Title: The role of macrophage migration inhibitory factor (MIF) family proteins in metabolic dysfunction and heart disease
Speaker: Prof. Dake Qi, University of Manitoba, Canada
Time: Oct 21st, Monday, 14:00 pm
Venue: Building 24#-C406
Host: Prof. Youcai Zhang
Macrophage migration inhibitory factor (MIF) is a pro-inflammatory factor that is widely expressed in multiple organ systems. MIF is released from pre-formed storage pools in response to stimulation and is classically involved in many diseases such as rheumatoid arthritis, atherosclerosis and sepsis. MIF also functions as a regulator of metabolism by increasing skeletal muscle glucose metabolism. In the heart, MIF acutely activates the “energy gauge” AMP-activated protein kinase (AMPK) during stress, implicating that MIF may also regulate cardiac metabolism. Thus, our major research interests focus on studying the role of MIF in regulating metabolism (whole body and tissue specific) during stress. MIF, cardiac metabolism and heart attack: Heartattack caused by partial or complete occlusion of coronary arteries is a leading cause for death around the world. In clinical practice, early and successful restoration of coronary blood flow by using thrombolytic therapy or primary percutaneous coronary intervention (PCI) is the most effective strategy to prevent ischemic injury and improve the clinical outcome. However, the recovery of blood flow simultaneously results in additional cardiac damage and complications, referred to as “reperfusion injury”. Our current research is to investigate how MIF and its homolog D-dopachrome tautomerase (DDT) acutely regulate cardiac metabolism during heart attack. MIF and insulin resistance: MIF expression is chronically augmented in monocytes and adipose tissue in obese individuals, and may contribute to the pathogenesis of insulin resistance by attenuating insulin signaling. Our second research direction is to explore the molecular mechanisms of MIF in mediating insulin resistance and metabolic syndrome.