Transamniotic mesenchymal stem cell therapy for neural tube defects preserves neural function through lesion-specific engraftment and regeneration
Neural tube defects (NTDs) lead to prenatal mortality and lifelong morbidity. Currently, surgical closure of NTD lesions results in limited functional recovery. We previously suggested that nerve regeneration was critical for NTD therapy. Here, we report that transamniotic bone marrow-derived mesenc...
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| Veröffentlicht in: | Cell death & disease 2020-07, Vol.11 (7), p.523-523, Article 523 |
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| creator | Wei, Xiaowei Ma, Wei Gu, Hui Liu, Dan Luo, Wenting Bai, Yuzuo Wang, Weilin Lui, Vincent Chi Hang Yang, Peixin Yuan, Zhengwei |
| description | Neural tube defects (NTDs) lead to prenatal mortality and lifelong morbidity. Currently, surgical closure of NTD lesions results in limited functional recovery. We previously suggested that nerve regeneration was critical for NTD therapy. Here, we report that transamniotic bone marrow-derived mesenchymal stem cell (BMSC) therapy for NTDs during early development may achieve beneficial functional recovery. In our ex vivo rat embryonic NTD model, BMSCs injected into the amniotic cavity spontaneously migrated into the defective neural tissue. Hepatocyte growth factor and its receptor c-MET were found to play critical roles in this NTD lesion-specific migration. Using the in vivo rat fetal NTD model, we further discovered that the engrafted BMSCs specifically differentiated into the cell types of the defective tissue, including skin and different types of neurons in situ. BMSC treatment triggered skin repair in fetuses, leading to a 29.9 ± 5.6% reduction in the skin lesion area. The electrophysiological functional recovery assay revealed a decreased latency and increased motor-evoked potential amplitude in the BMSC-treated fetuses. Based on these positive outcomes, ease of operation, and reduced trauma to the mother and fetus, we propose that transamniotic BMSC administration could be a new effective therapy for NTDs. |
| doi_str_mv | 10.1038/s41419-020-2734-3 |
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Currently, surgical closure of NTD lesions results in limited functional recovery. We previously suggested that nerve regeneration was critical for NTD therapy. Here, we report that transamniotic bone marrow-derived mesenchymal stem cell (BMSC) therapy for NTDs during early development may achieve beneficial functional recovery. In our ex vivo rat embryonic NTD model, BMSCs injected into the amniotic cavity spontaneously migrated into the defective neural tissue. Hepatocyte growth factor and its receptor c-MET were found to play critical roles in this NTD lesion-specific migration. Using the in vivo rat fetal NTD model, we further discovered that the engrafted BMSCs specifically differentiated into the cell types of the defective tissue, including skin and different types of neurons in situ. BMSC treatment triggered skin repair in fetuses, leading to a 29.9 ± 5.6% reduction in the skin lesion area. The electrophysiological functional recovery assay revealed a decreased latency and increased motor-evoked potential amplitude in the BMSC-treated fetuses. Based on these positive outcomes, ease of operation, and reduced trauma to the mother and fetus, we propose that transamniotic BMSC administration could be a new effective therapy for NTDs.</description><identifier>ISSN: 2041-4889</identifier><identifier>EISSN: 2041-4889</identifier><identifier>DOI: 10.1038/s41419-020-2734-3</identifier><identifier>PMID: 32655141</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/100 ; 13/109 ; 13/51 ; 14/35 ; 38/91 ; 45/77 ; 45/90 ; 631/532/1689 ; 692/699/375/361 ; 96/63 ; Animals ; Antibodies ; Biochemistry ; Biomedical and Life Sciences ; Bone marrow ; c-Met protein ; Cell Biology ; Cell Culture ; Cell Differentiation ; Cell therapy ; Embryogenesis ; Engraftment ; Fetuses ; Hepatocyte growth factor ; Humans ; Immunology ; Latency ; Life Sciences ; Mesenchymal Stem Cell Transplantation - methods ; Mesenchymal stem cells ; Mesenchymal Stem Cells - metabolism ; Morbidity ; Motor evoked potentials ; Nerve Regeneration - immunology ; Neural stem cells ; Neural tube defects ; Neural Tube Defects - therapy ; Rats ; Recovery of Function ; Regeneration ; Skin diseases ; Skin lesions ; Stem cells ; Trauma</subject><ispartof>Cell death & disease, 2020-07, Vol.11 (7), p.523-523, Article 523</ispartof><rights>The Author(s) 2020</rights><rights>The Author(s) 2020. 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Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-c97fbdc0b95a4f3a1fbd5f0daefc082f7b195389c550b668882a045b047ea0313</citedby><cites>FETCH-LOGICAL-c470t-c97fbdc0b95a4f3a1fbd5f0daefc082f7b195389c550b668882a045b047ea0313</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7354991/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7354991/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32655141$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wei, Xiaowei</creatorcontrib><creatorcontrib>Ma, Wei</creatorcontrib><creatorcontrib>Gu, Hui</creatorcontrib><creatorcontrib>Liu, Dan</creatorcontrib><creatorcontrib>Luo, Wenting</creatorcontrib><creatorcontrib>Bai, Yuzuo</creatorcontrib><creatorcontrib>Wang, Weilin</creatorcontrib><creatorcontrib>Lui, Vincent Chi Hang</creatorcontrib><creatorcontrib>Yang, Peixin</creatorcontrib><creatorcontrib>Yuan, Zhengwei</creatorcontrib><title>Transamniotic mesenchymal stem cell therapy for neural tube defects preserves neural function through lesion-specific engraftment and regeneration</title><title>Cell death & disease</title><addtitle>Cell Death Dis</addtitle><addtitle>Cell Death Dis</addtitle><description>Neural tube defects (NTDs) lead to prenatal mortality and lifelong morbidity. Currently, surgical closure of NTD lesions results in limited functional recovery. We previously suggested that nerve regeneration was critical for NTD therapy. Here, we report that transamniotic bone marrow-derived mesenchymal stem cell (BMSC) therapy for NTDs during early development may achieve beneficial functional recovery. In our ex vivo rat embryonic NTD model, BMSCs injected into the amniotic cavity spontaneously migrated into the defective neural tissue. Hepatocyte growth factor and its receptor c-MET were found to play critical roles in this NTD lesion-specific migration. Using the in vivo rat fetal NTD model, we further discovered that the engrafted BMSCs specifically differentiated into the cell types of the defective tissue, including skin and different types of neurons in situ. BMSC treatment triggered skin repair in fetuses, leading to a 29.9 ± 5.6% reduction in the skin lesion area. The electrophysiological functional recovery assay revealed a decreased latency and increased motor-evoked potential amplitude in the BMSC-treated fetuses. Based on these positive outcomes, ease of operation, and reduced trauma to the mother and fetus, we propose that transamniotic BMSC administration could be a new effective therapy for NTDs.</description><subject>13/100</subject><subject>13/109</subject><subject>13/51</subject><subject>14/35</subject><subject>38/91</subject><subject>45/77</subject><subject>45/90</subject><subject>631/532/1689</subject><subject>692/699/375/361</subject><subject>96/63</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Bone marrow</subject><subject>c-Met protein</subject><subject>Cell Biology</subject><subject>Cell Culture</subject><subject>Cell Differentiation</subject><subject>Cell therapy</subject><subject>Embryogenesis</subject><subject>Engraftment</subject><subject>Fetuses</subject><subject>Hepatocyte growth factor</subject><subject>Humans</subject><subject>Immunology</subject><subject>Latency</subject><subject>Life Sciences</subject><subject>Mesenchymal Stem Cell Transplantation - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death & disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wei, Xiaowei</au><au>Ma, Wei</au><au>Gu, Hui</au><au>Liu, Dan</au><au>Luo, Wenting</au><au>Bai, Yuzuo</au><au>Wang, Weilin</au><au>Lui, Vincent Chi Hang</au><au>Yang, Peixin</au><au>Yuan, Zhengwei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Transamniotic mesenchymal stem cell therapy for neural tube defects preserves neural function through lesion-specific engraftment and regeneration</atitle><jtitle>Cell death & disease</jtitle><stitle>Cell Death Dis</stitle><addtitle>Cell Death Dis</addtitle><date>2020-07-13</date><risdate>2020</risdate><volume>11</volume><issue>7</issue><spage>523</spage><epage>523</epage><pages>523-523</pages><artnum>523</artnum><issn>2041-4889</issn><eissn>2041-4889</eissn><abstract>Neural tube defects (NTDs) lead to prenatal mortality and lifelong morbidity. Currently, surgical closure of NTD lesions results in limited functional recovery. We previously suggested that nerve regeneration was critical for NTD therapy. Here, we report that transamniotic bone marrow-derived mesenchymal stem cell (BMSC) therapy for NTDs during early development may achieve beneficial functional recovery. In our ex vivo rat embryonic NTD model, BMSCs injected into the amniotic cavity spontaneously migrated into the defective neural tissue. Hepatocyte growth factor and its receptor c-MET were found to play critical roles in this NTD lesion-specific migration. Using the in vivo rat fetal NTD model, we further discovered that the engrafted BMSCs specifically differentiated into the cell types of the defective tissue, including skin and different types of neurons in situ. BMSC treatment triggered skin repair in fetuses, leading to a 29.9 ± 5.6% reduction in the skin lesion area. The electrophysiological functional recovery assay revealed a decreased latency and increased motor-evoked potential amplitude in the BMSC-treated fetuses. Based on these positive outcomes, ease of operation, and reduced trauma to the mother and fetus, we propose that transamniotic BMSC administration could be a new effective therapy for NTDs.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>32655141</pmid><doi>10.1038/s41419-020-2734-3</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/100 13/109 13/51 14/35 38/91 45/77 45/90 631/532/1689 692/699/375/361 96/63 Animals Antibodies Biochemistry Biomedical and Life Sciences Bone marrow c-Met protein Cell Biology Cell Culture Cell Differentiation Cell therapy Embryogenesis Engraftment Fetuses Hepatocyte growth factor Humans Immunology Latency Life Sciences Mesenchymal Stem Cell Transplantation - methods Mesenchymal stem cells Mesenchymal Stem Cells - metabolism Morbidity Motor evoked potentials Nerve Regeneration - immunology Neural stem cells Neural tube defects Neural Tube Defects - therapy Rats Recovery of Function Regeneration Skin diseases Skin lesions Stem cells Trauma |
| title | Transamniotic mesenchymal stem cell therapy for neural tube defects preserves neural function through lesion-specific engraftment and regeneration |
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