Maternal-Fetal Mitochondrial Metabolism

About the Program

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Given how crucial energy is at all stages of development, and the central role of mitochondria in generating that energy during most stages of development, the Maternal-Fetal Mitochondrial Metabolism Unit investigates normal function and dysfunction of mitochondria in development. Emphasis is on the role of mitochondrial dysfunction that leads to preterm birth as well as the role of inflammation in mitochondrial dysfunction. Members of the unit include Siddhesh Aras, MBBS, PhD, and Neeraja Purandare, PhD.

Objectives

  • Study of mitochondrial metabolism during development.
  • Analysis of mitochondrial function during preterm birth syndromes using animal models, cultured cells, and human samples.
  • Determination of mechanism by which mitochondria become dysfunctional in inflammation.
  • Development of drug therapies to restore mitochondrial function.

Research Highlights

  • Energy supply during pregnancy. Since the metabolic source of energy changes during pregnancy and mitochondrial dysfunction can promote preterm birth, we are focused on regulation of metabolism and on interventions to improve outcomes by restoring mitochondrial function.
  • Mitochondrial role in inflammation. As mitochondria have a special role in the placental response to inflammatory stimulus, we seek to identify linchpin mitochondrial targets to ameliorate placental inflammation.
  • Oxygen responsive genes. Given the role of oxygen level changes during development, we are focused on cellular regulators of hypoxic response and their role in mitochondrial function.

Select Publications

Mitochondrial Section

ABOUT THE PROGRAM

  • The regulation of mitochondrial function during normal placental development
  • Delineation of the effects of inflammation on mitochondrial function in a cell and tissue culture model and characterization of a pathway for the observed effects

OBJECTIVES

  • To understand how MNRR1 mediated mitochondrial function relates to organellar activity throughout pregnancy, and therefore the repercussions of an inflammatory insult on MNRR1-mediated mitochondrial dysfunction

Research Focus

  • How do inflammatory stimuli induce mitochondrial dysfunction?
  • What is the pathway by which LPS affects mitochondrial function?
  • How does stress regulator MNRR1 (CHCHD2) function during plaental inflammation?

IMPORTANT POINTS & DISCOVERIES

  • In preliminary data, MNRR1 decreases duering placental inflammation, inhibiting mitochondrial function.

SELECTED PUBLICATIONS

Faculty

 

DIRECTOR
Lawrence I. Grossman, Ph.D

Henry L. Brasza Professor of Molecular Medicine and Genetics, Professor of Internal Medicine, Director, Center for Molecular Medicine and Genetics

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