Human Adipose‐Derived Stromal/Stem Cells Protect Against STZ‐Induced Hyperglycemia: Analysis of hASC‐Derived Paracrine Effectors
Adipose‐derived stromal/stem cells (ASCs) ameliorate hyperglycemia in rodent models of islet transplantation and autoimmune diabetes, yet the precise human ASC (hASC)‐derived factors responsible for these effects remain largely unexplored. Here, we show that systemic administration of hASCs improved...
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| Published in | Stem cells (Dayton, Ohio) Vol. 32; no. 7; pp. 1831 - 1842 |
|---|---|
| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Oxford University Press
01.07.2014
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Adipose‐derived stromal/stem cells (ASCs) ameliorate hyperglycemia in rodent models of islet transplantation and autoimmune diabetes, yet the precise human ASC (hASC)‐derived factors responsible for these effects remain largely unexplored. Here, we show that systemic administration of hASCs improved glucose tolerance, preserved β cell mass, and increased β cell proliferation in streptozotocin‐treated nonobese diabetic/severe combined immunodeficient mice. Coculture experiments combining mouse or human islets with hASCs demonstrated that islet viability and function were improved by hASCs following prolonged culture or treatment with proinflammatory cytokines. Analysis of hASC‐derived factors revealed vascular endothelial growth factor and tissue inhibitor of metalloproteinase 1 (TIMP‐1) to be highly abundant factors secreted by hASCs. Notably, TIMP‐1 secretion increased in the presence of islet stress from cytokine treatment, while TIMP‐1 blockade was able to abrogate in vitro prosurvival effects of hASCs. Following systemic administration by tail vein injection, hASCs were detected in the pancreas and human TIMP‐1 was increased in the serum of injected mice, while recombinant TIMP‐1 increased viability in INS‐1 cells treated with interleukin‐1beta, interferon‐gamma, and tumor necrosis factor alpha. In aggregate, our data support a model whereby factors secreted by hASCs, such as TIMP‐1, are able to mitigate against β cell death in rodent and in vitro models of type 1 diabetes through a combination of local paracrine as well as systemic effects. Stem Cells 2014;32:1831–1842 |
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| AbstractList | Adipose-derived stromal/stem cells (ASCs) ameliorate hyperglycemia in rodent models of islet transplantation and autoimmune diabetes, yet the precise human ASC (hASC)-derived factors responsible for these effects remain largely unexplored. Here, we show that systemic administration of hASCs improved glucose tolerance, preserved β cell mass, and increased β cell proliferation in streptozotocin-treated nonobese diabetic/severe combined immunodeficient mice. Coculture experiments combining mouse or human islets with hASCs demonstrated that islet viability and function were improved by hASCs following prolonged culture or treatment with proinflammatory cytokines. Analysis of hASC-derived factors revealed vascular endothelial growth factor and tissue inhibitor of metalloproteinase 1 (TIMP-1) to be highly abundant factors secreted by hASCs. Notably, TIMP-1 secretion increased in the presence of islet stress from cytokine treatment, while TIMP-1 blockade was able to abrogate in vitro prosurvival effects of hASCs. Following systemic administration by tail vein injection, hASCs were detected in the pancreas and human TIMP-1 was increased in the serum of injected mice, while recombinant TIMP-1 increased viability in INS-1 cells treated with interleukin-1beta, interferon-gamma, and tumor necrosis factor alpha. In aggregate, our data support a model whereby factors secreted by hASCs, such as TIMP-1, are able to mitigate against β cell death in rodent and in vitro models of type 1 diabetes through a combination of local paracrine as well as systemic effects. Stem Cells 2014;32:1831–1842 Adipose-derived stromal/stem cells (ASCs) ameliorate hyperglycemia in rodent models of islet transplantation and autoimmune diabetes, yet the precise human ASC (hASC)-derived factors responsible for these effects remain largely unexplored. Here, we show that systemic administration of hASCs improved glucose tolerance, preserved β cell mass, and increased β cell proliferation in streptozotocin-treated nonobese diabetic/severe combined immunodeficient mice. Coculture experiments combining mouse or human islets with hASCs demonstrated that islet viability and function were improved by hASCs following prolonged culture or treatment with proinflammatory cytokines. Analysis of hASC-derived factors revealed vascular endothelial growth factor and tissue inhibitor of metalloproteinase 1 (TIMP-1) to be highly abundant factors secreted by hASCs. Notably, TIMP-1 secretion increased in the presence of islet stress from cytokine treatment, while TIMP-1 blockade was able to abrogate in vitro prosurvival effects of hASCs. Following systemic administration by tail vein injection, hASCs were detected in the pancreas and human TIMP-1 was increased in the serum of injected mice, while recombinant TIMP-1 increased viability in INS-1 cells treated with interleukin-1beta, interferon-gamma, and tumor necrosis factor alpha. In aggregate, our data support a model whereby factors secreted by hASCs, such as TIMP-1, are able to mitigate against β cell death in rodent and in vitro models of type 1 diabetes through a combination of local paracrine as well as systemic effects.Adipose-derived stromal/stem cells (ASCs) ameliorate hyperglycemia in rodent models of islet transplantation and autoimmune diabetes, yet the precise human ASC (hASC)-derived factors responsible for these effects remain largely unexplored. Here, we show that systemic administration of hASCs improved glucose tolerance, preserved β cell mass, and increased β cell proliferation in streptozotocin-treated nonobese diabetic/severe combined immunodeficient mice. Coculture experiments combining mouse or human islets with hASCs demonstrated that islet viability and function were improved by hASCs following prolonged culture or treatment with proinflammatory cytokines. Analysis of hASC-derived factors revealed vascular endothelial growth factor and tissue inhibitor of metalloproteinase 1 (TIMP-1) to be highly abundant factors secreted by hASCs. Notably, TIMP-1 secretion increased in the presence of islet stress from cytokine treatment, while TIMP-1 blockade was able to abrogate in vitro prosurvival effects of hASCs. Following systemic administration by tail vein injection, hASCs were detected in the pancreas and human TIMP-1 was increased in the serum of injected mice, while recombinant TIMP-1 increased viability in INS-1 cells treated with interleukin-1beta, interferon-gamma, and tumor necrosis factor alpha. In aggregate, our data support a model whereby factors secreted by hASCs, such as TIMP-1, are able to mitigate against β cell death in rodent and in vitro models of type 1 diabetes through a combination of local paracrine as well as systemic effects. Adipose-derived stromal/stem cells (ASCs) ameliorate hyperglycemia in rodent models of islet transplantation and autoimmune diabetes, yet the precise human ASC (hASC)-derived factors responsible for these effects remain largely unexplored. Here, we show that systemic administration of hASCs improved glucose tolerance, preserved β cell mass, and increased β cell proliferation in streptozotocin-treated nonobese diabetic/severe combined immunodeficient mice. Coculture experiments combining mouse or human islets with hASCs demonstrated that islet viability and function were improved by hASCs following prolonged culture or treatment with proinflammatory cytokines. Analysis of hASC-derived factors revealed vascular endothelial growth factor and tissue inhibitor of metalloproteinase 1 (TIMP-1) to be highly abundant factors secreted by hASCs. Notably, TIMP-1 secretion increased in the presence of islet stress from cytokine treatment, while TIMP-1 blockade was able to abrogate in vitro prosurvival effects of hASCs. Following systemic administration by tail vein injection, hASCs were detected in the pancreas and human TIMP-1 was increased in the serum of injected mice, while recombinant TIMP-1 increased viability in INS-1 cells treated with interleukin-1beta, interferon-gamma, and tumor necrosis factor alpha. In aggregate, our data support a model whereby factors secreted by hASCs, such as TIMP-1, are able to mitigate against β cell death in rodent and in vitro models of type 1 diabetes through a combination of local paracrine as well as systemic effects. Adipose-derived stromal/stem cells (ASCs) ameliorate hyperglycemia in rodent models of islet transplantation and autoimmune diabetes, yet the precise human ASC (hASC)-derived factors responsible for these effects remain largely unexplored. Here, we show that systemic administration of hASCs improved glucose tolerance, preserved [beta] cell mass, and increased [beta] cell proliferation in streptozotocin-treated nonobese diabetic/severe combined immunodeficient mice. Coculture experiments combining mouse or human islets with hASCs demonstrated that islet viability and function were improved by hASCs following prolonged culture or treatment with proinflammatory cytokines. Analysis of hASC-derived factors revealed vascular endothelial growth factor and tissue inhibitor of metalloproteinase 1 (TIMP-1) to be highly abundant factors secreted by hASCs. Notably, TIMP-1 secretion increased in the presence of islet stress from cytokine treatment, while TIMP-1 blockade was able to abrogate in vitro prosurvival effects of hASCs. Following systemic administration by tail vein injection, hASCs were detected in the pancreas and human TIMP-1 was increased in the serum of injected mice, while recombinant TIMP-1 increased viability in INS-1 cells treated with interleukin-1beta, interferon-gamma, and tumor necrosis factor alpha. In aggregate, our data support a model whereby factors secreted by hASCs, such as TIMP-1, are able to mitigate against [beta] cell death in rodent and in vitro models of type 1 diabetes through a combination of local paracrine as well as systemic effects. Stem Cells 2014;32:1831-1842 [PUBLICATION ABSTRACT] Adipose-derived stromal/stem cells (ASCs) ameliorate hyperglycemia in rodent models of islet transplantation and autoimmune diabetes, yet the precise human ASC (hASC)-derived factors responsible for these effects remain largely unexplored. Here, we show that systemic administration of hASCs improved glucose tolerance, preserved [beta] cell mass, and increased [beta] cell proliferation in streptozotocin-treated nonobese diabetic/severe combined immunodeficient mice. Coculture experiments combining mouse or human islets with hASCs demonstrated that islet viability and function were improved by hASCs following prolonged culture or treatment with proinflammatory cytokines. Analysis of hASC-derived factors revealed vascular endothelial growth factor and tissue inhibitor of metalloproteinase 1 (TIMP-1) to be highly abundant factors secreted by hASCs. Notably, TIMP-1 secretion increased in the presence of islet stress from cytokine treatment, while TIMP-1 blockade was able to abrogate in vitro prosurvival effects of hASCs. Following systemic administration by tail vein injection, hASCs were detected in the pancreas and human TIMP-1 was increased in the serum of injected mice, while recombinant TIMP-1 increased viability in INS-1 cells treated with interleukin-1beta, interferon-gamma, and tumor necrosis factor alpha. In aggregate, our data support a model whereby factors secreted by hASCs, such as TIMP-1, are able to mitigate against [beta] cell death in rodent and in vitro models of type 1 diabetes through a combination of local paracrine as well as systemic effects. Stem Cells 2014; 32:1831-1842 Adipose-derived stromal/stem cells (ASCs) ameliorate hyperglycemia in rodent models of islet transplantation and autoimmune diabetes, yet the precise human ASC (hASC)-derived factors responsible for these effects remain largely unexplored. Here, we show that systemic administration of hASCs improved glucose tolerance, preserved β cell mass, and increased β cell proliferation in STZ-treated NOD-SCID mice. Co-culture experiments combining mouse or human islets with hASCs demonstrated that islet viability and function were improved by hASCs following prolonged culture or treatment with pro-inflammatory cytokines. Analysis of hASC-derived factors revealed VEGF and TIMP-1 to be highly abundant factors secreted by hASCs. Notably, TIMP-1 secretion increased in the presence of islet stress from cytokine treatment, while TIMP-1 blockade was able to abrogate in vitro pro-survival effects of hASCs. Following systemic administration by tail vein injection, hASCs were detected in the pancreas and human TIMP-1 was increased in the serum of injected mice, while recombinant TIMP-1 increased viability in INS-1 cells treated with IL-1β, IFN-γ and TNF-α. In aggregate, our data support a model whereby factors secreted by hASCs, such as TIMP-1, are able to mitigate against β cell death in rodent and in vitro models of Type 1 diabetes through a combination of local paracrine as well as systemic effects. Adipose‐derived stromal/stem cells (ASCs) ameliorate hyperglycemia in rodent models of islet transplantation and autoimmune diabetes, yet the precise human ASC (hASC)‐derived factors responsible for these effects remain largely unexplored. Here, we show that systemic administration of hASCs improved glucose tolerance, preserved β cell mass, and increased β cell proliferation in streptozotocin‐treated nonobese diabetic/severe combined immunodeficient mice. Coculture experiments combining mouse or human islets with hASCs demonstrated that islet viability and function were improved by hASCs following prolonged culture or treatment with proinflammatory cytokines. Analysis of hASC‐derived factors revealed vascular endothelial growth factor and tissue inhibitor of metalloproteinase 1 (TIMP‐1) to be highly abundant factors secreted by hASCs. Notably, TIMP‐1 secretion increased in the presence of islet stress from cytokine treatment, while TIMP‐1 blockade was able to abrogate in vitro prosurvival effects of hASCs. Following systemic administration by tail vein injection, hASCs were detected in the pancreas and human TIMP‐1 was increased in the serum of injected mice, while recombinant TIMP‐1 increased viability in INS‐1 cells treated with interleukin‐1beta, interferon‐gamma, and tumor necrosis factor alpha. In aggregate, our data support a model whereby factors secreted by hASCs, such as TIMP‐1, are able to mitigate against β cell death in rodent and in vitro models of type 1 diabetes through a combination of local paracrine as well as systemic effects. Stem Cells 2014;32:1831–1842 |
| Author | March, Keith L. Moss, Dan R. Sims, Emily K. Kono, Tatsuyoshi M. Yamamoto, Wataru Evans‐Molina, Carmella Territo, Paul R. Traktuev, Dmitry O. Ahn, Geonyoung Hanenberg, Helmut Diamond, Julie Tong, Xin Day, Kathleen H. |
| AuthorAffiliation | 2 Department of Pediatrics, Indiana University School of Medicine, Indianapolis IN, USA 5 Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis IN, USA 4 Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis IN, USA 1 Department of Medicine, Indiana University School of Medicine, Indianapolis IN, USA 3 Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis IN, USA 6 Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis IN, USA |
| AuthorAffiliation_xml | – name: 3 Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis IN, USA – name: 2 Department of Pediatrics, Indiana University School of Medicine, Indianapolis IN, USA – name: 6 Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis IN, USA – name: 1 Department of Medicine, Indiana University School of Medicine, Indianapolis IN, USA – name: 4 Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis IN, USA – name: 5 Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis IN, USA |
| Author_xml | – sequence: 1 givenname: Tatsuyoshi M. surname: Kono fullname: Kono, Tatsuyoshi M. organization: Indiana University School of Medicine – sequence: 2 givenname: Emily K. surname: Sims fullname: Sims, Emily K. organization: Indiana University School of Medicine – sequence: 3 givenname: Dan R. surname: Moss fullname: Moss, Dan R. organization: Indiana University School of Medicine – sequence: 4 givenname: Wataru surname: Yamamoto fullname: Yamamoto, Wataru organization: Indiana University School of Medicine – sequence: 5 givenname: Geonyoung surname: Ahn fullname: Ahn, Geonyoung organization: Herman B Wells Center for Pediatric Research, Indiana University School of Medicine – sequence: 6 givenname: Julie surname: Diamond fullname: Diamond, Julie organization: Herman B Wells Center for Pediatric Research, Indiana University School of Medicine – sequence: 7 givenname: Xin surname: Tong fullname: Tong, Xin organization: Indiana University School of Medicine – sequence: 8 givenname: Kathleen H. surname: Day fullname: Day, Kathleen H. organization: Indiana University School of Medicine – sequence: 9 givenname: Paul R. surname: Territo fullname: Territo, Paul R. organization: Indiana University School of Medicine – sequence: 10 givenname: Helmut surname: Hanenberg fullname: Hanenberg, Helmut organization: Herman B Wells Center for Pediatric Research, Indiana University School of Medicine – sequence: 11 givenname: Dmitry O. surname: Traktuev fullname: Traktuev, Dmitry O. organization: Richard L. Roudebush Veterans Affairs Medical Center – sequence: 12 givenname: Keith L. surname: March fullname: March, Keith L. organization: Richard L. Roudebush Veterans Affairs Medical Center – sequence: 13 givenname: Carmella surname: Evans‐Molina fullname: Evans‐Molina, Carmella organization: Richard L. Roudebush Veterans Affairs Medical Center |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24519994$$D View this record in MEDLINE/PubMed |
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| Snippet | Adipose‐derived stromal/stem cells (ASCs) ameliorate hyperglycemia in rodent models of islet transplantation and autoimmune diabetes, yet the precise human ASC... Adipose-derived stromal/stem cells (ASCs) ameliorate hyperglycemia in rodent models of islet transplantation and autoimmune diabetes, yet the precise human ASC... |
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| SubjectTerms | Adipose stem cells Adult Adult Stem Cells - metabolism Adult Stem Cells - transplantation Animals Caspase Cell Size Cells, Cultured Cellular proliferation Coculture Techniques Cytokines - physiology Diabetes Diabetes Mellitus, Experimental - chemically induced Diabetes Mellitus, Experimental - therapy Diabetes Mellitus, Type 1 - chemically induced Diabetes Mellitus, Type 1 - therapy Female Glucose Intolerance Humans Hyperglycemia Hyperglycemia - chemically induced Hyperglycemia - therapy Insulin-Secreting Cells - pathology Male Mice, Inbred C57BL Mice, Inbred NOD Mice, SCID Pancreas Paracrine Communication Rodents Stem cells Streptozocin Subcutaneous Fat - cytology Tissue Inhibitor of Metalloproteinase-1 - metabolism Tissue regeneration |
| Title | Human Adipose‐Derived Stromal/Stem Cells Protect Against STZ‐Induced Hyperglycemia: Analysis of hASC‐Derived Paracrine Effectors |
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