Thomas H. Sanderson

ORCID: 0000-0003-0112-8164
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About
Contact & Profiles
Research Areas
  • Mitochondrial Function and Pathology
  • ATP Synthase and ATPases Research
  • Cardiac Arrest and Resuscitation
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Anesthesia and Neurotoxicity Research
  • Cardiac Ischemia and Reperfusion
  • Photoreceptor and optogenetics research
  • Autophagy in Disease and Therapy
  • Optical Imaging and Spectroscopy Techniques
  • Laser Applications in Dentistry and Medicine
  • Cell death mechanisms and regulation
  • Endoplasmic Reticulum Stress and Disease
  • Metabolism and Genetic Disorders
  • Neuroscience and Neuropharmacology Research
  • Respiratory Support and Mechanisms
  • Analytical Chemistry and Chromatography
  • Neuroinflammation and Neurodegeneration Mechanisms
  • RNA regulation and disease
  • Neonatal and fetal brain pathology
  • Heat shock proteins research
  • Amino Acid Enzymes and Metabolism
  • Analytical chemistry methods development
  • Mass Spectrometry Techniques and Applications
  • Coenzyme Q10 studies and effects
  • Cardiac Imaging and Diagnostics

University of Michigan
2018-2025

Wayne State University
2012-2024

Michigan United
2013-2024

Michigan Medicine
2022

Institut National de la Recherche Scientifique
2013-2019

Armand Frappier Museum
2013-2017

Cardiovascular Institute Hospital
2013

Centre National de la Recherche Scientifique
2013

Université Paris Cité
2013

Philipps University of Marburg
2011

The endoplasmic reticulum (ER) engages mitochondria at specialized ER domains known as mitochondria-associated membranes (MAMs). Here, we used three-dimensional high-resolution imaging to investigate the formation of pleomorphic "megamitochondria" with altered MAMs in brown adipocytes lacking Sel1L-Hrd1 protein complex ER-associated degradation (ERAD). Mice ERAD deficiency were cold sensitive and exhibited mitochondrial dysfunction. affected ER-mitochondria contacts dynamics, least part, by...

10.1126/science.aay2494 article EN Science 2020-03-19

Global brain ischemia/reperfusion induces neuronal damage in vulnerable regions, leading to mitochondrial dysfunction and subsequent death. Induction of death is mediated by release cytochrome c (cyt c) from the mitochondria though a well-characterized increase outer membrane permeability. However, for cyt be released it first necessary liberated cristae junctions which are gated Opa1 oligomers. has two known functions: maintenance junction fusion. These roles suggest that could play central...

10.1016/j.mcn.2016.08.010 article EN cc-by-nc-nd Molecular and Cellular Neuroscience 2016-08-30

Mitochondrial damage and dysfunction are hallmarks of neuronal injury during cerebral ischemia-reperfusion (I/R). Critical mitochondrial functions including energy production cell signaling perturbed I/R, often exacerbating contributing to secondary injury. The integrity the proteome is essential for efficient function. proteostasis mediated by cooperative forces mitophagy intramitochondrial proteolysis. aim this study was elucidate patterns protein dynamics their key regulators an in vitro...

10.1080/15548627.2025.2472586 article EN cc-by-nc-nd Autophagy 2025-02-27

In this study we tested the hypothesis that long-term neuropathological outcome is worsened by hyperoxic compared to normoxic reperfusion in a rat global cerebral ischemia model. Adult male rats were anesthetized and subjected bilateral carotid arterial occlusion plus bleeding hypotension for 10 min. The randomized one of four protocols: ischemia/normoxia (21% oxygen 1 h), ischemia/hyperoxia (100% sham/normoxia, sham/hyperoxia. Hippocampal CA1 neuronal survival activation microglia...

10.1089/neu.2009.1186 article EN Journal of Neurotrauma 2010-01-08

The interaction of light with biological tissue has been successfully utilized for multiple therapeutic purposes. Previous studies have suggested that near infrared (NIR) enhances the activity mitochondria by increasing cytochrome c oxidase (COX) activity, which we confirmed 810 nm NIR. In contrast, scanning NIR spectrum between 700 and 1000 revealed two wavelengths (750 950 nm) reduced isolated COX. COX-inhibitory mitochondrial respiration, membrane potential (ΔΨm), attenuated superoxide...

10.1038/s41598-018-21869-x article EN cc-by Scientific Reports 2018-02-16

Cytochrome c oxidase (COX) is the terminal enzyme of mitochondrial electron transport chain. The purpose this study was to analyze function lung-specific cytochrome subunit 4 isoform 2 (COX4i2) in vitro and COX4i2-knockout mice vivo. COX isolated from cow lung liver as control functionally analyzed. were generated effect gene knockout determined, including activity, tissue energy levels, noninvasive invasive function, pathology. These studies complemented by a comprehensive functional screen...

10.1096/fj.11-203273 article EN The FASEB Journal 2012-06-22

Brain ischemia/reperfusion injury results in death of vulnerable neurons and extensive brain damage. It is well known that mitochondrial release cytochrome c (cyto c) a hallmark neuronal death, however the molecular events underlying this are largely unknown. We tested hypothesis cyto regulated by breakdown cristae architecture maintenance protein, optic atrophy 1 (OPA1), located inner membrane. simulated isolated primary rat interrogated OPA1 from mitochondria, oligomeric breakdown,...

10.1016/j.neuroscience.2015.05.078 article EN cc-by-nc-nd Neuroscience 2015-06-06

Mitochondrial form and function are regulated by the opposing forces of mitochondrial dynamics: fission fusion. dynamics highly active consequential during neuronal ischemia/reperfusion (I/R) injury. fusion is executed at inner membrane Opa1. The balance long (L-Opa1) proteolytically cleaved short (S-Opa1) isoforms critical for efficient Oma1 predominant stress-responsive protease Opa1 processing. In cell models, we assessed regulation stress. an immortalized mouse hippocampal neuron line...

10.1096/fj.202400313r article EN cc-by-nc-nd The FASEB Journal 2024-09-23

Recent advancements in isolation techniques for cytochrome c (Cytc) have allowed us to discover post-translational modifications of this protein. We previously identified two distinct tyrosine phosphorylated residues on Cytc mammalian liver and heart that alter its electron transfer kinetics the ability induce apoptosis. Here we investigated phosphorylation status ischemic brain sought determine if insulin-induced neuroprotection inhibition release was associated with Cytc. Using an animal...

10.1371/journal.pone.0078627 article EN cc-by PLoS ONE 2013-11-05

Abstract The mitochondrial network continually undergoes events of fission and fusion. Under physiologic conditions, the is in equilibrium characterized by presence both elongated punctate mitochondria. However, this balanced, homeostatic profile can change morphologic distribution response to various stressors. Therefore, it imperative develop a method that robustly measures morphology with high accuracy. Here, we developed semi-automated image analysis pipeline for quantitation vitro vivo...

10.1038/s41598-021-84528-8 article EN cc-by Scientific Reports 2021-03-04

Abstract Mitochondrial dynamics and mitophagy are constitutive complex systems that ensure a healthy mitochondrial network through the segregation subsequent degradation of damaged mitochondria. Disruption these can lead to dysfunction has been established as central mechanism ischemia/reperfusion (I/R) injury. Emerging evidence suggests integrated systems; however, role this relationship in context I/R injury remains unclear. To investigate concept, we utilized primary cortical neurons...

10.1038/s41419-021-03752-2 article EN cc-by Cell Death and Disease 2021-05-12
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