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      Human amnion-derived mesenchymal stem cells alleviate lung injury induced by white smoke inhalation in rats

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          Abstract

          Background

          White smoke inhalation (WSI) is an uncommon but potentially deadly cause of acute lung injury and acute respiratory distress syndrome for which no effective pharmaceutical treatment has been developed. This study aimed to determine the protective effects of human amnion-derived mesenchymal stem cells (hAMSCs) against WSI-induced lung injury in rats.

          Methods

          hAMSCs were injected into rats via the tail vein 4 h after WSI. At 1, 3, 7, 14, and 28 days after cell injection, hAMSCs labeled with PKH26 in lung, heart, liver, and kidney tissues were observed by fluorescence microscopy. The lung injury score was determined by hematoxylin and eosin staining. Lung fibrosis was assessed by Masson’s trichrome staining. The computed tomography (CT) score was assessed by CT scanning. The wet/dry weight ratio was calculated. The levels of interleukin (IL)-1β, IL-6, and IL-10 were determined by enzyme-linked immunosorbent assays. The expression of surfactant protein (SP)-A, SP-C, and SP-D was measured by Western blotting.

          Results

          The injected hAMSCs were primarily distributed in the lung tissues in WSI-induced rats. Compared with the model and phosphate-buffered saline (PBS) group, hAMSC treatment led to reduced lung injury, lung fibrosis, CT score, and inflammation levels in WSI-induced mice. hAMSC treatment also resulted in increased cell retention in the lung, partial pressure of oxygen (PaO 2), and PaO 2/fraction of inspired oxygen (FiO 2) levels, and pulmonary SP-A, SP-C, and SP-D expression compared with that in the model and PBS group.

          Conclusions

          hAMSCs are a potential cell-based therapy for WSI-induced lung injury.

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          Most cited references33

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          Bleomycin-induced interstitial pulmonary disease in the nude, athymic mouse.

          S V Szapiel, Ronald G. Crystal, J Fulmer … (1979)
          Evidence from divergent sources suggests that some forms of interstitial pulmonary disease are associated with abnormalities of the cellular immune system. To evaluate whether cellular immune processes are necessary determinants for the development of parenchymal alveolitis and fibrosis secondary to bleomycin, we examined the effect of bleomycin on the NIH, outbred white mouse as compared to the homozygous nude, athymic mouse on the NIH outbred background. The nude mouse has virtually no detectable cell-mediated immune function; we therefore hypothesized that if this component of the immune system were necessary for the development of bleomycin-induced interstitial disease, bleomycin would not induce the same pulmonary lesion in the nude mouse as in the white mouse. However, both white and nude mice developed alveolitis and fibrosis after intraperitoneal administration of bleomycin. Comparison of the frequency and severity of these lesions in the 2 groups revealed no significant differences. These findings suggest that the presence of an intact cell-mediated immune system is not an absolute requirement for the development of bleomycin-induced interstitial disease in the mouse. To the extent that this model is an appropriate approximation of human bleomycin-induced pulmonary disease, these results are consistent with the hypothesis that T-lymphocyte mediated processes are not primary determinants of this lesion.
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            A cartilage ECM-derived 3-D porous acellular matrix scaffold for in vivo cartilage tissue engineering with PKH26-labeled chondrogenic bone marrow-derived mesenchymal stem cells.

            SHIBI LU, Jun Yao, Aiyuan Wang … (2008)
            We developed a natural, acellular, 3-D interconnected porous scaffold derived from cartilage extracellular matrix (ECM). Human cartilage was physically shattered, then decellularized sequentially with use of hypotonic buffer, TritonX-100, and a nuclease solution and made into a suspension. The scaffold was fabricated by simple freeze-drying and cross-linking techniques. On histology, scaffolds showed most of the ECM components after removal of the cell fragments, and scanning electron microscopy revealed a 3-D interconnected porous structure. Cellular viability assay revealed no cytotoxic effects. In vitro study showed that the novel scaffold could provide a suitable 3-D environment to support the adheration, proliferation and differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) to chondrocytes in culture with chondrogenic medium after 21 days. Chondrogenically induced BMSCs labeled with fluorescent dye PKH26 were then grown on scaffolds and implanted subcutaneously into nude mice. Four weeks later, cartilage-like tissue formed, with positive staining for Safranin O, tuoluidine blue and collagen II. Cells in the samples seemed to confirm that they originated from the labeled BMSCs, as confirmed by in vivo fluorescent imaging and immunofluorescence examination. In conclusion, the cartilage ECM-derived porous scaffold shows potential as biomaterial for cartilage tissue engineering, and PKH26 fluorescent labeling and in vivo fluorescent imaging can be useful for cell tracking and analyzing cell-scaffold constructs in vivo.
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              Mesenchymal stem cell-conditioned media recovers lung fibroblasts from cigarette smoke-induced damage.

              Ik Kim, Hyun Ji Julie Lee, H. Kim … (2012)
              Cigarette smoking causes apoptotic death, senescence, and impairment of repair functions in lung fibroblasts, which maintain the integrity of alveolar structure by producing extracellular matrix (ECM) proteins. Therefore, recovery of lung fibroblasts from cigarette smoke-induced damage may be crucial in regeneration of emphysematous lung resulting from degradation of ECM proteins and subsequent loss of alveolar cells. Recently, we reported that bone marrow-derived mesenchymal stem cell-conditioned media (MSC-CM) led to angiogenesis and regeneration of lung damaged by cigarette smoke. In this study, to further investigate reparative mechanisms for MSC-CM-mediated lung repair, we attempted to determine whether MSC-CM can recover lung fibroblasts from cigarette smoke-induced damage. In lung fibroblasts exposed to cigarette smoke extract (CSE), MSC-CM, not only inhibited apoptotic death, but also induced cell proliferation and reversed CSE-induced changes in the levels of caspase-3, p53, p21, p27, Akt, and p-Akt. MSC-CM also restored expression of ECM proteins and collagen gel contraction while suppressing CSE-induced expression of cyclooxygenase-2 and microsomal PGE(2) synthase-2. The CSE-opposing effects of MSC-CM on cell fate, expression of ECM proteins, and collagen gel contraction were partially inhibited by LY294002, a phosphatidylinositol 3-kinase (PI3K) inhibitor. In rats, MSC-CM administration also resulted in elevation of p-Akt and restored proliferation of lung fibroblasts, which was suppressed by exposure to cigarette smoke. Taken together, these data suggest that MSC-CM may recover lung fibroblasts from cigarette smoke-induced damage, possibly through inhibition of apoptosis, induction of proliferation, and restoration of lung fibroblast repair function, which are mediated in part by the PI3K/Akt pathway.
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                Author and article information

                Contributors
                Pei Cui: cpei1987@163.com
                Haiming Xin: xinhm123@163.com
                Yongming Yao: c_ff@sina.com
                Shichu Xiao: huangzhuoxiao4@hotmail.com
                Feng Zhu: 18801780080@163.com
                Zhenyu Gong: gzy_181@126.com
                Zhiping Tang: tzpmz0723@163.com
                Qiu Zhan: zhanqiu007@163.com
                Wei Qin: qwei2533598@163.com
                Yanhua Lai: wwwlaiyh@163.com
                Xiaohui Li: 15778027811@163.com
                Yalin Tong: +86-773-2081665 , scsyj_sys@163.com
                Zhaofan Xia: +86-21-65589829 , xiazhaofan_smmu@163.com
                Journal
                Journal ID (nlm-ta): Stem Cell Res Ther
                Journal ID (iso-abbrev): Stem Cell Res Ther
                Title: Stem Cell Research & Therapy
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1757-6512
                Publication date (Electronic): 12 April 2018
                Publication date PMC-release: 12 April 2018
                Publication date Collection: 2018
                Volume: 9
                Electronic Location Identifier: 101
                Affiliations
                [1 ]GRID grid.460041.7, Research Laboratory of Burns and Trauma, , the 181st Hospital of Chinese PLA, ; Guilin, 541002 People’s Republic of China
                [2 ]GRID grid.460041.7, Department of Burns, Plastic and Wound repair surgery, , the 181st Hospital of Chinese PLA, ; Guilin, 541002 People’s Republic of China
                [3 ]GRID grid.414889.8, Trauma Research Center, , First Hospital Affiliated to the Chinese PLA General Hospital, ; Beijing, 100048 People’s Republic of China
                [4 ]ISNI 0000 0004 0369 1599, GRID grid.411525.6, Department of Burn surgery, , Changhai Hospital, Naval Military Medical University, ; Shanghai, 200433 China
                Article
                Publisher ID: 856
                DOI: 10.1186/s13287-018-0856-7
                PMC ID: 5898065
                PubMed ID: 29650044
                SO-VID: 0ab27bb2-1672-4144-bd48-e5353a139267
                Copyright © © The Author(s). 2018
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 24 January 2018
                Date revision received : 17 March 2018
                Date accepted : 26 March 2018
                Funding
                Funded by: Academician workstation Program
                Funded by: Lijiang Scholars Program
                Funded by: Guilin science and technology project
                Award ID: 20170109-35
                Award Recipient :
                Funded by: Guangxi science and technology project
                Award ID: 1140003A-39
                Award Recipient :
                Categories
                Subject: Research
                Custom metadata
                issue-copyright-statement © The Author(s) 2018

                ScienceOpen disciplines: Molecular medicine
                Keywords: white smoke inhalation,human amnion-derived mesenchymal stem cells,lung injury,cell-based therapy
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: white smoke inhalation, human amnion-derived mesenchymal stem cells, lung injury, cell-based therapy

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