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Pharmacology and Therapeutics

MG53 Does Not Manifest the Development of Diabetes in db/db Mice

  1. Qiang Wang1,
  2. Zehua Bian1,
  3. Qiwei Jiang1,
  4. Xiaoliang Wang1,
  5. Xinyu Zhou1,
  6. Ki Ho Park1,
  7. Willa Hsueh2,
  8. Bryan A. Whitson1,
  9. Erin Haggard1,
  10. Haichang Li1,
  11. Ken Chen3,4,
  12. Chuanxi Cai1,
  13. Tao Tan1,5⇑,
  14. Hua Zhu1⇑ and
  15. Jianjie Ma1⇑
  1. 1Department of Surgery, The Ohio State University Wexner Medical Center, Columbus, OH
  2. 2Diabetes and Metabolism Research Center, Department of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, OH
  3. 3Department of Cardiology, The General Hospital of Western Theater Command, Chengdu, Sichuan, China
  4. 4Department of Cardiology, Daping Hospital, The Third Military Medical University, Chongqing, China
  5. 5TRIM-edicine, Inc., Columbus, OH
  1. Corresponding authors: Jianjie Ma, jianjie.ma{at}osumc.edu, Hua Zhu, hua.zhu{at}osumc.edu, and Tao Tan, ttan{at}trim-edicine.com
  1. Q.W., Z.B., and Q.J. contributed equally to this work.

Diabetes 2020 May; 69(5): 1052-1064. https://doi.org/10.2337/db19-0807
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Abstract

MG53 is a member of the TRIM protein family that is predominantly expressed in striated muscles and participates in cell membrane repair. Controversy exists regarding MG53’s role in insulin signaling and manifestation of diabetes. We generated db/db mice with either whole-body ablation or sustained elevation of MG53 in the bloodstream in order to evaluate the physiological function of MG53 in diabetes. To quantify the amount of MG53 protein in circulation, we developed a monoclonal antibody against MG53 with high specificity. Western blot using this antibody revealed lower or no change of serum MG53 levels in db/db mice or patients with diabetes compared with control subjects. Neither whole-body ablation of MG53 nor sustained elevation of MG53 in circulation altered insulin signaling and glucose handling in db/db mice. Instead, mice with ablation of MG53 were more susceptible to streptozotocin-induced dysfunctional handling of glucose compared with the wild-type littermates. Alkaline-induced corneal injury demonstrated delayed healing in db/db mice, which was restored by topical administration of recombinant human (rh)MG53. Daily intravenous administration of rhMG53 in rats at concentrations up to 10 mg/kg did not produce adverse effects on glucose handling. These findings challenge the hypothetical function of MG53 as a causative factor for the development of diabetes. Our data suggest that rhMG53 is a potentially safe and effective biologic to treat diabetic oculopathy in rodents.

Footnotes

  • This article contains Supplementary Data online at https://diabetes.diabetesjournals.org/lookup/suppl/doi:10.2337/db19-0807/-/DC1.

  • Received August 14, 2019.
  • Accepted February 25, 2020.
  • © 2020 by the American Diabetes Association
https://www.diabetesjournals.org/content/license

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. More information is available at https://www.diabetesjournals.org/content/license.

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May 2020, 69(5)
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MG53 Does Not Manifest the Development of Diabetes in db/db Mice
Qiang Wang, Zehua Bian, Qiwei Jiang, Xiaoliang Wang, Xinyu Zhou, Ki Ho Park, Willa Hsueh, Bryan A. Whitson, Erin Haggard, Haichang Li, Ken Chen, Chuanxi Cai, Tao Tan, Hua Zhu, Jianjie Ma
Diabetes May 2020, 69 (5) 1052-1064; DOI: 10.2337/db19-0807

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MG53 Does Not Manifest the Development of Diabetes in db/db Mice
Qiang Wang, Zehua Bian, Qiwei Jiang, Xiaoliang Wang, Xinyu Zhou, Ki Ho Park, Willa Hsueh, Bryan A. Whitson, Erin Haggard, Haichang Li, Ken Chen, Chuanxi Cai, Tao Tan, Hua Zhu, Jianjie Ma
Diabetes May 2020, 69 (5) 1052-1064; DOI: 10.2337/db19-0807
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