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Hua Sun, MD, PhD

Contact information: 

Office: E-202 GH
Phone: 678-7151
Faculty Profile

Brief description of current research:

My research of interest is the molecular mechanism of human podocyte disease (also termed “podocytopathy”), with a special focus on cytoskeleton and vesicle trafficking related pathophysiology. My resent transcriptome data analysis in diabetic nephropathy shifted my interest to dysregulated protein trafficking mediated by dynein, a motor protein complex for microtubule-based vesicle trafficking. Being the first group of investigators studying dynein in podocyte biology, my work is extending the understanding and technical platforms used in other target cells of diabetes to podocytes.   

My lab uses various techniques and models to study dynein mediated mechanism of diabetic podocytopathy, including classic molecular cloning and molecular cell biology experiments, live cell imaging and analysis of cytoskeletal and trafficking dynamics using mathematical models, podocyte specific transgenic mouse models in combination with type I and type 2 diabetes models, and CRISPR facilitated transgenic podocyte cell lines. Specifically, my research aims to address the following questions: 1) How is dynein-mediated trafficking of podocyte proteins activated in type I and Type 2 diabetes;  2) What is the impact of activated dynein-mediated trafficking in the homeostasis od podocyte protein, architecture and function;  3) How specially is dynein regulated in podocytes; 4) What are dynein-mediated biomarkers in human diabetic podocytopathy and do they have values in predicting disease prognosis or guide treatments; 4) Can dynein-driven pathogenesis be used as a therapeutic target to modify the progress and outcome of diabetic nephropathy.

3 most influential diabetes/obesity/metabolism publications:

  • Sun H, Chandra Perez, Schlöndorff JS, Subramanian B, Pollak MR. Dysregulated dynein mediated trafficking of nephrin causes INF2 related podocytopathy. J Am Soc Nephrol. 2021; 32 (2): 307-22. PMID: 3344305
  • Sun H, Al-Romaih KI, MacRae CA, Pollak MR. Human Kidney Disease-causing INF2 Mutations Perturb Rho/Dia Signaling in the Glomerulus. EBioMedicine. 2014; 1(2-3): 107-15. PMID: 26086034; PMCID: PMC4457406
  • ​Sun H, Schlöndorff J, Brown E, Higgs H, Pollak MR. Rho activation of mDia formins is modulated by an interaction with INF2. PNAS. 2011; 108 (7):2933-8. PMID: 21278336; PMCID: PMC3041098

Quote:

Diabetic nephropathy is no longer an “adult-only” condition. An early recognition and intervention in pediatric diabetic population may prepare them for a healthier adulthood and a bright future.