Endothelial progenitor cell transplantation attenuates lipopolysaccharide-induced acute lung injury via regulating miR-10a/b-5p

Jin, Yan; Yang, Chen; Sui, Xintong; Cai, Quan; Guo, Liang; Liu, Zhi

doi:10.1186/s12944-019-1079-3

Cited by 10 publications

(10 citation statements)

References 35 publications

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“…4e). Coexpression of α7nAChR and VE-cadherin was found in the periphery of blood vessels or capillaries in the bone It has been reported that EPC transplantation could improve LPS-induced acute lung injury [27,[39][40][41]. In 23 patients with pneumonia, the proportion of EPCs in peripheral blood MNCs was increased.…”

Section: Discussionmentioning

confidence: 97%

Vagal α7nAChR signaling regulates α7nAChR+Sca1+ cells during lung injury repair

Chen

Song

et al. 2020

Stem Cell Res Ther

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Background: The distal airways of the lung and bone marrow are innervated by the vagus nerve. Vagal α7nAChR signaling plays a key role in regulating lung infection and inflammation; however, whether this pathway regulates α7nAChR + Sca1 + cells during lung injury repair remains unknown. We hypothesized that vagal α7nAChR signaling controls α7nAChR + Sca1 + cells, which contribute to the resolution of lung injury. Methods: Pneumonia was induced by intratracheal challenge with E. coli. The bone marrow mononuclear cells (BM-MNCs) were isolated from the bone marrow of pneumonia mice for immunofluorescence. The bone marrow, blood, BAL, and lung cells were isolated for flow cytometric analysis by labeling with anti-Sca1, VE-cadherin, p-Akt1, or Flk1 antibodies. Immunofluorescence was also used to examine the coexpression of α7nAChR, VE-cadherin, and p-Akt1. Sham, vagotomized, α7nAChR knockout, and Akt1 knockout mice were infected with E. coli to study the regulatory role of vagal α7nAChR signaling and Akt1 in Sca1 + cells. Results: During pneumonia, BM-MNCs were enriched with α7nAChR + Sca1 + cells, and this cell population proliferated. Transplantation of pneumonia BM-MNCs could mitigate lung injury and increase engraftment in recipient pneumonia lungs. Activation of α7nAChR by its agonist could boost α7nAChR + Sca1 + cells in the bone marrow, peripheral blood, and bronchoalveolar lavage (BAL) in pneumonia. Immunofluorescence revealed that α7nAChR, VE-cadherin, and p-Akt1 were coexpressed in the bone marrow cells. Vagotomy could reduce α7nAChR + VE-cadherin + and VE-cadherin + p-Akt1 + cells in the bone marrow in pneumonia. Knockout of α7nAChR reduced VE-cadherin + cells and p-Akt1 + cells in the bone marrow. Deletion of Akt1 reduced Sca1 + cells in the bone marrow and BAL. More importantly, 91.3 ± 4.9% bone marrow and 77.8 ± 4.9% lung α7nAChR + Sca1 + VE-cadherin + cells expressed Flk1, which is a key marker of endothelial progenitor cells (EPCs). Vagotomy reduced α7nAChR + Sca1 + VE-cadherin + p-Akt1 + cells in the bone marrow and lung from pneumonia mice. Treatment with cultured EPCs reduced ELW compared to PBS treatment in E. coli pneumonia mice at 48 h. The ELW was further reduced by treatment with EPCs combining with α7nAChR agonist-PHA568487 compared to EPC treatments only.

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Section: Discussionmentioning

confidence: 97%

Vagal α7nAChR signaling regulates α7nAChR+Sca1+ cells during lung injury repair

Chen

Song

et al. 2020

Stem Cell Res Ther

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“…miRNAs inhibit translation or induce the degradation of targeted mRNA by binding to the 3' untranslated region (UTR) [9]. Increasing number of evidences have proved that miRNAs associated with certain inflammatory lung diseases.…”

Section: Introductionmentioning

confidence: 99%

miR-128-3p enhances the protective effect of dexmedetomidine on acute lung injury in septic mice by targeted inhibition of MAPK14

Ding¹,

Gao²,

Yu³

et al. 2020

J Bioenerg Biomembr

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Background: To investigate the role of miR-128-3p and MAPK14 in the dexmedetomidine treatment of acute lung injury in septic mice. Methods: SPF C57BL/6 mice were divided into 8 groups. The pathological changes and wet/dry weight ratio (W/D), PaO 2 , PaCO 2 , MDA, SOD and MPO levels in lung tissue and the serum levels of inflammation factors were observed. Dual luciferase reporter assay was used to detect the targeting relationship of miR-128-3p and MAPK14, and qPCR and WB were used to detect the expression of miR-128-3p and MAPK14. Results: Compared with the Normal group, other groups had lower MDA, MPO, inflammatory factors levels and the expression level of MAPK14, while the content of SOD and the expression level of miR-128-3p was significantly decreased (all p < 0.05). Compared with the Model group, the contents of MDA, MPO, inflammatory factors in the DEX group and miR-128-3p mimic group were significantly decreased, and the content SOD was significantly increased, however, opposite results were occurred in oe-MAPK14 group (all p < 0.05). Compared with the DEX group, all the indicators in miR-128-3p mimic+DEX group showed significant improvement (all p < 0.05). Compared with the miR-128-3p mimic group, all the indicators were deteriorated in the miR-128-3p mimic+oe-MAPK14 group (all p < 0.05). The combination of DEX and oe-MAPK14 blocked the protective effect of dexmedetomidine on acute lung injury in septic mice. Conclusion: miR-128-3p can further enhance the protective effect of dexmedetomidine on acute lung injury in septic mice by targeting and inhibiting MAPK14 expression.

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“…MicroRNAs (miRNAs) are endogenous small non-coding RNAs with a length of 21-23 nucleotides. miRNAs inhibit translation or induce the degradation of targeted mRNA by binding to the 3' untranslated region (UTR) [12]. Increasing number of evidences have proved that miRNAs associated with certain in ammatory lung diseases.…”

Section: Introductionmentioning

confidence: 99%

miR-128-3p enhances the protective effect of dexmedetomidine on acute lung injury in septic mice by targeted inhibition of MAPK14

Ding

Gao

et al. 2020

Preprint

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Background: To investigate the mechanism of miR-128-3p and MAPK14 on the protective effect of dexmedetomidine on acute lung injury in septic mice.Methods: SPF C57BL/6 mice were divided into 8 groups. The pathological changes and wet/dry weight ratio (W/D), PaO2, PaCO2, MDA, SOD and MPO levels in lung tissue and the serum levels of inflammation factors were observed. Dual luciferase reporter assay was used to verify the targeting relationship between miR-128-3p and MAPK14. qPCR and WB were used to detect the expression of miR-128-3p and MAPK14.Results: Compared with the Normal group, other groups had lower MDA, MPO, inflammatory factors levels and the expression level of MAPK14, while the content of SOD and the expression level of miR-128-3p was significantly decreased. DEX treatment and up-regulation of miR-128-3p could significantly decrease the contents of MDA, MPO, inflammatory factor levels and significantly increase the SOD content in model mice, however, MAPK14 over-expression had opposite effects. miR-128-3p up-regulation enhanced the changes of above indicators caused by DEX treatment and MAPK14 over-expression could block the protective effect of DEX on acute lung injury in septic mice. miR-128-3p up-regulation reversed the effects of MAPK14 over-expression in model mice.Conclusion: miR-128-3p can further enhance the protective effect of dexmedetomidine on acute lung injury in septic mice by targeting and inhibiting MAPK14 expression.

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Endothelial progenitor cell transplantation attenuates lipopolysaccharide-induced acute lung injury via regulating miR-10a/b-5p

Cited by 10 publications

References 35 publications

Vagal α7nAChR signaling regulates α7nAChR+Sca1+ cells during lung injury repair

Vagal α7nAChR signaling regulates α7nAChR+Sca1+ cells during lung injury repair

miR-128-3p enhances the protective effect of dexmedetomidine on acute lung injury in septic mice by targeted inhibition of MAPK14

miR-128-3p enhances the protective effect of dexmedetomidine on acute lung injury in septic mice by targeted inhibition of MAPK14

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