Li Li, PhD
Elliman Building, Rm 2146
421 E. Canfield Avenue
Detroit, MI 48201
University of Texas Health Science Center at Houston, PhD, 1991
We are studying the molecular mechanisms of smooth muscle cell (SMC) phenotypic modulation during development and in vascular diseases using tissue culture cells and transgenic/knockout mouse disease models. We have been using comprehensive cellular, molecular, genomic and genetic approaches to address these issues. Understanding the molecular mechanisms of cardiovascular development is critical for developing therapeutic strategies to improve treatment of human vascular diseases. We use mouse models for vascular restenosis, atherosclerosis, aneurysms and Marfan syndrome.
Currently, we have two major projects: (1) Characterizing the molecular mechanisms of SM22 (aka Transgelin) in regulating smooth muscle cell phenotypic modulation and contributing to the pathogenesis of vascular diseases. We are particularly interested in how cytoskeletal proteins, transcription factors, epigenetic factors and changes in TGF-beta signaling lead to SMC dysfunction in the pathogenesis of aneurysms and atherosclerosis. (2) Characterizing the interplay of transcriptional regulatory network and signal pathways for SMC gene expression in different SMC subtypes.
Another line of research in the lab is to investigate the regulatory mechanisms for the hematopoietic factor Hemogen (aka HEMGN, EDAG), which is specifically expressed in blood islands, active hematopoietic sites and spermatids during development. Characterizing the function of Hemogen will provide insights on the molecular mechanism of hematopoiesis, vasculogenesis, spermatogenesis and stem cell differentiation.
Xiaohua Dai1, Jianbin Shen1, Neeraja Priyanka Annam, Hong Jiang, Edi Levi, Charles M. Schworer, Gerard Tromp, Anandita Arora, Mary Higgins, Xiao-Fan Wang, Maozhou Yang, Hui J. Li, Kezhong Zhang, Helena Kuivaniemi and Li Li SMAD3 deficiency promotes vessel wall remodeling, collagen fiber reorganization and leukocyte infiltration in an inflammatory abdominal aortic aneurysm mouse model. Sci. Rep. (2015). 5:10180 (www.nature.com/search?facets=new&journal=srep&q=SREP10180). PMID: 25985281.
Zhonghui Xu1, Guangdong Ji1, Jianbin Shen, Xiao Wang, Jiliang Zhou and Li Li. SOX9 and Myocardin counteract each other in regulating vascular smooth muscle cell differentiation. Biochem Biophys Res Commun . (2012). 422(2):285-90 PMID: 22580282.
Jianbin Shen; Maozhou Yang; Hong Jiang; Donghong Ju; Jian-Pu Zheng; Zhonghui Xu; Tang-Dong Liao and Li Li. Arterial injury promotes medial chondrogenesis in Sm22 knockout mice Cardiovascular Research (2011) 90:28. PMID: 21183509.
Jianbin Shen, Maozhou Yang, Donghong Ju, Hong Jiang, Jian-pu Zheng and Li Li. Disruption of SM22 promotes inflammation after artery injury via Nuclear Factor kB activation. Circulation Research, 2010 106:1351-62.
Jian-Pu Zheng, Donghong Ju, Jianbin Shen, Maozhou Yang, Li Li. Disruption of actin cytoskeleton mediates loss of tensile stress induced early phenotypic modulation of vascular smooth muscle cells in aorta organ culture. Experimental Molecular Pathology 2010 88: 52-57.
Maozhou Yang, Hong Jiang, and Li Li. Sm22α transcription occurs at the early onset of the cardiovascular system and the intron 1 is dispensable for its transcription in smooth muscle cells during mouse development. International Journal of Physiology, Pathophysiology and Pharmacology 2010;2(1):12-19.