The long-term goal of our lab is to understand the systemic network governed by epigenetic factors in stem cells. We want to dissect the mechanisms that makes a stem cell a stem cell (cell identity), maintains as a stem cell (stemness) or goes to a specific lineage (cell fate determination). We adopted a well established system to dissect the interactive network controlling adult stem cells and cancer stem cells, and differentiated blood cells functions from the angle of non-coding RNAs.

Several major direction that we are currently interested in are:

  1. The regulation of microRNAs in hematopoietic stem cell function
  2. Mechanism of microRNAs in macrophage activation and obesity induced cardiac vascular diseases

The regulation of microRNAs in hematopoietic stem cell function

Limited self-renewal and differentiation of hematopoietic stem cells (HSCs) and their progenies rely on a well-orchestrated regulatory network, mainly comprising transcription factors, cytokines and their receptors mediated signaling pathways, and a group of newly discovered microRNAs (miRNAs). Even though there are experimental evidences suggesting the important roles played by miRNAs in this network, the detailed picture is largely unknown. Our lab is interested in investigating the regulation network governed by miRNAs in hematopoiesis, in particular lymphopoiesis. In addition, abnormal miRNA expression, along with gene mutations, can transform hematopoietic stem cells and progenitor cells to “indefinite self-renewal” cancer stem cells, thus lead to hematopoietic malignancies, such as leukemia and lymphoma.

Hematopoiesis Picture

microRNAs regulated macrophage function in obesity induced adipose inflammation

Leukocytes are not only crucial cells for immune responses, but also pivotal in regulators for other tissues’ function. A new dimension of our research is to investigate the interactions between leukocytes and connective tissue cells that composite the micro-environment after their emigration. Cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM) are the leading causes of mortality and morbidity in the United States. Among various CVDs, atherosclerosis associated complications account for more than half of the year mortality. Meanwhile, it is well accepted obesity and its associated type 2 diabetes mellitus (T2DM) are major contributors for the high incidence of CVD, including atherosclerosis. Growing evidences indicated the pivotal role of macrophage mediated inflammation is one of the crucial factors for the pathogenesis of both atherosclerosis and T2DM. However, the detailed picture of how macrophage function remains vague. Our long-term goal is to elucidate the underlying mechanism of CVD risk and providing crucial information for new therapeutic strategy development for obesity induced CVD.