L
Louis J. Ignarro
Researcher at University of California, Los Angeles
Publications - 335
Citations - 47353
Louis J. Ignarro is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Nitric oxide & Nitric oxide synthase. The author has an hindex of 106, co-authored 335 publications receiving 46008 citations. Previous affiliations of Louis J. Ignarro include Boston University & Konkuk University.
Papers
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Journal ArticleDOI
Nuclear Fusion-Independent Smooth Muscle Differentiation of Human Adipose-Derived Stem Cells Induced by a Smooth Muscle Environment
Rong Zhang,Rong Zhang,Gregory S. Jack,Nagesh Rao,Patricia A. Zuk,Louis J. Ignarro,Benjamin M. Wu,Larissa V. Rodriguez,Larissa V. Rodriguez +8 more
TL;DR: It is concluded that cell plasticity is present in hASCs, and their differentiation is accomplished in the absence of nuclear fusion.
Journal ArticleDOI
Evidence for the presence of an unusual nitric oxide- and citrulline-producing enzyme in rat kidney.
TL;DR: The results suggest the possible existence of another isoform of nitric oxide synthase with very distinct properties from the known isoforms.
Book ChapterDOI
Neurotransmitters and cytokines in CNS pathology.
Branislava Mitrovic,Fredricka C. Martin,Andrew Charles,Louis J. Ignarro,Peter A. Anton,Fergus Shanahan,Jean E. Merrill +6 more
TL;DR: An in vitro model for oligodendrocyte cell death that may be relevant to events in formation of lesions in multiple sclerosis is demonstrated, suggesting that the plaque formation is cell-mediated.
Journal ArticleDOI
Biphasic regulation of tissue plasminogen activator activity in ischemic rat brain and in cultured neural cells: Essential role of astrocyte-derived plasminogen activator inhibitor-1
Ji Woon Kim,Sung Hoon Lee,Hyun Myung Ko,Kyoung Ja Kwon,Kyu Suk Cho,Chang Soon Choi,Jin Hee Park,Hahn Young Kim,Jongmin Lee,Seol Heui Han,Louis J. Ignarro,Louis J. Ignarro,Jae Hoon Cheong,Won Ki Kim,Chan Young Shin +14 more
TL;DR: The results from the present study suggest that neurons are the major source of tPA and that the glutamate-induced stimulated release is mainly governed by neurons in the acute phase, while the massive up-regulation of PAI-1 in astrocytes during subchronic and chronic inflammatory conditions, leads to decreased tPA activity in the later stages of MCAO.
Journal Article
Oppositional effects of acetylcholine and isoproterenol on isometric tension and cyclic nucleotide concentrations in rabbit atria.
TL;DR: The hypothesis that changes in intracellular levels of cyclic AMP and cyclic GMP may mediate the positive and negative inotropic effects of adrenergic and cholinergic agents is supported.