Loretta Ma
Ottawa Hospital Research Institute
9 Papers
101 Citations
Loretta Ma is an academic researcher from Ottawa Hospital Research Institute. The author has contributed to research in topics: ABCA1 & ATP Binding Cassette Transporter 1. The author has an hindex of 6, co-authored 9 publications. Previous affiliations of Loretta Ma include University of Ottawa.
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Papers
ABCA1-mediated cholesterol efflux generates microparticles in addition to HDL through processes governed by membrane rigidity.
Shilpi Nandi,Loretta Ma,Maxime Denis,Joel Karwatsky,Zhiqiang Li,Xian-Cheng Jiang,Xiaohui Zha +6 more
TL;DR: It is demonstrated that ABCA1 also directly mediates the production of apoA-I free microparticles, and suggested that both HDL and microparticle release is favored by a more fluid plasma membrane.
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Human Apolipoprotein A-II Protects Against Diet-Induced Atherosclerosis in Transgenic Rabbits
Yao Wang,Manabu Niimi,Kazutoshi Nishijima,Ahmed Bilal Waqar,Ying Yu,Tomonari Koike,Shuji Kitajima,Enqi Liu,Tomohiro Inoue,Masayuki Kohashi,Yuka Keyamura,Tomohiro Yoshikawa,Jifeng Zhang,Loretta Ma,Xiaohui Zha,Teruo Watanabe,Yujiro Asada,Y. Eugene Chen,Jianglin Fan,Jianglin Fan +19 more
TL;DR: Results suggest that enrichment of apo A-II in high-density lipoprotein particles has atheroprotective effects and apo B-II may become a target for the treatment of atherosclerosis.
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Ht31, a protein kinase A anchoring inhibitor, induces robust cholesterol efflux and reverses macrophage foam cell formation through ATP-binding cassette transporter A1.
TL;DR: It is reported that a protein kinase A (PKA)-anchoring inhibitor, st-Ht31, induces robust cholesterol/phospholipid efflux, and ATP-binding cassette transporter A1 (ABCA1) greatly facilitates this process, and it is found that st- Ht31 completely reverses foam cell formation, and this process is ABCA1-dependent.
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Cholesterol efflux to apoA-I in ABCA1-expressing cells is regulated by Ca2+-dependent calcineurin signaling
TL;DR: It is concluded that this Ca2+-dependent calcineurin/JAK2 pathway is specifically responsible for apoA-I lipidation without directly modifying ABCA1 activity.
28
ABCA1 increases extracellular ATP to mediate cholesterol efflux to ApoA-I
TL;DR: It is concluded that, through direct or indirect mechanisms, ABCA1 functions to raise ATP levels in the medium, which is required forABCA1-mediated cholesterol efflux to apoA-I.