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Anna-Liisa Nieminen PhD

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  • Associate Professor
  • College of Pharmacy
  • COP Drug Discovery and Biomedical Sciences
Academic Focus
  • Mitochondrial pathophysiology related to liver diseases
  • Oxygen free radicals
  • Mechanisms of cell death
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Dr. Nieminen has a long-standing interest in research related to mechanisms of mitochondrial dysfunction employing various models of oxidative stress, photodynamic therapy, sensitization of pancreatic cancer to conventional chemotherapy, and applying nanoparticles to treat head and neck cancers.  Her most recent research focuses on iron-mediated mitochondrial dysfunction related to liver injury.

Mitochondria are the site of biosynthesis of heme and Fe-S clusters.  Substantial evidence also implicates mitochondrial iron as an important contributor to liver pathology, including acetaminophen (APAP) toxicity, ischemia-reperfusion, oxidative stress, and iron overload in hemochromatosis. Toxicity from redox-active iron occurs by one-electron exchange reactions promoting oxidative stress by the Fenton reaction, which produces highly toxic and reactive hydroxyl radical (•OH) which is highly damaging to DNA, proteins and membranes. Given the central role of mitochondria in reactive oxygen species (ROS) generation, mitochondrial iron must be tightly regulated to provide sufficient supply of iron for processes for which iron is a co-factor but at the same time prevent formation of toxic •OH. However, the molecular pathways by which mitochondria regulate iron remain controversial and incompletely understood.

The current studies in the lab aim to elucidate pathways of mitochondrial iron uptake, specifically whether iron is taken up by two independent pathways, mitoferrin (Mfrn) and mitochondrial calcium uniporter (MCU), or whether Mfrn and MCU act synergistically to transport Fe2+. In the iron field, Mfrn is still considered the main mitochondrial iron transporter, whereas in the calcium field the MCU complex is studied almost exclusively as a calcium transporter. The goal is to determine whether these two transporters interact and how both contribute to mitochondrial Fe2+ uptake. To address these fundamental hypotheses, she has assembled a unique tool kit including: hepatocyte-specific Mfrn1 and Mfrn2 knock out, Mfrn1/2 double knock out, MCU knock out and DMT1 knock out mice; affinity enrichment-mass spectrometry (AE/MS); confocal/super-resolution microscopy; the newly developed mitochondrial iron sensor; novel assays of mitochondrial iron uptake and release; and in vivo and in vitro models of iron-dependent hepatotoxicity. AE/MS allows to detect binding partners with Mfrn2 whose functional importance in mitochondrial iron homeostasis will then be evaluated. The short-term impact of the studies is acquisition of fundamental new and unique knowledge of the molecular pathways of mitochondrial iron uptake. The long-term impact is that a better understanding of mitochondrial iron handling will lead to new and more specific interventions against toxicities and diseases promoted by iron overload.  An important issue associated with iron chelation therapy is that chelators currently in use are unselective for different organs and subcellular compartments and therefore chelate iron indiscriminately, a hazard especially in elderly patients. New information from the studies will form the basis for developing safer therapeutic interventions to target iron-overloaded mitochondria selectively in specific tissues, while maintaining the bioavailable iron pool required for hematopoiesis and other essential processes.