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Effects of mesenchymal stromal cells on type 1 diabetes mellitus rat muscles
ABSTRACT Introduction: Type 1 diabetes mellitus (DM) causes marked skeletal muscle atrophy. Mesenchymal stromal cells (MSC) are an attractive therapy to avoid diabetic complications because of their ability to modify the microenvironment at sites of tissue injury. The objective of this study was to...
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Published in: | Muscle & nerve 2018-10, Vol.58 (4), p.583-591 |
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Introduction: Type 1 diabetes mellitus (DM) causes marked skeletal muscle atrophy. Mesenchymal stromal cells (MSC) are an attractive therapy to avoid diabetic complications because of their ability to modify the microenvironment at sites of tissue injury. The objective of this study was to evaluate the effects of MSC transplantation on muscle adaptation caused by diabetes. Methods: DM was induced by streptozotocin (STZ), and the diabetic animals received systemic MSC transplantation. The von Frey test and footprint analysis were used to assess sensation and sensory motor performance, respectively. Tibialis anterior muscles were investigated by morphology; molecular markers atrogin‐1/muscle RING‐finger protein‐1, nuclear factor κB/p38 mitogen‐activated protein kinase, tumor necrosis‐like weak inducer of apoptosis/fibroblast growth factor‐inducible 14, myostatin, myogenic differentiation 1, and insulin‐like growth factor 1 were also assessed. Results: MSC transplantation improved sensation and walking performance and also decreased muscle fibrosis in DM rats by modulating atrogenes but did not prevent muscle atrophy. Discussion: MSCs can reduce muscle and functional complications that result from type 1 DM in rats. Muscle Nerve 58: 583–591, 2018 |
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Introduction: Type 1 diabetes mellitus (DM) causes marked skeletal muscle atrophy. Mesenchymal stromal cells (MSC) are an attractive therapy to avoid diabetic complications because of their ability to modify the microenvironment at sites of tissue injury. The objective of this study was to evaluate the effects of MSC transplantation on muscle adaptation caused by diabetes. Methods: DM was induced by streptozotocin (STZ), and the diabetic animals received systemic MSC transplantation. The von Frey test and footprint analysis were used to assess sensation and sensory motor performance, respectively. Tibialis anterior muscles were investigated by morphology; molecular markers atrogin‐1/muscle RING‐finger protein‐1, nuclear factor κB/p38 mitogen‐activated protein kinase, tumor necrosis‐like weak inducer of apoptosis/fibroblast growth factor‐inducible 14, myostatin, myogenic differentiation 1, and insulin‐like growth factor 1 were also assessed. Results: MSC transplantation improved sensation and walking performance and also decreased muscle fibrosis in DM rats by modulating atrogenes but did not prevent muscle atrophy. Discussion: MSCs can reduce muscle and functional complications that result from type 1 DM in rats. Muscle Nerve 58: 583–591, 2018</description><identifier>ISSN: 0148-639X</identifier><identifier>EISSN: 1097-4598</identifier><identifier>DOI: 10.1002/mus.26196</identifier><identifier>PMID: 30028527</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Animals ; Apoptosis ; Atrophy ; cellular therapy ; Complications ; Diabetes ; Diabetes mellitus ; Diabetes mellitus (insulin dependent) ; Diabetes Mellitus, Experimental - complications ; Diabetes Mellitus, Experimental - metabolism ; Diabetes Mellitus, Type 1 - complications ; Diabetes Mellitus, Type 1 - metabolism ; Disease Models, Animal ; Fibroblast growth factors ; Fibrosis ; Footprint analysis ; Growth factors ; Insulin ; Insulin-Like Growth Factor I - metabolism ; Kinases ; Male ; Mesenchymal Stem Cell Transplantation ; Mesenchymal stem cells ; Mesenchyme ; Metabolic syndrome ; Morphology ; Motor task performance ; muscle atrophy ; Muscle Proteins - metabolism ; Muscle, Skeletal - metabolism ; Muscle, Skeletal - pathology ; Muscle, Skeletal - physiopathology ; Muscles ; Muscular Atrophy - metabolism ; Muscular Atrophy - pathology ; Muscular Diseases - etiology ; Muscular Diseases - metabolism ; Muscular Diseases - pathology ; Muscular Diseases - physiopathology ; MyoD Protein - metabolism ; Myostatin ; Myostatin - metabolism ; Necrosis ; NF-kappa B - metabolism ; p38 Mitogen-Activated Protein Kinases - metabolism ; Protein kinase ; Proteins ; Rats ; Rats, Wistar ; Sensorimotor integration ; Signal Transduction ; Skeletal muscle ; SKP Cullin F-Box Protein Ligases - metabolism ; Somatosensory Disorders - physiopathology ; Streptozocin ; Stromal cells ; Touch - physiology ; Transplantation ; Tripartite Motif Proteins - metabolism ; TWEAK Receptor - metabolism ; Ubiquitin-Protein Ligases - metabolism ; Walking</subject><ispartof>Muscle & nerve, 2018-10, Vol.58 (4), p.583-591</ispartof><rights>2018 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3536-5197bcf1389ce1f981dbcac898897b3a4c138eb2fb978d600d1c469b0782072e3</citedby><cites>FETCH-LOGICAL-c3536-5197bcf1389ce1f981dbcac898897b3a4c138eb2fb978d600d1c469b0782072e3</cites><orcidid>0000-0003-3454-5327</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30028527$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sabadine, Maria Augusta</creatorcontrib><creatorcontrib>Russo, Thiago Luiz</creatorcontrib><creatorcontrib>Luna, Genoveva Flores</creatorcontrib><creatorcontrib>Oliveira Leal, Angela Merice</creatorcontrib><title>Effects of mesenchymal stromal cells on type 1 diabetes mellitus rat muscles</title><title>Muscle & nerve</title><addtitle>Muscle Nerve</addtitle><description>ABSTRACT
Introduction: Type 1 diabetes mellitus (DM) causes marked skeletal muscle atrophy. Mesenchymal stromal cells (MSC) are an attractive therapy to avoid diabetic complications because of their ability to modify the microenvironment at sites of tissue injury. The objective of this study was to evaluate the effects of MSC transplantation on muscle adaptation caused by diabetes. Methods: DM was induced by streptozotocin (STZ), and the diabetic animals received systemic MSC transplantation. The von Frey test and footprint analysis were used to assess sensation and sensory motor performance, respectively. Tibialis anterior muscles were investigated by morphology; molecular markers atrogin‐1/muscle RING‐finger protein‐1, nuclear factor κB/p38 mitogen‐activated protein kinase, tumor necrosis‐like weak inducer of apoptosis/fibroblast growth factor‐inducible 14, myostatin, myogenic differentiation 1, and insulin‐like growth factor 1 were also assessed. Results: MSC transplantation improved sensation and walking performance and also decreased muscle fibrosis in DM rats by modulating atrogenes but did not prevent muscle atrophy. Discussion: MSCs can reduce muscle and functional complications that result from type 1 DM in rats. Muscle Nerve 58: 583–591, 2018</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Atrophy</subject><subject>cellular therapy</subject><subject>Complications</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (insulin dependent)</subject><subject>Diabetes Mellitus, Experimental - complications</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetes Mellitus, Type 1 - complications</subject><subject>Diabetes Mellitus, Type 1 - metabolism</subject><subject>Disease Models, Animal</subject><subject>Fibroblast growth factors</subject><subject>Fibrosis</subject><subject>Footprint analysis</subject><subject>Growth factors</subject><subject>Insulin</subject><subject>Insulin-Like Growth Factor I - metabolism</subject><subject>Kinases</subject><subject>Male</subject><subject>Mesenchymal Stem Cell Transplantation</subject><subject>Mesenchymal stem cells</subject><subject>Mesenchyme</subject><subject>Metabolic syndrome</subject><subject>Morphology</subject><subject>Motor task performance</subject><subject>muscle atrophy</subject><subject>Muscle Proteins - metabolism</subject><subject>Muscle, Skeletal - metabolism</subject><subject>Muscle, Skeletal - pathology</subject><subject>Muscle, Skeletal - physiopathology</subject><subject>Muscles</subject><subject>Muscular Atrophy - metabolism</subject><subject>Muscular Atrophy - pathology</subject><subject>Muscular Diseases - etiology</subject><subject>Muscular Diseases - metabolism</subject><subject>Muscular Diseases - pathology</subject><subject>Muscular Diseases - physiopathology</subject><subject>MyoD Protein - metabolism</subject><subject>Myostatin</subject><subject>Myostatin - metabolism</subject><subject>Necrosis</subject><subject>NF-kappa B - metabolism</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Protein kinase</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Sensorimotor integration</subject><subject>Signal Transduction</subject><subject>Skeletal muscle</subject><subject>SKP Cullin F-Box Protein Ligases - metabolism</subject><subject>Somatosensory Disorders - physiopathology</subject><subject>Streptozocin</subject><subject>Stromal cells</subject><subject>Touch - physiology</subject><subject>Transplantation</subject><subject>Tripartite Motif Proteins - metabolism</subject><subject>TWEAK Receptor - metabolism</subject><subject>Ubiquitin-Protein Ligases - metabolism</subject><subject>Walking</subject><issn>0148-639X</issn><issn>1097-4598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp1kEtLw0AUhQdRbK0u_AMy4EYXaeeRTGaWUuoDKi604G6YTO5gStLUTILk3zsh1YXg6i7Odz8OB6FLSuaUELaoOj9ngipxhKaUqDSKEyWP0ZTQWEaCq_cJOvN-SwihUqSnaMLDl0xYOkXrlXNgW49rhyvwsLMffWVK7NumHq6FsgzhDrf9HjDFeWEyaMEHuCyLtvO4MS0OBWwJ_hydOFN6uDjcGdrcr96Wj9H65eFpebeOLE-4iBKq0sw6yqWyQJ2SNM-ssVJJGQJuYhsiyJjLVCpzQUhObSxURlLJSMqAz9DN6N039WcHvtVV4YemZgd153WgOGdKEhHQ6z_otu6aXWinGaUikTxmPFC3I2Wb2vsGnN43RWWaXlOih4l1NWiHiQN7dTB2WQX5L_mzaQAWI_BVlND_b9LPm9dR-Q1MtoRl</recordid><startdate>201810</startdate><enddate>201810</enddate><creator>Sabadine, Maria Augusta</creator><creator>Russo, Thiago Luiz</creator><creator>Luna, Genoveva Flores</creator><creator>Oliveira Leal, Angela Merice</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TS</scope><scope>7U7</scope><scope>7U9</scope><scope>C1K</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-3454-5327</orcidid></search><sort><creationdate>201810</creationdate><title>Effects of mesenchymal stromal cells on type 1 diabetes mellitus rat muscles</title><author>Sabadine, Maria Augusta ; Russo, Thiago Luiz ; Luna, Genoveva Flores ; Oliveira Leal, Angela Merice</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3536-5197bcf1389ce1f981dbcac898897b3a4c138eb2fb978d600d1c469b0782072e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Atrophy</topic><topic>cellular therapy</topic><topic>Complications</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes mellitus (insulin dependent)</topic><topic>Diabetes Mellitus, Experimental - complications</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Diabetes Mellitus, Type 1 - complications</topic><topic>Diabetes Mellitus, Type 1 - metabolism</topic><topic>Disease Models, Animal</topic><topic>Fibroblast growth factors</topic><topic>Fibrosis</topic><topic>Footprint analysis</topic><topic>Growth factors</topic><topic>Insulin</topic><topic>Insulin-Like Growth Factor I - metabolism</topic><topic>Kinases</topic><topic>Male</topic><topic>Mesenchymal Stem Cell Transplantation</topic><topic>Mesenchymal stem cells</topic><topic>Mesenchyme</topic><topic>Metabolic syndrome</topic><topic>Morphology</topic><topic>Motor task performance</topic><topic>muscle atrophy</topic><topic>Muscle Proteins - metabolism</topic><topic>Muscle, Skeletal - metabolism</topic><topic>Muscle, Skeletal - pathology</topic><topic>Muscle, Skeletal - physiopathology</topic><topic>Muscles</topic><topic>Muscular Atrophy - metabolism</topic><topic>Muscular Atrophy - pathology</topic><topic>Muscular Diseases - etiology</topic><topic>Muscular Diseases - metabolism</topic><topic>Muscular Diseases - pathology</topic><topic>Muscular Diseases - physiopathology</topic><topic>MyoD Protein - metabolism</topic><topic>Myostatin</topic><topic>Myostatin - metabolism</topic><topic>Necrosis</topic><topic>NF-kappa B - metabolism</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Protein kinase</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Sensorimotor integration</topic><topic>Signal Transduction</topic><topic>Skeletal muscle</topic><topic>SKP Cullin F-Box Protein Ligases - metabolism</topic><topic>Somatosensory Disorders - physiopathology</topic><topic>Streptozocin</topic><topic>Stromal cells</topic><topic>Touch - physiology</topic><topic>Transplantation</topic><topic>Tripartite Motif Proteins - metabolism</topic><topic>TWEAK Receptor - metabolism</topic><topic>Ubiquitin-Protein Ligases - metabolism</topic><topic>Walking</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sabadine, Maria Augusta</creatorcontrib><creatorcontrib>Russo, Thiago Luiz</creatorcontrib><creatorcontrib>Luna, Genoveva Flores</creatorcontrib><creatorcontrib>Oliveira Leal, Angela Merice</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Muscle & nerve</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sabadine, Maria Augusta</au><au>Russo, Thiago Luiz</au><au>Luna, Genoveva Flores</au><au>Oliveira Leal, Angela Merice</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of mesenchymal stromal cells on type 1 diabetes mellitus rat muscles</atitle><jtitle>Muscle & nerve</jtitle><addtitle>Muscle Nerve</addtitle><date>2018-10</date><risdate>2018</risdate><volume>58</volume><issue>4</issue><spage>583</spage><epage>591</epage><pages>583-591</pages><issn>0148-639X</issn><eissn>1097-4598</eissn><abstract>ABSTRACT
Introduction: Type 1 diabetes mellitus (DM) causes marked skeletal muscle atrophy. Mesenchymal stromal cells (MSC) are an attractive therapy to avoid diabetic complications because of their ability to modify the microenvironment at sites of tissue injury. The objective of this study was to evaluate the effects of MSC transplantation on muscle adaptation caused by diabetes. Methods: DM was induced by streptozotocin (STZ), and the diabetic animals received systemic MSC transplantation. The von Frey test and footprint analysis were used to assess sensation and sensory motor performance, respectively. Tibialis anterior muscles were investigated by morphology; molecular markers atrogin‐1/muscle RING‐finger protein‐1, nuclear factor κB/p38 mitogen‐activated protein kinase, tumor necrosis‐like weak inducer of apoptosis/fibroblast growth factor‐inducible 14, myostatin, myogenic differentiation 1, and insulin‐like growth factor 1 were also assessed. Results: MSC transplantation improved sensation and walking performance and also decreased muscle fibrosis in DM rats by modulating atrogenes but did not prevent muscle atrophy. Discussion: MSCs can reduce muscle and functional complications that result from type 1 DM in rats. Muscle Nerve 58: 583–591, 2018</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>30028527</pmid><doi>10.1002/mus.26196</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0003-3454-5327</orcidid></addata></record> |
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subjects | Animals Apoptosis Atrophy cellular therapy Complications Diabetes Diabetes mellitus Diabetes mellitus (insulin dependent) Diabetes Mellitus, Experimental - complications Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Type 1 - complications Diabetes Mellitus, Type 1 - metabolism Disease Models, Animal Fibroblast growth factors Fibrosis Footprint analysis Growth factors Insulin Insulin-Like Growth Factor I - metabolism Kinases Male Mesenchymal Stem Cell Transplantation Mesenchymal stem cells Mesenchyme Metabolic syndrome Morphology Motor task performance muscle atrophy Muscle Proteins - metabolism Muscle, Skeletal - metabolism Muscle, Skeletal - pathology Muscle, Skeletal - physiopathology Muscles Muscular Atrophy - metabolism Muscular Atrophy - pathology Muscular Diseases - etiology Muscular Diseases - metabolism Muscular Diseases - pathology Muscular Diseases - physiopathology MyoD Protein - metabolism Myostatin Myostatin - metabolism Necrosis NF-kappa B - metabolism p38 Mitogen-Activated Protein Kinases - metabolism Protein kinase Proteins Rats Rats, Wistar Sensorimotor integration Signal Transduction Skeletal muscle SKP Cullin F-Box Protein Ligases - metabolism Somatosensory Disorders - physiopathology Streptozocin Stromal cells Touch - physiology Transplantation Tripartite Motif Proteins - metabolism TWEAK Receptor - metabolism Ubiquitin-Protein Ligases - metabolism Walking |
title | Effects of mesenchymal stromal cells on type 1 diabetes mellitus rat muscles |
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