Conditions and Treatments
- Professor, Department of Medicine at NYU Grossman School of Medicine
- Professor, Department of Biochemistry and Molecular Pharmacology at NYU Grossman School of Medicine
- Director, Clinical and Translational Science Institute Education and Careers Unit
- Chief of Rheumatology, VA NY Harbor Health Care System
- Director, Rheumatology Fellowship Program
- American Board of Internal Medicine (Rheumatology), 1992
Education and Training
- Fellowship, New York University School of Medicine, Rheumatology, 1993
- Residency, Jacobi Medical Center, Internal Medicine, 1990
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Michael H. Pillinger, MD does not accept insurance.
Research My Research
signal transduction and the regulation of cells involved in inflammation and rheumatoid arthritis
In rheumatoid arthritis (RA) the tissues of the involved joints assume inflammatory, autoimmune and pseudoneoplastic features. The cells contributing to these phenotypes include neutrophils, which accumulate in the RA joint space, and synovial fibroblasts (SFs), which proliferate in great numbers in the RA synovium (pannus) and secrete matrix metalloproteinases (MMPs) that participate in the destruction of cartilage.
The mitogen-activated protein kinases (MAPKs) include the Erks, Jnks and p38. Our laboratory is interested in the role of MAPKs on neutrophils and SF regulation. We are especially interested in the role of Erks. We have observed that, in neutrophils, Erk is rapidly activated in response to chemoattractants and regulates neutrophil adhesion, a critical early step in the acute inflammation. In SFs we have shown that Erk regulates proliferation, but also the release of some (MMP-1,3,9) but not other (MMP-13) metalloproteinases. Interestingly, high-dose salicylates (doses achievable in patients but in excess of those needed to inhibit cyclooxygenase) inhibit Erk in both neutrophils and SFs, and concordantly inhibit neutrophil adhesion and SF MMP release. Non-salicylate nonsteroidals also inhibit cyclooxygenase but do not reproduce these effects. Indeed, COX inhibition actually leads to enhancement of MMP release from synovial fibroblasts.
Our present aims are threefold: 1) to understand the mechanisms through which Erk positively regulates neutrophil adhesion; 2) to understand the cross talk between prostaglandin production and Erk activation in SF responses; 3) to understand the mechanisms through which salicylates inhibit Erk, as a clue into how Erk, and other signaling pathways, may be pharmacologically targeted. A better understanding of these phenomena may lead to new approaches, and new agents, for the treatment of RA.}
Research Interests Timeline
Clinical Trials and Research Studies
Current rheumatology reports. 2023 May ; 25(5):83-97
Colchicine Use and Major Adverse Cardiovascular Events in Male Patients with Gout and Established Coronary Artery Disease: A Veterans Affairs Nested Retrospective Cohort Study
Gout, urate, & crystal deposition disease. 2023; 1(1):11-24
Mayo Clinic proceedings. 2022 07 ; 97(7):1345-1362