Mitochondrial Targeting with Antioxidant Peptide SS-31 Prevents Mitochondrial Depolarization, Reduces Islet Cell Apoptosis, Increases Islet Cell Yield, and Improves Posttransplantation Function

Thomas, Dolca A.; Stauffer, Craig; Zhao, Kesheng; Yang, Hua; Sharma, Vijay K.; Szeto, Hazel H.; Suthanthiran, Manikkam

doi:10.1681/asn.2006080825

Cited by 84Pancreatic function and diabetesDiabetes and associated disordersMitochondrial Function and Pathology

Mitochondrial Targeting with Antioxidant Peptide SS-31 Prevents Mitochondrial Depolarization, Reduces Islet Cell Apoptosis, Increases Islet Cell Yield, and Improves Posttransplantation Function

Thomas, Dolca A., Stauffer, Craig, Zhao, Kesheng, Yang, Hua, Sharma, Vijay K., Szeto, Hazel H., Suthanthiran, Manikkam·2007·Journal of the American Society of Nephrology

DOI 10.1681/asn.2006080825

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Abstract

Apoptotic cell death is a defined pathway for islet cell demise, and mitochondrial dysfunction contributes to islet cell apoptosis. The hypothesis that the novel peptide D-Arg-2', 6'-dimethyltyrosine-Lys-Phe-NH2 (SS-31), previously shown to target inner mitochondrial membrane and prevent oxidative damage of neuronal cells and other cell types, optimizes pancreatic islet isolation and improves posttransplantation function in recipients with diabetes was investigated. Herein is demonstrated that SS-31 readily penetrates intact mouse islets, preserves mitochondrial polarization, reduces islet cell apoptosis, and increases islet cell yield. Optimization of islet isolation is demonstrable after SS-31 pretreatment of islet (pancreas) donor mice and with the addition of SS-31 to reagents that are used in the isolation of mouse islets. The supplementation of in vitro culture medium with SS-31 reduced islet cell apoptosis and increased the viability of human islets, as ascertained by dual-parameter flow cytometry analysis. In a stringent marginal islet cell mass transplantation model (200 mouse islets transplanted under the renal capsule of syngeneic diabetic mice) and using islets that were derived from old mice (>24 wk), SS-31 treatment was associated with prompt and sustained normoglycemia, whereas the untreated islet graft recipients remained diabetic. Our data suggest a novel strategy to optimize islet isolation and reduce the need for multiple pancreata to achieve insulin independence in the recipient with type 1 diabetes. Because SS-31 was effective with "extended" islet donors, it is hypothesized that the antioxidant SS-31 may serve to increase the pool of eligible organ donors.

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In type 2 diabetes, animal models and human islet and leukocyte samples provide evidence that elamipretide restores glucose levels.
“restoring glucose levels290”
From Mitochondrial and metabolic dysfunction in ageing and age-related diseases (2022) · cites this paper as [290]
Such peptides reduce intracellular ROS and cell death in neuronal and pancreatic islet cells and reduce skeletal myocyte H2O2 production and preserve insulin sensitivity in rats fed a high-fat diet.
“Such peptides reduce intracellular ROS and cell death in neuronal (256) and pancreatic islet cells (309) and recently were reported to reduce skeletal myocyte H2O2 production and to preserve insulin sensitivity in rats fed a high-fat diet (14).”
From Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010) · cites this paper as [309]

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Authors: Thomas, D. A., Stauffer, C., Zhao, K., Yang, H., Sharma, V. K., Szeto, H. H., & Suthanthiran, M.
Affiliations: NewYork–Presbyterian Hospital (US)
Corresponding author: Thomas, Dolca A.
Stauffer, Craig
Yang, Hua
Sharma, Vijay K.
Suthanthiran, Manikkam
ORCID: Yang, Hua
Sharma, Vijay K.
Szeto, Hazel H.
Suthanthiran, Manikkam
Venue: Journal of the American Society of Nephrology
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2007-01
Volume: 18
Issue: 1
Pages: 213-222
ISSN: 1046-6673 (ISSN-L)
DOI: 10.1681/asn.2006080825
OpenAlex: W2149486238
Cited by: 84
References: 48
Citations by year: 2026: 1 · 2025: 4 · 2024: 1 · 2023: 1 · 2022: 5 · 2021: 7 · 2020: 7 · 2019: 6 · 2018: 6 · 2017: 2 · 2016: 2 · 2015: 7 · 2014: 2 · 2013: 4 · 2012: 7
FWCI: 3.36
Type: journal article
Language: en
Open access: closed
Locations: Journal of the American Society of Nephrology (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (5r21dk060186-02)
National Institute on Drug Abuse (P01DA008924)
National Institute of Diabetes and Digestive and Kidney Diseases (R21 DK 60186)
National Institute of Neurological Disorders and Stroke (R21NS048295)
Topics: Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords: SS-31, mitochondrial peptides, antioxidant peptides, islet transplantation, islet isolation, islet cell apoptosis, mitochondrial depolarization, mitochondrial dysfunction, type 1 diabetes, islet graft function, insulin independence
MeSH terms: Animals, Antioxidants, Biological Transport, Active, Diabetes Mellitus, Experimental, Humans, Male, Mice, Inbred DBA, Mitochondria, Oligopeptides, Transplantation, Isogeneic, Islets of Langerhans Transplantation, Apoptosis, Mice, Membrane Potential, Mitochondrial, In Vitro Techniques

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Mitochondrial Targeting with Antioxidant Peptide SS-31 Prevents Mitochondrial Depolarization, Reduces Islet Cell Apoptosis, Increases Islet Cell Yield, and Improves Posttransplantation Function

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