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Shikata Y Rios A Kawkitinarong K DePaola N Garcia JG Birukov KG 《Experimental cell research》2005,304(1):40-49
Regulation of endothelial cell (EC) permeability by bioactive molecules is associated with specific patterns of cytoskeletal and cell contact remodeling. A role for mechanical factors such as shear stress (SS) and cyclic stretch (CS) in cytoskeletal rearrangements and regulation of EC permeability becomes increasingly recognized. This paper examined redistribution of focal adhesion (FA) proteins, site-specific focal adhesion kinase (FAK) phosphorylation, small GTPase activation and barrier regulation in human pulmonary EC exposed to laminar shear stress (15 dyn/cm2) or cyclic stretch (18% elongation) in vitro. SS caused peripheral accumulation of FAs, whereas CS induced randomly distributed FAs attached to the ends of newly formed stress fibers. SS activated small GTPase Rac without effects on Rho, whereas 18% CS activated without effect on Rac. SS increased transendothelial electrical resistance (TER) in EC monolayers, which was further elevated by barrier-protective phospholipid sphingosine 1-phosphate. Finally, SS induced FAK phosphorylation at Y576, whereas CS induced FAK phosphorylation at Y397 and Y576. These results demonstrate for the first time differential effects of SS and CS on Rho and Rac activation, FA redistribution, site-specific FAK phosphorylation, and link them with SS-mediated barrier enhancement. Thus, our results suggest common signaling and cytoskeletal mechanisms shared by mechanical and chemical factors involved in EC barrier regulation. 相似文献
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Arunee Thitithanyanont Monkol Uiprasertkul Suwimon Wiboon-ut Amporn Limsalakpetch Kosol Yongvanitchit Pimprapa Rukyen Kamon Kawkitinarong Pongsak Utaisincharoen Carl J. Mason Sathit Pichyangkul 《Biochemical and biophysical research communications》2010,398(4):752-758
Information on the immune response against H5N1 within the lung is lacking. Here we describe the sustained antiviral immune responses, as indicated by the expression of MxA protein and IFN-α mRNA, in autopsy lung tissue from an H5N1-infected patient. H5N1 infection of primary bronchial/tracheal epithelial cells and lung microvascular endothelial cells induced IP-10, and also up-regulated the retinoic acid-inducible gene-I (RIG-I). Down-regulation of RIG-I gene expression decreased IP-10 response. Co-culturing of H5N1-infected pulmonary cells with TNF-α led to synergistically enhanced production of IP-10. In the absence of viral infection, TNF-α and IFN-α also synergistically enhanced IP-10 response. Methylprednisolone showed only a partial inhibitory effect on this chemokine response. Our findings strongly suggest that both the H5N1 virus and the locally produced antiviral cytokines; IFN-α and TNF-α may have an important role in inducing IP-10 hyperresponse, leading to inflammatory damage in infected lung. 相似文献
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Chumpa Nuntana Kawkitinarong Kamon Rotcheewaphan Suwatchareeporn Sawatpanich Ajcharaporn Petsong Suthidee Tumwasorn Somying Suwanpimolkul Gompol 《Molecular biology reports》2020,47(4):2501-2508
Molecular Biology Reports - To determine the accuracy of multiplex real-time PCR (Anyplex? II MTB/MDR kit) in detecting Isoniazid (INH)- and Rifampin (RIF)-resistant Mycobacterium... 相似文献
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