The immunoglobulin-like cell adhesion molecule nectin and its associated protein afadin.
- Y. Takai, W. Ikeda, H. Ogita, Y. Rikitake
- Biology, ChemistryAnnual Review of Cell and Developmental Biology
- 6 October 2008
Nectins are immunoglobulin-like cell adhesion molecules (CAMs) that compose a family of four members that homophilic and heterophilically interact in trans with each other to form cell-cell adhesions and regulate many other cellular activities in cooperation with other CAMs and cell surface membrane receptors.
Rho GTPases, statins, and nitric oxide.
- Y. Rikitake, J. Liao
- Biology, ChemistryCirculation Research
- 9 December 2005
The lipid-lowering drugs, 3-hydroxy-3-methylgulutaryl-coenzyme A (HMG-CoA) reductase inhibitors or statins, are used in the prevention and treatment of cardiovascular diseases. Recent experimental…
Inhibition of Rho Kinase (ROCK) Leads to Increased Cerebral Blood Flow and Stroke Protection
- Y. Rikitake, Hyung-Hwan Kim, J. Liao
- Medicine, BiologyStroke
- 1 October 2005
Findings indicate that the neuroprotective effect of ROCK inhibition is mediated by endothelium-derived NO and suggest that ROCK may be an important therapeutic target for ischemic stroke.
Decreased Perivascular Fibrosis but Not Cardiac Hypertrophy in ROCK1+/− Haploinsufficient Mice
- Y. Rikitake, Naotsugu Oyama, J. Liao
- Medicine, BiologyCirculation
- 8 November 2005
Findings indicate ROCK1 is critical for the development of cardiac fibrosis, but not hypertrophy, in response to various pathological conditions and suggest that signaling pathways leading to the hypertrophic and profibrotic response of the heart are distinct.
Inhibition of Rho-Kinase Leads to Rapid Activation of Phosphatidylinositol 3-Kinase/Protein Kinase Akt and Cardiovascular Protection
- S. Wolfrum, A. Dendorfer, J. Liao
- Biology, MedicineArteriosclerosis, Thrombosis and Vascular Biology
- 1 October 2004
Findings suggest that Rho-kinase may play an important role in mediating the inflammatory response to ischemia-reperfusion injury and cardiovascular protection.
Critical Role of Endothelial Notch1 Signaling in Postnatal Angiogenesis
- K. Takeshita, M. Satoh, J. Liao
- BiologyCirculation Research
- 5 January 2007
It is shown that blood flow recovery and postnatal neovascularization in response to hindlimb ischemia in haploinsufficient global or endothelial-specific Notch1-specific mice, but not Notch4−/− mice, were impaired compared with wild-type mice, and that Notch 1 is critical for VEGF-induced postnatal angiogenesis.
Endothelial Cell–Derived Endothelin-1 Promotes Cardiac Fibrosis in Diabetic Hearts Through Stimulation of Endothelial-to-Mesenchymal Transition
- B. Widyantoro, N. Emoto, K. Hirata
- Medicine, BiologyCirculation
- 8 June 2010
New insights are provided suggesting that diabetes mellitus–induced cardiac fibrosis is associated with the emergence of fibroblasts from endothelial cells and that this endothelial-to-mesenchymal transition process is stimulated by ET-1.
Regulation of Tight Junction Permeability and Occludin Phosphorylation by RhoA-p160ROCK-dependent and -independent Mechanisms*
- T. Hirase, S. Kawashima, J. Staddon
- BiologyJournal of Biological Chemistry
- 30 March 2001
Although RhoA T19N and Y-27632 blocked the cytoskeletal events induced by histamine, they had no effect on the stimulation of occludin phosphorylation or increased tracer flux, indicating that occluding phosphorylated may regulate tight junction permeability independently of cytoskeleton events.
ROCK1 mediates leukocyte recruitment and neointima formation following vascular injury.
- K. Noma, Y. Rikitake, J. Liao
- GeologyJournal of Clinical Investigation
- 1 May 2008
It is indicated that ROCK1 in BM-derived cells mediates neointima formation following vascular injury and suggest that ROCK 1 may represent a promising therapeutic target in vascular inflammatory diseases.
Mechanisms of reduced nitric oxide/cGMP-mediated vasorelaxation in transgenic mice overexpressing endothelial nitric oxide synthase.
- T. Yamashita, S. Kawashima, M. Yokoyama
- Biology, MedicineHYPERTENSION
- 1 July 2000
Observations indicate that chronic overexpression of eNOS in the endothelium resulted in resistance to the NO/cGMP-mediated vasodilators and that at least 2 distinct mechanisms might be involved: one is reduced sGC activity, and the other is a decrease in PKG protein levels.
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