Shaoning Jiang

My main research interest has been studying epigenetic mechanisms linking inflammation and energy metabolism in the pathogenesis of diabetes and obesity and related metabolic disorders. Specifically, my research has focused on two main directions:

1) Macrophages, microRNAs, and adipose stem cells crosstalk in the regulation of brown/beige adipogenesis in obesity. This project studies a bone marrow-derived microRNA cluster of miR-130b and miR-301b, which suppresses adipose tissue stem cells beige differentiation and energy metabolism. By in vivo approaches using a global and a macrophage-specific knockout mouse model for miRNA-130b/301b and in vitro culture of bone marrow and adipose stem cells, the goal is to further delineate cell subtype-specific actions and explore therapeutic potential of extracellular vesicle (EV)-mediated miR-130b/301b inhibition in obesity and related metabolic disorders.

2) Epigenetic mechanisms of developmental programming of metabolic diseases in maternal obesity and diabetes. Adverse intrauterine environment, including diabetes and obesity, impacts fetal development and growth and predispose offspring to type 2 diabetes, obesity, and other metabolic diseases later in life, which has been known as “Developmental Origins of Health and Disease (DoHad)”. The overall aim of my research is to better understand the molecular mechanisms of DoHad and explore new therapeutic options for early prevention of metabolic diseases at the time of their origin, focusing on a) Roles of AMP-activated protein kinase (AMPK) and epigenetic pathways in placenta and fetal development and offspring long-term health in response to maternal overnutrition (obesity and diabetes); b) Effects of maternal overnutrition on peroxisomal and mitochondrial programming during fetal development, and how those alterations impact adipose tissue development and offspring obesity and fatty liver diseases later in life.