Clathrin and Lipid Raft-dependent Internalization of Porphyromonas gingivalis in Endothelial Cells.
- Author:
Sang Yong KIM
1
;
So Hee KIM
;
Eun Kyoung CHOI
;
Yun Woong PAEK
;
In Chol KANG
Author Information
1. Department of Oral Microbiology, School of Dentistry, Chonnam National University, Gwangju, 500-757, Republic of Korea. ickang@jnu.ac.kr
- Publication Type:Original Article
- Keywords:
Porphyromonas gingivalis;
endothelial cell;
bacterial internalization;
clathrin;
lipid raft
- MeSH:
Actins;
Caveolae;
Caveolin 1;
Clathrin*;
Endothelial Cells*;
GTP Phosphohydrolases;
Human Umbilical Vein Endothelial Cells;
Humans;
Microtubules;
Phosphatidylinositol 3-Kinase;
Phosphotransferases;
Polymerization;
Polymers;
Porphyromonas gingivalis*;
RNA, Small Interfering;
src-Family Kinases
- From:International Journal of Oral Biology
2014;39(3):131-136
- CountryRepublic of Korea
- Language:English
-
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.
