Hagir Suliman

Overview:

Dr. Suliman is an expert in the molecular and cell biology of mammalian diseases, particularly in the molecular regulation of oxidant inflammatory responses in the heart and lung. She has a strong interest and expertise in the transcriptional control of cell metabolism, especially mitochondrial biogenesis and mitochondrial-mediated apoptosis and necrosis. Her recent publications have focused on the redox-regulation of nuclear transcription factors involved in both mitochondrial biogenesis and cellular adaptation to oxidative and nitrosative stress. Specifically, she has undertaken promoter analyses of nuclear respiratory factors-1 and -2 that indicate that these transcription factor genes are controlled by redox-regulated signaling networks activated by reactive oxygen and nitrogen species, and carbon monoxide. Dr. Suliman and her colleagues have reported that the cancer chemotherapeutic, doxorubicin, disrupts cardiac mitochondrial biogenesis through mitochondrial oxidant production, which promotes intrinsic apoptosis, while heme oxygenase-1 up-regulates adaptive mitochondrial biogenesis and opposes apoptosis through close regulation of mitochondrial ROS signaling by physiological CO production, thus forestalling fibrosis and cardiomyopathy. Most recently I have been defining the role of mitochondrial transcription factors in regulating cell survival, proliferation and differentiation including in embryonic stem cells and pluripotent cells.

Positions:

Associate Professor in Anesthesiology

Anesthesiology
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

Ph.D. 1996

Virginia Polytech Institute and State University

Grants:

Regulation of mitochondrial biogenesis by heme oxygenase-1

Administered By
Medicine, Pulmonary, Allergy, and Critical Care Medicine
Awarded By
National Institutes of Health
Role
Co Investigator
Start Date
End Date

Lung Injury Protection by Coagulation Blockade

Administered By
Medicine, Pulmonary, Allergy, and Critical Care Medicine
Awarded By
National Institutes of Health
Role
Co Investigator
Start Date
End Date

Novel Combinatorial Screening for NTFs, NPCs, MMPs, and CCs in relevance to Autoantibodies in the Serum and CSF of Veterans with GWI

Administered By
Pharmacology & Cancer Biology
Awarded By
Department of Defense
Role
Collaborator
Start Date
End Date

Mitochondrial quality control and alveolar damage resolution after acute lung injury

Administered By
Medicine, Pulmonary, Allergy, and Critical Care Medicine
Awarded By
National Institutes of Health
Role
Co Investigator
Start Date
End Date

Oxidative tissue damage mitigation after exposure to HBO2 using FDA approved anti-epileptic drugs (AEDs)

Administered By
Medicine, Pulmonary, Allergy, and Critical Care Medicine
Awarded By
Office of Naval Research
Role
Investigator
Start Date
End Date

Publications:

Erratum: Skeletal muscle mitochondrial fragmentation and impaired bioenergetics from nutrient overload are prevented by carbon monoxide (American Journal of Physiology - Cell Physiology (2020) 319 (C746-C756) DOI: 10.1152/ajpcell.00016.2020)

Skeletal muscle mitochondrial fragmentation and impaired bioenergetics from nutrient overload are prevented by carbon monoxide. Am J Physiol Cell Physiol 319: C746–C756, 2020. First published August 26, 2020; https://doi.org/ 10.1152/ajpcell.00016.2020.—In the published version of this article, the RESULTS section “CO and moderate exercise training on skeletal muscle mitochondrial morphology, dynamic regulation, and biogenesis in rats during diet-induced obesity” refers to Fig. 5C when it should be Fig. 6, B and C. The two corrected sentences are as follows: “Despite a reduction in the distribution of mitochondria, exercise increased mitochondrial size and citrate synthase protein expression (Fig. 6, B and C), thus density, and morphological parameters.” “The responses were not accompanied by changes in the protein expression of PGC-1a, Mfn2, Drp1 (Fig. 6, B and C), or IL-10 (data not shown).” The revisions do not change the scientific conclusions of the study.
Authors
Gasier, HG; Dohl, J; Suliman, HB; Piantadosi, CA; Yu, T
MLA Citation
Gasier, H. G., et al. “Erratum: Skeletal muscle mitochondrial fragmentation and impaired bioenergetics from nutrient overload are prevented by carbon monoxide (American Journal of Physiology - Cell Physiology (2020) 319 (C746-C756) DOI: 10.1152/ajpcell.00016.2020).” American Journal of Physiology  Cell Physiology, vol. 319, no. 6, Dec. 2020, p. C1163. Scopus, doi:10.1152/ajpcell.00016.2020_COR.
URI
https://scholars.duke.edu/individual/pub1471502
Source
scopus
Published In
American Journal of Physiology. Cell Physiology
Volume
319
Published Date
Start Page
C1163
DOI
10.1152/ajpcell.00016.2020_COR

ecSOD overexpression in transgenic mice attenuates inflammation and lung injury following hyperoxia

Authors
Folz, RJ; Abushamaa, A; Suliman, HB
MLA Citation
Folz, R. J., et al. “ecSOD overexpression in transgenic mice attenuates inflammation and lung injury following hyperoxia.” Free Radical Biology and Medicine, vol. 25, PERGAMON-ELSEVIER SCIENCE LTD, 1998, pp. S31–S31.
URI
https://scholars.duke.edu/individual/pub917180
Source
wos
Published In
Free Radical Biology and Medicine
Volume
25
Published Date
Start Page
S31
End Page
S31

The toxic effects of hyperbaric oxygen in S-nitrosoglutathione reductase null mice

Authors
Gasier, H; Demchenko, I; Kraft, B; Suliman, H; Piantadosi, C
MLA Citation
Gasier, Heath, et al. The toxic effects of hyperbaric oxygen in S-nitrosoglutathione reductase null mice. Undersea and Hyperbaric Medical Society.
URI
https://scholars.duke.edu/individual/pub1415216
Source
manual

Skeletal muscle mitochondrial fragmentation and impaired bioenergetics from nutrient overload are prevented by carbon monoxide.

Nutrient excess increases skeletal muscle oxidant production and mitochondrial fragmentation that may result in impaired mitochondrial function, a hallmark of skeletal muscle insulin resistance. This led us to explore whether an endogenous gas molecule, carbon monoxide (CO), which is thought to prevent weight gain and metabolic dysfunction in mice consuming high-fat diets, alters mitochondrial morphology and respiration in C2C12 myoblasts exposed to high glucose (15.6 mM) and high fat (250 µM BSA-palmitate) (HGHF). Also, skeletal muscle mitochondrial morphology, distribution, respiration, and energy expenditure were examined in obese resistant (OR) and obese prone (OP) rats that consumed a high-fat and high-sucrose diet for 10 wk with or without intermittent low-dose inhaled CO and/or exercise training. In cells exposed to HGHF, superoxide production, mitochondrial membrane potential (ΔΨm), mitochondrial fission regulatory protein dynamin-related protein 1 (Drp1) and mitochondrial fragmentation increased, while mitochondrial respiratory capacity was reduced. CO decreased HGHF-induced superoxide production, Drp1 protein levels and mitochondrial fragmentation, maintained ΔΨm, and increased mitochondrial respiratory capacity. In comparison with lean OR rats, OP rats had smaller skeletal muscle mitochondria that contained disorganized cristae, a normal mitochondrial distribution, but reduced citrate synthase protein expression, normal respiratory responses, and a lower energy expenditure. The combination of inhaled CO and exercise produced the greatest effect on mitochondrial morphology, increasing ADP-stimulated respiration in the presence of pyruvate, and preventing a decline in resting energy expenditure. These data support a therapeutic role for CO and exercise in preserving mitochondrial morphology and respiration during metabolic overload.
Authors
Gasier, HG; Dohl, J; Suliman, HB; Piantadosi, CA; Yu, T
MLA Citation
Gasier, Heath G., et al. “Skeletal muscle mitochondrial fragmentation and impaired bioenergetics from nutrient overload are prevented by carbon monoxide.Am J Physiol Cell Physiol, vol. 319, no. 4, Oct. 2020, pp. C746–56. Pubmed, doi:10.1152/ajpcell.00016.2020.
URI
https://scholars.duke.edu/individual/pub1457175
PMID
32845721
Source
pubmed
Published In
Am J Physiol Cell Physiol
Volume
319
Published Date
Start Page
C746
End Page
C756
DOI
10.1152/ajpcell.00016.2020

Transgenic mice with overexpression of human extracellular superoxide dismutase in the lungs are tolerant to pulmonary oxygen toxicity

Authors
Folz, RJ; Suliman, HB
MLA Citation
Folz, R. J., and H. B. Suliman. “Transgenic mice with overexpression of human extracellular superoxide dismutase in the lungs are tolerant to pulmonary oxygen toxicity.” Molecular Biology of the Cell, vol. 8, AMER SOC CELL BIOLOGY, 1997, pp. 1352–1352.
URI
https://scholars.duke.edu/individual/pub917185
Source
wos
Published In
Molecular Biology of the Cell
Volume
8
Published Date
Start Page
1352
End Page
1352