Lee Ann MacMillan-Crow
Researcher
Also affiliated: Arkansas Children's Hospital (2009); University of Alabama (2001–2003); University of Alabama at Birmingham (1994–2003)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Lee Ann MacMillan-Crow's research program focuses on understanding the molecular mechanisms of kidney injury, particularly in the context of transplantation and ischemia-reperfusion. Her work investigates the role of oxidative stress and mitochondrial dysfunction in cellular damage. Recent publications have examined how cold storage protocols affect the proteome and phosphoproteome of rat kidney transplants and how hypothermic machine perfusion can mitigate oxidative stress and tubular injury compared to static cold storage.
Her investigations also delve into the processing of mitochondrial proteins, such as OPA1, and the enzymes involved, like OMA1. MacMillan-Crow has explored how overexpression of manganese superoxide dismutase (MnSOD) can protect against cold storage-induced mitochondrial injury. Her lab has also developed fluorescence-based assays for measuring enzyme activity. Collaborations include work with Dinesh Bhattarai, Nirmala Parajuli, Julia Tobacyk, and Samuel G. Mackintosh at the University of Arkansas for Medical Sciences. MacMillan-Crow is recognized as a highly cited researcher, with an h-index of 31 and over 9,000 citations across her 84 publications.
Metrics
- h-index: 32
- Publications: 86
- Citations: 9,475
Selected Publications
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Heat shock protein 72 is a druggable target during cold storage to improve graft outcome after kidney transplantation (2026)
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Influence of Hypothermic Machine Perfusion on Markers of Oxidative Stress and Early Tubular Injury in Rat Donor Kidneys Before Transplantation (2026)
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Compared with Static Cold Storage, Hypothermic Machine Perfusion Mitigates Oxidative Stress and Tubular Injury in Rat Kidneys (2025)
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Cold Storage Disrupts the Proteome and Phosphoproteome Landscape in Rat Kidney Transplants (2024)
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Differentiation activates mitochondrial OPA1 processing in myoblast cell lines (2024)
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Normal Proteasome Function Is Needed to Prevent Kidney Graft Injury during Cold Storage Followed by Transplantation (2024)
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Does Disruption of Optic Atrophy-1 (OPA1) Contribute to Cell Death in HL-1 Cardiomyocytes Subjected to Lethal Ischemia-Reperfusion Injury? (2022)
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Inhibition of Na‐H exchanger 3 ameliorates lower limb ischemia/reperfusion‐induced acute kidney injury through preservation of mitochondrial biogenesis in mice (2022)
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Non-Canonical Cannabinoid Receptors with Distinct Binding and Signaling Properties in Prostate and Other Cancer Cell Types Mediate Cell Death (2022)
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Overexpression of MnSOD Protects against Cold Storage-Induced Mitochondrial Injury but Not against OMA1-Dependent OPA1 Proteolytic Processing in Rat Renal Proximal Tubular Cells (2021)
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Fluorescence-Based Assay For Measuring OMA1 Activity (2021)
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Association Between L-OPA1 Cleavage and Cardiac Dysfunction During Ischemia-Reperfusion Injury in Rats (2020)
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The BK activator NS11021 partially protects rat kidneys from cold storage and transplantation-induced mitochondrial and renal injury (2020)
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Association Between L‐OPA1 Cleavage/OMA1 Activity and Cardiac Function During Ischemia‐Reperfusion Injury in the Rat (2020)
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Specific BK Channel Activator NS11021 Protects Rat Renal Proximal Tubular Cells from Cold Storage—Induced Mitochondrial Injury In Vitro (2019)
Collaboration Network
Top Collaborators
- Normal Proteasome Function Is Needed to Prevent Kidney Graft Injury during Cold Storage Followed by Transplantation
- Cold Storage Disrupts the Proteome and Phosphoproteome Landscape in Rat Kidney Transplants
- Compared with Static Cold Storage, Hypothermic Machine Perfusion Mitigates Oxidative Stress and Tubular Injury in Rat Kidneys
- Normal Proteasome Function Is Needed to Prevent Kidney Graft Injury during Cold Storage Followed by Transplantation
- Cold Storage Disrupts the Proteome and Phosphoproteome Landscape in Rat Kidney Transplants
- Compared with Static Cold Storage, Hypothermic Machine Perfusion Mitigates Oxidative Stress and Tubular Injury in Rat Kidneys
- Fluorescence-Based Assay For Measuring OMA1 Activity
- Overexpression of MnSOD Protects against Cold Storage-Induced Mitochondrial Injury but Not against OMA1-Dependent OPA1 Proteolytic Processing in Rat Renal Proximal Tubular Cells
- Overexpression of MnSOD Protects against Cold Storage-Induced Mitochondrial Injury but Not against OMA1-Dependent OPA1 Proteolytic Processing in Rat Renal Proximal Tubular Cells
- Non-Canonical Cannabinoid Receptors with Distinct Binding and Signaling Properties in Prostate and Other Cancer Cell Types Mediate Cell Death
- Non-Canonical Cannabinoid Receptors with Distinct Binding and Signaling Properties in Prostate and Other Cancer Cell Types Mediate Cell Death
- Non-Canonical Cannabinoid Receptors with Distinct Binding and Signaling Properties in Prostate and Other Cancer Cell Types Mediate Cell Death
- Non-Canonical Cannabinoid Receptors with Distinct Binding and Signaling Properties in Prostate and Other Cancer Cell Types Mediate Cell Death
- Does Disruption of Optic Atrophy-1 (OPA1) Contribute to Cell Death in HL-1 Cardiomyocytes Subjected to Lethal Ischemia-Reperfusion Injury?
- Does Disruption of Optic Atrophy-1 (OPA1) Contribute to Cell Death in HL-1 Cardiomyocytes Subjected to Lethal Ischemia-Reperfusion Injury?
- Does Disruption of Optic Atrophy-1 (OPA1) Contribute to Cell Death in HL-1 Cardiomyocytes Subjected to Lethal Ischemia-Reperfusion Injury?
- Does Disruption of Optic Atrophy-1 (OPA1) Contribute to Cell Death in HL-1 Cardiomyocytes Subjected to Lethal Ischemia-Reperfusion Injury?
- Does Disruption of Optic Atrophy-1 (OPA1) Contribute to Cell Death in HL-1 Cardiomyocytes Subjected to Lethal Ischemia-Reperfusion Injury?
- Does Disruption of Optic Atrophy-1 (OPA1) Contribute to Cell Death in HL-1 Cardiomyocytes Subjected to Lethal Ischemia-Reperfusion Injury?
- Normal Proteasome Function Is Needed to Prevent Kidney Graft Injury during Cold Storage Followed by Transplantation
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