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Role of matricellular proteins in cardiac tissue remodeling after myocardial infarction

World Journal of Biological Chemistry 2010年第5期1卷 69-80页

作者： Yutaka Matsui Junko Morimoto Toshimitsu Uede Department of Matrix Medicine Institute for Genetic MedicineHokkaido UniversityKita-15Nishi-7Kita-kuSapporo 060-0815Japan Division of Molecular Immunology Institute for Genetic MedicineHokkaido UniversityKita-15Nishi-7Kita-kuSapporo 060-0815Japan

After onset of myocardial infarction(MI),the left ventricle(LV) undergoes a continuum of molecular,cellular,and extracellular responses that result in LV wall thinning,dilatation,and *** dynamic changes in LV shape,size,and function are termed cardiac *** the cardiac healing after MI does not proceed properly,it could lead to cardiac rupture or maladaptive cardiac remodeling,such as further LV dilatation and dysfunction,and ultimately *** the precise molecular mechanisms in this cardiac healing process have not been fully elucidated,this process is strictly coordinated by the interaction of cells with their surrounding extracellular matrix(ECM) *** components of ECM include basic structural proteins such as collagen,elastin and specialized proteins such as fibronectin,proteoglycans and matricellular *** proteins are a class of non-structural and secreted proteins that probably exert regulatory functions through direct binding to cell surface receptors,other matrix proteins,and soluble extracellular factors such as growth factors and *** small group of proteins,which includesosteopontin,thrombospondin-1/2,tenascin,periostin,and secreted protein,acidic and rich in cysteine,shows a low level of expression in normal adult tissue,but is markedly upregulated during wound healing and tissue remodeling,including *** this review,we focus on the regulatory functions of matricellular proteins during cardiac tissue healing and remodeling after MI.

关键词： matricellular proteins Myocardial infarction Cardiac healing Cardiac remodeling Extracellular matrix

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Potential therapeutic molecular targets for blood-brain barrier disruption after subarachnoid hemorrhage

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Neural Regeneration Research 2019年第7期14卷 1138-1143页

作者： Hideki Kanamaru Hidenori Suzuki Department of Neurosurgery Mie University Graduate School of Medicine

Aneurysmal subarachnoid hemorrhage remains serious hemorrhagic stroke with high morbidities and *** rupture causes arterial bleeding-induced mechanical brain tissue injuries and elevated intracranial pressure,followed by global cerebral ***-subarachnoid hemorrhage ischemia,tissue injuries as well as extravasated blood components and the breakdown products activate microglia,astrocytes and Toll-like receptor 4,and disrupt blood-brain barrier associated with the induction of many inflammatory and other *** blood-brain barrier is disrupted,brain tissues are directly exposed to harmful blood contents and immune cells,which aggravate brain injuries ***-brain barrier disruption after subarachnoid hemorrhage may be developed by a variety of mechanisms including endothelial cell apoptosis and disruption of tight junction *** molecules and pathways have been reported to disrupt the blood-brain barrier after subarachnoid hemorrhage,but the exact mechanisms remain *** independent and/or interconnected signaling pathways may be involved in blood-brain barrier disruption after subarachnoid *** review provides recent understandings of the mechanisms and the potential therapeutic targets of blood-brain barrier disruption after subarachnoid hemorrhage.

关键词： blood-brain barrier early brain injury endothelial cell subarachnoid hemorrhage tight junction inflammation matricellular protein Toll-like receptor 4 TLR4

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