Information

Related Research Units

Nephrology Research
Computational Health Informatics Program Research

Research Overview

Dr. Wedel’s research focuses on the identification of novel cell types and signaling pathways that regulate T cell-dependent immune responses of broad clinical relevance. He is particularly interested in identifying new molecular mechanisms and pharmacological targets that can be used to modulate alloimmune responses, resolve inflammation and promote tolerance following transplantation.

Research Background

Dr. Wedel is an Assistant Professor in Pediatrics at Harvard Medical School, Research Associate within the Division of Nephrology and the Transplant Research Program, and Affiliate Faculty Member of the Computational Health Informatics Program (CHIP).

Publications

  1. A Combination therapy using an mTOR inhibitor and Honokiol effectively induces autophagy through the modulation of AXL and Rubicon in renal cancer cells and restricts renal tumor growth following organ transplantation. Carcinogenesis. 2022 05 19; 43(4):360-370. View Abstract
  2. Inhibition of mevalonate metabolism by statins augments the immunoregulatory phenotype of vascular endothelial cells and inhibits the costimulation of CD4+ T cells. Am J Transplant. 2022 03; 22(3):947-954. View Abstract
  3. T Cell-Specific Adaptor Protein Regulates Mitochondrial Function and CD4+ T Regulatory Cell Activity In Vivo following Transplantation. J Immunol. 2019 10 15; 203(8):2328-2338. View Abstract
  4. Treatment with 2,4-Dihydroxybenzoic Acid Prevents FSGS Progression and Renal Fibrosis in Podocyte-Specific Coq6 Knockout Mice. J Am Soc Nephrol. 2019 Mar; 30(3):393-405. View Abstract
  5. DEPTOR modulates activation responses in CD4+ T cells and enhances immunoregulation following transplantation. Am J Transplant. 2019 01; 19(1):77-88. View Abstract
  6. Vitamin D inhibits lymphangiogenesis through VDR-dependent mechanisms. Sci Rep. 2017 03 17; 7:44403. View Abstract
  7. The intragraft microenvironment as a central determinant of chronic rejection or local immunoregulation/tolerance. Curr Opin Organ Transplant. 2017 Feb; 22(1):55-63. View Abstract
  8. Pharmacological Inhibition of Vanin Activity Attenuates Transplant Vasculopathy in Rat Aortic Allografts. Transplantation. 2016 08; 100(8):1656-66. View Abstract
  9. Netrin-1 Augments Chemokinesis in CD4+ T Cells In Vitro and Elicits a Proinflammatory Response In Vivo. J Immunol. 2016 08 15; 197(4):1389-98. View Abstract
  10. N-octanoyl Dopamine Attenuates the Development of Transplant Vasculopathy in Rat Aortic Allografts Via Smooth Muscle Cell Protective Mechanisms. Transplantation. 2016 Jan; 100(1):80-90. View Abstract
  11. Translational implications of endothelial cell dysfunction in association with chronic allograft rejection. Pediatr Nephrol. 2016 Jan; 31(1):41-51. View Abstract
  12. Chronic allograft rejection: a fresh look. Curr Opin Organ Transplant. 2015 Feb; 20(1):13-20. View Abstract
  13. N-acyl dopamine derivates as lead compound for implementation in transplantation medicine. Transplant Rev (Orlando). 2015 Jul; 29(3):109-13. View Abstract
  14. Simultaneous subcutaneous implantation of two osmotic minipumps connected to a jugular vein catheter in the rat. Lab Anim. 2014 Oct; 48(4):338-41. View Abstract
  15. N-octanoyl dopamine treatment of endothelial cells induces the unfolded protein response and results in hypometabolism and tolerance to hypothermia. PLoS One. 2014; 9(6):e99298. View Abstract
  16. N-Octanoyl dopamine transiently inhibits T cell proliferation via G1 cell-cycle arrest and inhibition of redox-dependent transcription factors. J Leukoc Biol. 2014 Sep; 96(3):453-62. View Abstract
  17. Different design of enzyme-triggered CO-releasing molecules (ET-CORMs) reveals quantitative differences in biological activities in terms of toxicity and inflammation. Redox Biol. 2014; 2:739-48. View Abstract
  18. N-octanoyl dopamine inhibits the expression of a subset of ?B regulated genes: potential role of p65 Ser276 phosphorylation. PLoS One. 2013; 8(9):e73122. View Abstract
  19. N-octanoyl-dopamine is a potent inhibitor of platelet function. Platelets. 2013; 24(6):428-34. View Abstract
  20. N-octanoyl-dopamine is an agonist at the capsaicin receptor TRPV1 and mitigates ischemia-induced [corrected] acute kidney injury in rat. PLoS One. 2012; 7(8):e43525. View Abstract
  21. Anserine inhibits carnosine degradation but in human serum carnosinase (CN1) is not correlated with histidine dipeptide concentration. Clin Chim Acta. 2011 Jan 30; 412(3-4):263-7. View Abstract

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