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Int J Oral Biol. 2014 Sep;39(3):131-136. English. Original Article. https://doi.org/10.11620/IJOB.2014.39.3.131
Kim SY , Kim SH , Choi EK , Paek YW , Kang IC .
Department of Oral Microbiology, School of Dentistry, Chonnam National University, Gwangju, 500-757, Republic of Korea. ickang@jnu.ac.kr
Department of Physical Therapy, Gwangju Health University, Gwangju, 506-701, Republic of Korea.
Abstract

Porphyromonas gingivalis is one of the most important periodontal pathogens and has been to known to invade various types of cells, including endothelial cells. The present study investigated the mechanisms involved in the internalization of P. gingivalis in human umbilical vein endothelial cells (HUVEC). P. gingivalis internalization was reduced by clathrin and lipid raft inhibitors, as well as a siRNA knockdown of caveolin-1, a principal molecule of lipid raft-related caveolae. The internalization was also reduced by perturbation of actin rearrangement, while microtubule polymerization was not required. Furthermore, we found that Src kinases are critical for the internalization of P. gingivalis into HUVEC, while neither Rho family GTPases nor phosphatidylinositol 3-kinase are required. Taken together, this study indicated that P. gingivalis internalization into endothelial cells involves clathrin and lipid rafts and requires actin rearrangement associated with Src kinase activation.

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