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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
Main Authors: Sabadine, Maria Augusta, Russo, Thiago Luiz, Luna, Genoveva Flores, Oliveira Leal, Angela Merice
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container_title Muscle & nerve
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creator Sabadine, Maria Augusta
Russo, Thiago Luiz
Luna, Genoveva Flores
Oliveira Leal, Angela Merice
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
doi_str_mv 10.1002/mus.26196
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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 &amp; 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 &amp; 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 &amp; Medical Complete (Alumni)</collection><collection>Nursing &amp; Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Muscle &amp; 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 &amp; 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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