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The Jiang lab is interested in the cellular and molecular control of adipogenesis, with the ultimate goal of understanding and treating obesity and other metabolic diseases. Adipocyte comes from the activation and expansion of adipose stem cells, and subsequent differentiation and maturation of their progenies. We are particularly interested in the developmental origin and plasticity of adipose stem cells. To do so, we use cutting-edge tissue specific, inducible knockout and lineage tracing mouse models, coupled with cell culture approaches and advanced genomics and imaging technologies. Our current research centers on the following directions:
1. Adipose lineage development
The prevalence of childhood obesity nearly doubled over the past three decades. Thus there is a critical need to understand how adipocytes develop. Using genetic mouse tools, one of our most exciting findings is that Developmental and Adult adipose stem cells are distinct in origin and have distinct controlling mechanisms. We are currently probing to understand the adipose cell lineage development and identify genes and pathways that are critical for normal and diseased developing adipose tissues.
2. Beige adipocytes and energy metabolism
Adipose tissue contains white, beige and brown adipocytes. Unlike white adipocytes that store fat and their excessive accumulation are associated with obesity, brown/beige adipocytes consume glucose and free fatty acid, presenting a potential tool to diminish adiposity and address the combined obesity and diabetes epidemic. However, after discontinuing the beiging stimulus (cold temperature), beige adipocytes rapidly convert to “white-like” adipocytes at room temperature. We are interested to identify the molecular mechanism(s) involved in maintaining beige cell identity and their perdurance. This study will not only help us to understand beige adipocyte cell biology, but also will provide molecular targets to extend beige adipocyte lifespan thereby improving metabolic health.
3. Adipose tissue aging
Aging is a progressive decline in many tissues throughout the body, including adipose tissues. For instance, both white and beige adipogenesis fail in older individuals, who constitute a large percentage of this epidemic. We are interested in understanding the cellular and molecular basis of adipose tissue decline and aging, and to determine if aspects of these aging processes can be rejuvenated. Our work in mice and human cells has led us to identify that cellular senescence contributes to adipose stem cell aging and that affect adipose stem cell dynamics and function. An ongoing project is to evaluate the role of nutrient overloading in stem cell aging. Key questions we are asking include: how do adipose stem cells integrate environmental stimuli (food, stress, etc? Do these mechanisms regulate aging and lifespan? Are they reversible? The overarching theme of this research proposal is to define the molecular basis of tissue deterioration in aging and obesity.