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NMDA receptor activation inhibits the antifibrotic effect of BM-MSCs on bleomycin-induced pulmonary fibrosis

Endogenous glutamate (Glu) release and N-methyl-d-aspartate (NMDA) receptor (NMDAR) activation are associated with lung injury in different animal models. However, the underlying mechanism is unclear. Bone marrow-derived mesenchymal stem cells (BM-MSCs), which show potential use for immunomodulation... Full description

Journal Title: American Journal of Physiology Sep 2018, Vol.315(3), p.L404
Main Author: Li, Xiaohong
Other Authors: Li, Chen , Tang, Yiting , Huang, Yanhong , Cheng, Qingmei , Huang, Xiaoting , Zhao, Feiyan , Hao, Caixia , Feng, Dandan , Xu, Jianping , Han, Jianzhong , Tang, Siyuan , Liu, Wei , Yue, Shaojie , Luo, Ziqiang
Format: Electronic Article Electronic Article
Language: English
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ID: ISSN: 10400605 ; E-ISSN: 15221504
Link: http://search.proquest.com/docview/2125760038/?pq-origsite=primo
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title: NMDA receptor activation inhibits the antifibrotic effect of BM-MSCs on bleomycin-induced pulmonary fibrosis
format: Article
creator:
  • Li, Xiaohong
  • Li, Chen
  • Tang, Yiting
  • Huang, Yanhong
  • Cheng, Qingmei
  • Huang, Xiaoting
  • Zhao, Feiyan
  • Hao, Caixia
  • Feng, Dandan
  • Xu, Jianping
  • Han, Jianzhong
  • Tang, Siyuan
  • Liu, Wei
  • Yue, Shaojie
  • Luo, Ziqiang
subjects:
  • Pulmonary Fibrosis
  • Lung Diseases
  • Stem Cells
  • Genes
  • Extracellular Matrix
  • Transplantation
  • Glutamic Acid Receptors (Ionotropic)
  • Homing Behavior
  • Stem Cells
  • Cell Migration
  • Inhibition
  • Sex Determination
  • Stem Cells
  • Animal Models
  • Growth Factors
  • Excitotoxicity
  • Bone Marrow
  • Proteins
  • Fibrosis
  • Fluorescence
  • Gene Expression
  • Fluorescence
  • Lung Diseases
  • Animal Models
  • Gene Expression
  • Transplantation
  • Paracrine Signalling
  • Epithelial Cells
  • Fibrosis
  • Bone Marrow
  • Activation
  • Transforming Growth Factor
  • Mice
  • Mice
  • Immunomodulation
  • Fibroblasts
  • Receptor Mechanisms
  • Glutamic Acid Receptors
  • Extracellular Matrix
  • Homing
  • Bleomycin
  • Leukocyte Migration
  • Sdf-1 Protein
  • N-Methyl-D-Aspartic Acid Receptors
  • Lungs
  • Mesenchyme
  • Stem Cell Transplantation
  • Stem Cells
  • Bone Marrow
  • Fibroblasts
ispartof: American Journal of Physiology, Sep 2018, Vol.315(3), p.L404
description: Endogenous glutamate (Glu) release and N-methyl-d-aspartate (NMDA) receptor (NMDAR) activation are associated with lung injury in different animal models. However, the underlying mechanism is unclear. Bone marrow-derived mesenchymal stem cells (BM-MSCs), which show potential use for immunomodulation and tissue protection, play a protective role in pulmonary fibrosis (PF) process. Here, we found the increased Glu release from the BM cells of bleomycin (BLM)-induced PF mice in vivo. BLM stimulation also increased the extracellular Glu in BM-MSCs via the antiporter system xc− in vitro. The gene expression of each subunit of NMDAR was detected in BM-MSCs. NMDAR activation inhibited the proliferation, migration, and paracrine function of BM-MSCs in vitro. BM-MSCs were derived from male C57BL/6 mice, transfected with lentiviral vectors carrying the enhanced green fluorescence protein gene, pretreated with NMDA, and transplanted into the female recipient mice that were intratracheally injected with BLM to induce PF. Transplantation of NMDA-pretreated BM-MSCs significantly aggravated PF as compared with that in the normal BM-MSCs transplantation group. The sex determination gene Y chromosome and green fluorescence protein genes of BM-MSCs were detected to observe BM-MSCs homing in the fibrotic lungs. Moreover, NMDAR activation inhibited BM-MSC migration by downregulating the stromal cell-derived factor-1/C-X-C chemokine receptor type 4 signaling axis. NMDAR activation aggravated the transforming growth factor-β1-induced extracellular matrix production in alveolar epithelial cells and fibroblasts through the paracrine effects of BM-MSCs. In summary, these findings suggested that NMDAR activation-mediated Glu excitotoxicity induced by BLM in BM-MSCs abolished the therapeutic effects of normal BM-MSCs transplantation on BLM-induced PF.
language: eng
source:
identifier: ISSN: 10400605 ; E-ISSN: 15221504
fulltext: no_fulltext
issn:
  • 10400605
  • 1040-0605
  • 15221504
  • 1522-1504
url: Link


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titleNMDA receptor activation inhibits the antifibrotic effect of BM-MSCs on bleomycin-induced pulmonary fibrosis
creatorLi, Xiaohong ; Li, Chen ; Tang, Yiting ; Huang, Yanhong ; Cheng, Qingmei ; Huang, Xiaoting ; Zhao, Feiyan ; Hao, Caixia ; Feng, Dandan ; Xu, Jianping ; Han, Jianzhong ; Tang, Siyuan ; Liu, Wei ; Yue, Shaojie ; Luo, Ziqiang
ispartofAmerican Journal of Physiology, Sep 2018, Vol.315(3), p.L404
identifierISSN: 10400605 ; E-ISSN: 15221504
subjectPulmonary Fibrosis ; Lung Diseases ; Stem Cells ; Genes ; Extracellular Matrix ; Transplantation ; Glutamic Acid Receptors (Ionotropic) ; Homing Behavior ; Stem Cells ; Cell Migration ; Inhibition ; Sex Determination ; Stem Cells ; Animal Models ; Growth Factors ; Excitotoxicity ; Bone Marrow ; Proteins ; Fibrosis ; Fluorescence ; Gene Expression ; Fluorescence ; Lung Diseases ; Animal Models ; Gene Expression ; Transplantation ; Paracrine Signalling ; Epithelial Cells ; Fibrosis ; Bone Marrow ; Activation ; Transforming Growth Factor ; Mice ; Mice ; Immunomodulation ; Fibroblasts ; Receptor Mechanisms ; Glutamic Acid Receptors ; Extracellular Matrix ; Homing ; Bleomycin ; Leukocyte Migration ; Sdf-1 Protein ; N-Methyl-D-Aspartic Acid Receptors ; Lungs ; Mesenchyme ; Stem Cell Transplantation ; Stem Cells ; Bone Marrow ; Fibroblasts
descriptionEndogenous glutamate (Glu) release and N-methyl-d-aspartate (NMDA) receptor (NMDAR) activation are associated with lung injury in different animal models. However, the underlying mechanism is unclear. Bone marrow-derived mesenchymal stem cells (BM-MSCs), which show potential use for immunomodulation and tissue protection, play a protective role in pulmonary fibrosis (PF) process. Here, we found the increased Glu release from the BM cells of bleomycin (BLM)-induced PF mice in vivo. BLM stimulation also increased the extracellular Glu in BM-MSCs via the antiporter system xc− in vitro. The gene expression of each subunit of NMDAR was detected in BM-MSCs. NMDAR activation inhibited the proliferation, migration, and paracrine function of BM-MSCs in vitro. BM-MSCs were derived from male C57BL/6 mice, transfected with lentiviral vectors carrying the enhanced green fluorescence protein gene, pretreated with NMDA, and transplanted into the female recipient mice that were intratracheally injected with BLM to induce PF. Transplantation of NMDA-pretreated BM-MSCs significantly aggravated PF as compared with that in the normal BM-MSCs transplantation group. The sex determination gene Y chromosome and green fluorescence protein genes of BM-MSCs were detected to observe BM-MSCs homing in the fibrotic lungs. Moreover, NMDAR activation inhibited BM-MSC migration by downregulating the stromal cell-derived factor-1/C-X-C chemokine receptor type 4 signaling axis. NMDAR activation aggravated the transforming growth factor-β1-induced extracellular matrix production in alveolar epithelial cells and fibroblasts through the paracrine effects of BM-MSCs. In summary, these findings suggested that NMDAR activation-mediated Glu excitotoxicity induced by BLM in BM-MSCs abolished the therapeutic effects of normal BM-MSCs transplantation on BLM-induced PF.
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titleNMDA receptor activation inhibits the antifibrotic effect of BM-MSCs on bleomycin-induced pulmonary fibrosis
descriptionEndogenous glutamate (Glu) release and N-methyl-d-aspartate (NMDA) receptor (NMDAR) activation are associated with lung injury in different animal models. However, the underlying mechanism is unclear. Bone marrow-derived mesenchymal stem cells (BM-MSCs), which show potential use for immunomodulation and tissue protection, play a protective role in pulmonary fibrosis (PF) process. Here, we found the increased Glu release from the BM cells of bleomycin (BLM)-induced PF mice in vivo. BLM stimulation also increased the extracellular Glu in BM-MSCs via the antiporter system xc− in vitro. The gene expression of each subunit of NMDAR was detected in BM-MSCs. NMDAR activation inhibited the proliferation, migration, and paracrine function of BM-MSCs in vitro. BM-MSCs were derived from male C57BL/6 mice, transfected with lentiviral vectors carrying the enhanced green fluorescence protein gene, pretreated with NMDA, and transplanted into the female recipient mice that were intratracheally injected with BLM to induce PF. Transplantation of NMDA-pretreated BM-MSCs significantly aggravated PF as compared with that in the normal BM-MSCs transplantation group. The sex determination gene Y chromosome and green fluorescence protein genes of BM-MSCs were detected to observe BM-MSCs homing in the fibrotic lungs. Moreover, NMDAR activation inhibited BM-MSC migration by downregulating the stromal cell-derived factor-1/C-X-C chemokine receptor type 4 signaling axis. NMDAR activation aggravated the transforming growth factor-β1-induced extracellular matrix production in alveolar epithelial cells and fibroblasts through the paracrine effects of BM-MSCs. In summary, these findings suggested that NMDAR activation-mediated Glu excitotoxicity induced by BLM in BM-MSCs abolished the therapeutic effects of normal BM-MSCs transplantation on BLM-induced PF.
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titleNMDA receptor activation inhibits the antifibrotic effect of BM-MSCs on bleomycin-induced pulmonary fibrosis
authorLi, Xiaohong ; Li, Chen ; Tang, Yiting ; Huang, Yanhong ; Cheng, Qingmei ; Huang, Xiaoting ; Zhao, Feiyan ; Hao, Caixia ; Feng, Dandan ; Xu, Jianping ; Han, Jianzhong ; Tang, Siyuan ; Liu, Wei ; Yue, Shaojie ; Luo, Ziqiang
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1Lung Diseases
2Stem Cells
3Genes
4Extracellular Matrix
5Transplantation
6Glutamic Acid Receptors (Ionotropic)
7Homing Behavior
8Cell Migration
9Inhibition
10Sex Determination
11Animal Models
12Growth Factors
13Excitotoxicity
14Bone Marrow
15Proteins
16Fibrosis
17Fluorescence
18Gene Expression
19Paracrine Signalling
20Epithelial Cells
21Activation
22Transforming Growth Factor
23Mice
24Immunomodulation
25Fibroblasts
26Receptor Mechanisms
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abstractEndogenous glutamate (Glu) release and N-methyl-d-aspartate (NMDA) receptor (NMDAR) activation are associated with lung injury in different animal models. However, the underlying mechanism is unclear. Bone marrow-derived mesenchymal stem cells (BM-MSCs), which show potential use for immunomodulation and tissue protection, play a protective role in pulmonary fibrosis (PF) process. Here, we found the increased Glu release from the BM cells of bleomycin (BLM)-induced PF mice in vivo. BLM stimulation also increased the extracellular Glu in BM-MSCs via the antiporter system xc− in vitro. The gene expression of each subunit of NMDAR was detected in BM-MSCs. NMDAR activation inhibited the proliferation, migration, and paracrine function of BM-MSCs in vitro. BM-MSCs were derived from male C57BL/6 mice, transfected with lentiviral vectors carrying the enhanced green fluorescence protein gene, pretreated with NMDA, and transplanted into the female recipient mice that were intratracheally injected with BLM to induce PF. Transplantation of NMDA-pretreated BM-MSCs significantly aggravated PF as compared with that in the normal BM-MSCs transplantation group. The sex determination gene Y chromosome and green fluorescence protein genes of BM-MSCs were detected to observe BM-MSCs homing in the fibrotic lungs. Moreover, NMDAR activation inhibited BM-MSC migration by downregulating the stromal cell-derived factor-1/C-X-C chemokine receptor type 4 signaling axis. NMDAR activation aggravated the transforming growth factor-β1-induced extracellular matrix production in alveolar epithelial cells and fibroblasts through the paracrine effects of BM-MSCs. In summary, these findings suggested that NMDAR activation-mediated Glu excitotoxicity induced by BLM in BM-MSCs abolished the therapeutic effects of normal BM-MSCs transplantation on BLM-induced PF.
copBethesda
pubAmerican Physiological Society
urlhttp://search.proquest.com/docview/2125760038/
doi10.1152/ajplung.00002.2018
pagesL404-L421
date2018-09-01