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Improvement of ventilator-induced lung injury by IPS cell-derived conditioned medium via inhibition of PI3K/Akt pathway and IP-10-dependent paracrine regulation

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Title: Improvement of ventilator-induced lung injury by IPS cell-derived conditioned medium via inhibition of PI3K/Akt pathway and IP-10-dependent paracrine regulation
Authors: Li, Li-Fu1,2,3, Liu, Yung-Yang4,5, Yang, Cheng-Ta1,2,3, Chien, Yueh6,7, Twu, Nae-Fang8,9, Wang, Mong-Lien5, Wang, Chien-Ying9,10, Huang, Chung-Chi1,2,3, Kao, Kuo-Chin1,2,3, Hsu, Han-Shui9,10, Wu, Cheng-Wen5,9, Chiou, Shih-Hwa6,7,9 shchiou@vghtpe.gov.tw
Source: Biomaterials. Jan2013, Vol. 34 Issue 1, p78-91. 14p.
Subjects: Lung injuries, Paracrine mechanisms, Artificial respiration, Pluripotent stem cells, Transmission electron microscopy, Interferons
Abstract: Abstract: Mechanical ventilation in patients may increase the risk of an acute lung injury (ALI), termed ventilator-induced lung injury (VILI). Induced pluripotent stem cells (iPSCs) have previously been shown to improve tissue repair in different disease models, including ALI. However, the therapeutic efficacy of iPSCs-derived conditioned medium (iPSC-CM) on ALI or VILI remains unknown. Here, we demonstrated that both iPSCs and iPSC-CM effectively decrease high-tidal-volume-induced VILI-related inflammatory processes and HMGB1 and PAI-1 production, predominantly through suppressing PI3K/Akt signaling. Notably, iPSC-CM suppressed production of macrophage inflammatory protein-2, malondialdehyde, and increased total glutathione content. Transmission electron microscopy revealed that iPSC-CM potentially restored the bronchial microstructure. This iPSC-CM efficacy could be mimicked by PI3K inhibitor LY294002 or Akt heterozygous knockout, and either treatment showed no further improvement on VILI in iPSC-CM recipients. Furthermore, iPSC-CM increased interferon gamma-induced protein 10 (IP-10) production in injured lungs. Administration of IP-10-neutralizing antibodies increased neutrophil infiltration, impaired lung oxygenation and deteriorated the protective effects mediated by iPSC-CM. Our data provide a preclinical indication regarding the therapeutic potential of iPSC-CM in VILI and suggest that inhibiting PI3K/Akt pathway or increasing IP-10 is a prospective diagnostic and therapeutic target for VILI patients. [Copyright &y& Elsevier]
Copyright of Biomaterials is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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DbLabel: Engineering Source
An: 82840648
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  Data: Improvement of ventilator-induced lung injury by IPS cell-derived conditioned medium via inhibition of PI3K/Akt pathway and IP-10-dependent paracrine regulation
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  Data: <searchLink fieldCode="AR" term="%22Li%2C+Li-Fu%22">Li, Li-Fu</searchLink><relatesTo>1,2,3</relatesTo><br /><searchLink fieldCode="AR" term="%22Liu%2C+Yung-Yang%22">Liu, Yung-Yang</searchLink><relatesTo>4,5</relatesTo><br /><searchLink fieldCode="AR" term="%22Yang%2C+Cheng-Ta%22">Yang, Cheng-Ta</searchLink><relatesTo>1,2,3</relatesTo><br /><searchLink fieldCode="AR" term="%22Chien%2C+Yueh%22">Chien, Yueh</searchLink><relatesTo>6,7</relatesTo><br /><searchLink fieldCode="AR" term="%22Twu%2C+Nae-Fang%22">Twu, Nae-Fang</searchLink><relatesTo>8,9</relatesTo><br /><searchLink fieldCode="AR" term="%22Wang%2C+Mong-Lien%22">Wang, Mong-Lien</searchLink><relatesTo>5</relatesTo><br /><searchLink fieldCode="AR" term="%22Wang%2C+Chien-Ying%22">Wang, Chien-Ying</searchLink><relatesTo>9,10</relatesTo><br /><searchLink fieldCode="AR" term="%22Huang%2C+Chung-Chi%22">Huang, Chung-Chi</searchLink><relatesTo>1,2,3</relatesTo><br /><searchLink fieldCode="AR" term="%22Kao%2C+Kuo-Chin%22">Kao, Kuo-Chin</searchLink><relatesTo>1,2,3</relatesTo><br /><searchLink fieldCode="AR" term="%22Hsu%2C+Han-Shui%22">Hsu, Han-Shui</searchLink><relatesTo>9,10</relatesTo><br /><searchLink fieldCode="AR" term="%22Wu%2C+Cheng-Wen%22">Wu, Cheng-Wen</searchLink><relatesTo>5,9</relatesTo><br /><searchLink fieldCode="AR" term="%22Chiou%2C+Shih-Hwa%22">Chiou, Shih-Hwa</searchLink><relatesTo>6,7,9</relatesTo><i> shchiou@vghtpe.gov.tw</i>
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  Data: <searchLink fieldCode="JN" term="%22Biomaterials%22">Biomaterials</searchLink>. Jan2013, Vol. 34 Issue 1, p78-91. 14p.
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  Data: <searchLink fieldCode="DE" term="%22Lung+injuries%22">Lung injuries</searchLink><br /><searchLink fieldCode="DE" term="%22Paracrine+mechanisms%22">Paracrine mechanisms</searchLink><br /><searchLink fieldCode="DE" term="%22Artificial+respiration%22">Artificial respiration</searchLink><br /><searchLink fieldCode="DE" term="%22Pluripotent+stem+cells%22">Pluripotent stem cells</searchLink><br /><searchLink fieldCode="DE" term="%22Transmission+electron+microscopy%22">Transmission electron microscopy</searchLink><br /><searchLink fieldCode="DE" term="%22Interferons%22">Interferons</searchLink>
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  Label: Abstract
  Group: Ab
  Data: Abstract: Mechanical ventilation in patients may increase the risk of an acute lung injury (ALI), termed ventilator-induced lung injury (VILI). Induced pluripotent stem cells (iPSCs) have previously been shown to improve tissue repair in different disease models, including ALI. However, the therapeutic efficacy of iPSCs-derived conditioned medium (iPSC-CM) on ALI or VILI remains unknown. Here, we demonstrated that both iPSCs and iPSC-CM effectively decrease high-tidal-volume-induced VILI-related inflammatory processes and HMGB1 and PAI-1 production, predominantly through suppressing PI3K/Akt signaling. Notably, iPSC-CM suppressed production of macrophage inflammatory protein-2, malondialdehyde, and increased total glutathione content. Transmission electron microscopy revealed that iPSC-CM potentially restored the bronchial microstructure. This iPSC-CM efficacy could be mimicked by PI3K inhibitor LY294002 or Akt heterozygous knockout, and either treatment showed no further improvement on VILI in iPSC-CM recipients. Furthermore, iPSC-CM increased interferon gamma-induced protein 10 (IP-10) production in injured lungs. Administration of IP-10-neutralizing antibodies increased neutrophil infiltration, impaired lung oxygenation and deteriorated the protective effects mediated by iPSC-CM. Our data provide a preclinical indication regarding the therapeutic potential of iPSC-CM in VILI and suggest that inhibiting PI3K/Akt pathway or increasing IP-10 is a prospective diagnostic and therapeutic target for VILI patients. [Copyright &y& Elsevier]
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  Data: <i>Copyright of Biomaterials is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1016/j.biomaterials.2012.09.042
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        Text: English
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      – SubjectFull: Lung injuries
        Type: general
      – SubjectFull: Paracrine mechanisms
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      – SubjectFull: Artificial respiration
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              Text: Jan2013
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