Faculty and Staff
|Title:||Associate Professor of Cell Biology & Anatomy
|Department:||Cell Biology and Anatomy
School of Medicine Columbia
|Office:||Basic Science Bldg 1|
|Resources:||Lab Phone: 803-216-3833|
1989 The 4th Military Medical University – M.D. – P.R. China
2001 Ehime University School of Medicine – Ph.D. – Molecular Medicine
Dr. Cui has a research interest in understanding the nature of cardiac adaptation as well as maladaptive remodeling and dysfunction in diverse pathological settings. In addition, Dr. Cui has a research interest in investigating the source of resident vascular stem cells (VSCs) as well as the role of resident (VSCs) in vascular lesion formation, repair, and regeneration. Dr. Cui’s laboratory takes multi-disciplinary approaches to explore the key molecules which coordinate the proteasome- and autophagy-dependent protein degradation pathways contributing to cardiac adaptation as well as cardiac maladaptation and dysfunction, and to identify the novel determinants in controlling resident VSC generation and resident VSC-mediated vascular lesion formation, repair, and regeneration.
There are four areas of technical strengths in Dr. Cui’s laboratory: 1) molecular
biology including most of the routine DNA, RNA and protein techniques; 2) cellular
biology including primary culture of vascular smooth muscle cells, endothelial cells,
macrophages and adipocytes, dissection of signal transduction pathways involved in
cellular metabolism, migration and proliferation as well as inflammatory responses;
3) development and characterization of animal models of vascular disease through transgenic
approaches; 4) vascular physiology analyses in cell, organ and whole animal levels.
Two major projects currently underway include:
- To identify novel regulators of proteasome- and autophagy-dependent protein quality control in the heart.
- To identify the molecular switch of vascular and lesion formation, repair, and regeneration.
Ongoing Research Support
- I01 CX002062, VA, CRS&D Merit Award, Cui (PI), 04/01/2021-03/31/2025. To explore the potential of UCH-L1 as a novel therapeutic and diagnostic target in heart failure.
- R01 HL131667, NIH, NHLBI, Cui (MPI), 04/01/2017-03/31/2022. Role of Nrf2-p62 axis in the crosstalk between proteasomal and lysosomal degradation.
- Wu W, Qin Q, Ding Y, Li DS, Nagarkatti M, Nagarkatti P, Wang W, Wang X, Cui T*. Autophagy controls Nrf2-mediated dichotomy in pressure overloaded hearts. Front Physiol. 2021 in press.
- Zang H, Wu W, Qi L, Wenbin Tan, Nagarkatti M, Nagarkatti P, Wang X, Cui T*. Autophagy inhibition enables Nrf2 to exaggerate the progression of diabetic cardiomyopathy in mice. Diabetes. 2020 Dec;69(12): 2720-2734.
- Zang H, Mathew RO, Cui T*. The dark side of Nrf2 in the heart. Front Physiol. 2020 Jul 9;11: 722. Invited review.
- Qi L, Zang H, Wu W, Nagarkatti P, Nagarkatti M, Liu Q, Robbins J, Wang X, Cui T*. CYLD exaggerates pressure overload-induced cardiomyopathy via suppressing autolysosome efflux in cardiomyocytes. J Mol Cell Cardiol. 2020 Jun 14;145: 59-73.
- Wu W, Wang C, Zang H, Qi L, Azhar M, Nagarkatti M, Nagarkatti P, Cai G, Weiser-Evans MCM, Cui T*. Mature vascular smooth muscle cells, but not endothelial cells, serve as the major cellular source of intimal hyperplasia in vein grafts. Arterioscler Thromb Vasc Biol. 2020 Aug;40(8): 1870-1890.
- Li KC, Wang CH, Zou JJ, Qu C, Wang XL, Tian XS, Liu HW, Cui T*. Loss of Atg7 in endothelia cells enhanced cutaneous wound healing in a mouse model. J Surg Res. 2020, 249: 145-155.
- Wang X, Cui T*. Autophagy modulation—A potential therapeutic approach in cardiac hypertrophy. Am J Physiol Heart Circ Physiol. 2017 Aug 1;313(2):H304-H319. Invited Review.
- Qin Q, Qu C, Niu T, Zang H, Lyu L, Wang X, Nagarkatti M, Nagarkatti P, Janicki JS, Wang XL, Cui T*. Nrf2-mediated cardiac maladaptive remodeling and dysfunction in a setting of autophagy insufficiency. Hypertension. 2016 Jan;67(1): 107-17.
- Lyu L, Wang H, Li B, Qin Q, Qi L, Janicki JS, Nagarkatti M, Nagarkatti P, Janicki JS, Wang XL, Cui T*. A critical role of cardiac fibroblast-derived exosomes in activating renin angiotensin system in cardiomyocytes. J Mol Cell Cardiol. 2015 Dec;89 (Pt B): 268-79.
- Wang H, Lai Y, Mathis BJ, Wang W, Li S, Qu C, Li B, Shao L, Song H, Janicki JS, Sun SC, Wang XL, Tang D, Cui T*. Deubiquitinating enzyme CYLD mediates pressure overload-induced cardiac maladaptive remodeling and dysfunction via downregulating Nrf2. J Mol Cell Cardiol. 2015 Apr 30;84: 143-153.