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Start Over Author "Changjun Yang" Publisher american physiological society
2 results on '"Changjun Yang"'

1. Neuroinflammatory mechanisms of blood-brain barrier damage in ischemic stroke

Author

Changjun Yang, Kimberly E. Hawkins, Sylvain Doré, and Eduardo Candelario-Jalil

Subjects
0301 basic medicine, Chemokine, Physiology, medicine.disease_cause, Blood–brain barrier, Permeability, Brain Ischemia, Tight Junctions, 03 medical and health sciences, 0302 clinical medicine, Immune system, medicine, Animals, Humans, Stroke, Neuroinflammation, biology, Tight junction, business.industry, Endothelial Cells, Biological Transport, Cell Biology, Neurovascular bundle, medicine.disease, Oxidative Stress, 030104 developmental biology, medicine.anatomical_structure, nervous system, Blood-Brain Barrier, cardiovascular system, biology.protein, Inflammation Mediators, business, Neuroscience, Theme, 030217 neurology & neurosurgery, Oxidative stress
Abstract

As part of the neurovascular unit, the blood-brain barrier (BBB) is a unique, dynamic regulatory boundary that limits and regulates the exchange of molecules, ions, and cells between the blood and the central nervous system. Disruption of the BBB plays an important role in the development of neurological dysfunction in ischemic stroke. Blood-borne substances and cells have restricted access to the brain due to the presence of tight junctions between the endothelial cells of the BBB. Following stroke, there is loss of BBB tight junction integrity, leading to increased paracellular permeability, which results in vasogenic edema, hemorrhagic transformation, and increased mortality. Thus, understanding principal mediators and molecular mechanisms involved in BBB disruption is critical for the development of novel therapeutics to treat ischemic stroke. This review discusses the current knowledge of how neuroinflammation contributes to BBB damage in ischemic stroke. Specifically, we provide an updated overview of the role of cytokines, chemokines, oxidative and nitrosative stress, adhesion molecules, matrix metalloproteinases, and vascular endothelial growth factor as well as the role of different cell types in the regulation of BBB permeability in ischemic stroke.

Published
2019
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2. Identification of a PKCϵ-dependent regulation of myocardial contraction by epicatechin-3-gallate.

Author

Daxiang Li, Changjun Yang, Ying Chen, Jiang Tian, Lijun Liu, Qiuping Dai, Xiaochun Wan, and Zijian Xie

Subjects
*CATECHIN, *CARDIAC contraction, *ELECTROCARDIOGRAPHY, *PERFUSION, *MYOCARDIUM, *CYSTEINE proteinases
Abstract

In this study, the effects of tea catechins and tea theaflavins on myocardial contraction were examined in isolated rat hearts using a Langendorff-perfusion system. We found that both tea catechins and theafiavins had positive inotropic effects on the myocardium. Of the tested chemicals, epicatechin-3-gallate (ECG) and theafiavin-3,3–-digallate (TF4) appear to be the most effective tea catechin and theafiavin, respectively. Further studies of ECG-induced positive inotropy revealed the following insights. First, unlike digitalis drugs, ECO had no effect on intracellular Ca2+ level in cultured adult cardiac myocytes. Second, it activated PKCϵ, but not PKCα, in the isolated hearts as well as in cultured cells. Neither a phospholipase C (PLC) inhibitor (U73122) nor the antioxidant N-acetyl cysteine (NAC) affected the ECG-induced activation of PKCϵ. Third, inhibition of PKCϵ by either chelerythrine chloride (CHE) or PKCϵ translocation inhibitor peptide (TIP) caused a partial reduction of ECG-induced increases in myocardial contraction. Moreover, NAC was also effective in reducing the effects of ECG on myocardial contraction. Finally, pretreatment of the heart with both CHE and NAC completely abolished ECG-induced inotropic effects on the heart. Together, these findings indicate that ECG can regulate myocardial contractility via a novel PKCϵ-dependent signaling pathway. [ABSTRACT FROM AUTHOR]

Published
2008
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