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Katherine H. Gotlinger

Researcher at New York Medical College

Publications -  50
Citations -  5985

Katherine H. Gotlinger is an academic researcher from New York Medical College. The author has contributed to research in topics: Resolvin & Angiotensin II. The author has an hindex of 29, co-authored 50 publications receiving 5440 citations. Previous affiliations of Katherine H. Gotlinger include Harvard University & Brigham and Women's Hospital.

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A role for docosahexaenoic acid-derived neuroprotectin D1 in neural cell survival and Alzheimer disease.

TL;DR: Results indicate that NPD1 promotes brain cell survival via the induction of antiapoptotic and neuroprotective gene-expression programs that suppress Abeta42-induced neurotoxicity.
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Molecular Circuits of Resolution: Formation and Actions of Resolvins and Protectins

TL;DR: The first molecular resolution circuits and their major components activated by specific novel lipid mediators (i.e., resolvin E1 and 10,17S-docosatriene) to promote resolution are characterized.
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Resolvin D1 and Its Aspirin-triggered 17R Epimer STEREOCHEMICAL ASSIGNMENTS, ANTI-INFLAMMATORY PROPERTIES, AND ENZYMATIC INACTIVATION

TL;DR: The stereochemistry of the conjugated double bonds and chirality of alcohols present in resolvin D1 and its aspirin-triggered 17R epimer (AT-RvD1) with compounds prepared by total organic synthesis are established and demonstrate the stereoselective basis for their enzymatic inactivation.
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Anti-Inflammatory Actions of Neuroprotectin D1/Protectin D1 and Its Natural Stereoisomers: Assignments of Dihydroxy-Containing Docosatrienes

TL;DR: Comparisons showed that PD1 from human cells carrying potent bioactivity is 10R,17S-dihydroxy-docosa-4Z,7Z,11E,13E,15Z,19Z-hexaenoic acid, whereas PD1 formation proceeded via an epoxide, indicating sequential lipoxygenation.
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Atherosclerosis: evidence for impairment of resolution of vascular inflammation governed by specific lipid mediators

TL;DR: Results indicate that 12/15‐lipoxy‐genase expression protects mice against atherosclerosis via its role in the local biosynthesis of lipid mediators, including lipoxin A4, resolvin D1, and protectin D1.