D
David S. Milstone
Researcher at Brigham and Women's Hospital
Publications - 38
Citations - 5137
David S. Milstone is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: Peroxisome proliferator-activated receptor & Trophoblast. The author has an hindex of 23, co-authored 36 publications receiving 4824 citations. Previous affiliations of David S. Milstone include Howard Hughes Medical Institute & Boston Children's Hospital.
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Journal ArticleDOI
PPARγ Is Required for the Differentiation of Adipose Tissue In Vivo and In Vitro
Evan D. Rosen,Pasha Sarraf,Amy E Troy,Gary Bradwin,Kathryn J. Moore,David S. Milstone,Bruce M. Spiegelman,Richard M. Mortensen +7 more
TL;DR: It is demonstrated here that mice chimeric for wild-type and PPARγ null cells show little or no contribution of null cells to adipose tissue, whereas most other organs examined do not require PParγ for proper development.
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A major role for VCAM-1, but not ICAM-1, in early atherosclerosis
Myron I. Cybulsky,Kaeko Iiyama,Hongmei Li,Su-Ning Zhu,Mian Chen,Motoi Iiyama,Vannessa M. Davis,Jose-Carlos Gutierrez-Ramos,Philip W. Connelly,David S. Milstone +9 more
TL;DR: The data indicate that VCAM-1 plays a dominant role in the initiation of atherosclerosis in mice generated from heterozygous intercrosses and fed a cholesterol-enriched diet for 8 weeks.
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The role of PPAR-γ in macrophage differentiation and cholesterol uptake
Kathryn J. Moore,Evan D. Rosen,Michael L. Fitzgerald,Felix Randow,Lorna P. Andersson,David Altshuler,David Altshuler,David S. Milstone,David S. Milstone,Richard M. Mortensen,Bruce M. Spiegelman,Mason W. Freeman +11 more
TL;DR: In wild-type macrophages, TZD treatment divergently regulated CD36 and class A macrophage-scavenger receptor expression and failed to induce significant cellular cholesterol accumulation, indicating that TZDs may not exacerbate Macrophage foam-cell formation.
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Cardiomyocyte-Specific Knockout and Agonist of Peroxisome Proliferator–Activated Receptor-γ Both Induce Cardiac Hypertrophy in Mice
Sheng-Zhong Duan,Christine Y. Ivashchenko,Mark W. Russell,David S. Milstone,David S. Milstone,Richard M. Mortensen +5 more
TL;DR: It is shown that cardiomyocyte PPAR-γ suppresses cardiac growth and embryonic gene expression and inhibits nuclear factor &kgr;B activity in vivo and rosiglitazone causes cardiac hypertrophy at least partially independent of PPar-γ inCardiomyocytes and through different mechanisms from CM-PGKO.
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Hypotension, lipodystrophy, and insulin resistance in generalized PPARγ-deficient mice rescued from embryonic lethality
Sheng-Zhong Duan,Christine Y. Ivashchenko,Steven E. Whitesall,Louis G. D'Alecy,Damon Duquaine,Frank C. Brosius,Frank J. Gonzalez,Charles Vinson,Melissa A. Pierre,David S. Milstone,Richard M. Mortensen +10 more
TL;DR: It is demonstrated that PPargamma is required to maintain normal adiposity and insulin sensitivity in adult mice and genetic loss of PPARgamma function, like activation by agonists, lowered blood pressure, likely through a mechanism involving increased vascular relaxation.