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Leo E. Otterbein

Researcher at Beth Israel Deaconess Medical Center

Publications -  228
Citations -  24913

Leo E. Otterbein is an academic researcher from Beth Israel Deaconess Medical Center. The author has contributed to research in topics: Heme oxygenase & Heme. The author has an hindex of 79, co-authored 221 publications receiving 22713 citations. Previous affiliations of Leo E. Otterbein include Veterans Health Administration & Johns Hopkins University School of Medicine.

Papers
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Journal ArticleDOI

Carbon Monoxide Preserves Circadian Rhythm to Reduce the Severity of Subarachnoid Hemorrhage in Mice.

Nils Schallner, +6 more
- 26 Jul 2017 - 
TL;DR: Clock gene expression regulates, in part, the severity of SAH and requires myeloid HO-1 activity to clear the erythrocyte burden and inhibit neuronal apoptosis and thus merits further investigation in patients with SAH.
Journal ArticleDOI

Biliverdin modulates the expression of C5aR in response to endotoxin in part via mTOR signaling

Kavita Bisht, +6 more
- 20 Jun 2014 - 
TL;DR: Biliverdin mitigates LPS-dependent C5aR expression in macrophages in part via mTOR and promotes phosphorylation of Akt and PS6 and decreases L PS-mediated induction of C 5aR-associated cytokines.
Patent

Methods of treating vascular disease

Leo E. Otterbein, +3 more
TL;DR: In this paper, a method of treating patients suffering from, or at risk for, intimal hyperplasia and/or arteriosclerosis was proposed, which includes administering a pharmaceutical composition that includes carbon monoxide to the patient.
Journal ArticleDOI

Differential Modulation by Exogenous Carbon Monoxide of TNF-α Stimulated Mitogen-Activated Protein Kinases in Rat Pulmonary Artery Endothelial Cells

Jigme M. Sethi, +2 more
- 01 Apr 2002 - 
TL;DR: In this article, the authors showed that carbon monoxide (CO), a major catalytic byproduct of HO-1, may mediate this anti-inflammatory effect by modulating signal transduction pathways, in particular the mitogen-activated protein (MAP) kinase pathway.
Journal ArticleDOI

Deficiency in the c-Jun NH2-terminal kinase signaling pathway confers susceptibility to hyperoxic lung injury in mice.

Danielle Morse, +7 more
- 01 Jul 2003 - 
TL;DR: Results indicate that JNK pathways participate in adaptive responses to hyperoxia in mice, which generates an oxidative stress in the mouse lung, which activates the major stress-inducible kinase pathways, including c-Jun NH2-terminal kinase (JNK).