rat pups were exposed to either room air (RA) or oxygen-enriched atmosphere (O2) treatment from postnatal days 1 to 14. Human MSCs (1 × 105 cells) in 0.03 mL of normal saline (NS) were administered intratracheally on postnatal day 5, and four study groups were obtained: RA + NS, RA + MSCs, O2 + NS, and O2 + MSCs. The lungs were excised for cytokine, expression of RAS components, and histological analyses on postnatal day 14. Body and lung weights were significantly lower in rats reared in hyperoxia than in those reared in RA. The rats reared in hyperoxia and treated with NS exhibited significantly higher tumor necrosis factor (TNF)-α and interleukin (IL)-6 levels, mean linear intercept (MLI), and expression of angiotensin II, angiotensin II type 1 receptor, and angiotensin-converting enzyme than those reared in RA and treated with NS or MSCs did. Administering MSC to hyperoxia-exposed rats reduced TNF-α and IL-6 levels, improved MLI, and decreased expression of angiotensin II, angiotensin II type 1 receptor, and angiotensin-converting enzyme to normoxic levels. Thus, human MSCs attenuated hyperoxia-induced lung injury through inhibition of the RAS in newborn rats.",
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N2 - Hyperoxia induces activation of the renin-angiotensin system (RAS) in newborn rat lungs. This study investigated the therapeutic effects of human mesenchymal stem cells (MSCs) on lung development and RAS expression in neonatal rats exposed to hyperoxia. Sprague-Dawley rat pups were exposed to either room air (RA) or oxygen-enriched atmosphere (O2) treatment from postnatal days 1 to 14. Human MSCs (1 × 105 cells) in 0.03 mL of normal saline (NS) were administered intratracheally on postnatal day 5, and four study groups were obtained: RA + NS, RA + MSCs, O2 + NS, and O2 + MSCs. The lungs were excised for cytokine, expression of RAS components, and histological analyses on postnatal day 14. Body and lung weights were significantly lower in rats reared in hyperoxia than in those reared in RA. The rats reared in hyperoxia and treated with NS exhibited significantly higher tumor necrosis factor (TNF)-α and interleukin (IL)-6 levels, mean linear intercept (MLI), and expression of angiotensin II, angiotensin II type 1 receptor, and angiotensin-converting enzyme than those reared in RA and treated with NS or MSCs did. Administering MSC to hyperoxia-exposed rats reduced TNF-α and IL-6 levels, improved MLI, and decreased expression of angiotensin II, angiotensin II type 1 receptor, and angiotensin-converting enzyme to normoxic levels. Thus, human MSCs attenuated hyperoxia-induced lung injury through inhibition of the RAS in newborn rats.

AB - Hyperoxia induces activation of the renin-angiotensin system (RAS) in newborn rat lungs. This study investigated the therapeutic effects of human mesenchymal stem cells (MSCs) on lung development and RAS expression in neonatal rats exposed to hyperoxia. Sprague-Dawley rat pups were exposed to either room air (RA) or oxygen-enriched atmosphere (O2) treatment from postnatal days 1 to 14. Human MSCs (1 × 105 cells) in 0.03 mL of normal saline (NS) were administered intratracheally on postnatal day 5, and four study groups were obtained: RA + NS, RA + MSCs, O2 + NS, and O2 + MSCs. The lungs were excised for cytokine, expression of RAS components, and histological analyses on postnatal day 14. Body and lung weights were significantly lower in rats reared in hyperoxia than in those reared in RA. The rats reared in hyperoxia and treated with NS exhibited significantly higher tumor necrosis factor (TNF)-α and interleukin (IL)-6 levels, mean linear intercept (MLI), and expression of angiotensin II, angiotensin II type 1 receptor, and angiotensin-converting enzyme than those reared in RA and treated with NS or MSCs did. Administering MSC to hyperoxia-exposed rats reduced TNF-α and IL-6 levels, improved MLI, and decreased expression of angiotensin II, angiotensin II type 1 receptor, and angiotensin-converting enzyme to normoxic levels. Thus, human MSCs attenuated hyperoxia-induced lung injury through inhibition of the RAS in newborn rats.

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