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LPS-induced vascular endothelial growth factor expression in rat lung pericytes

 Chang Oh Kim  ;  Ae Jung Huh  ;  Myung Soo Kim  ;  Bum Sik Chin  ;  Sang Hoon Han  ;  Suk Hoon Choi  ;  Su Jin Jeong  ;  Hee Kyung Choi  ;  Jun Yong Choi  ;  Young Goo Song  ;  June Myung Kim 
 SHOCK, Vol.30(1) : 92-97, 2008 
Journal Title
Issue Date
Animals ; Cells, Cultured ; Imidazoles/pharmacology ; Lipopolysaccharides/pharmacology* ; Lung/cytology* ; Lung/drug effects ; Male ; Nitric Oxide Synthase Type II/physiology ; Pericytes/drug effects ; Pericytes/metabolism* ; Pyridines/pharmacology ; RNA, Messenger/metabolism ; Rats ; Rats, Sprague-Dawley ; Respiratory Distress Syndrome, Adult/physiopathology ; Vascular Endothelial Growth Factor A/biosynthesis* ; p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors ; p38 Mitogen-Activated Protein Kinases/physiology*
KEYWORDS—LPS ; sepsis ; VEGF ; pericyte ; p38 MAP kinase
Vascular endothelial growth factor (VEGF) is a potent angiogenic and vascular permeability factor. Recent studies have shown that the VEGF levels increase in several cell types, for example, macrophages and smooth muscle cells after LPS stimulation, suggesting that it is important in the initiation and development of sepsis. In particular, LPS-regulated contractility in lung pericytes may play an important role in mediating pulmonary microvascular fluid hemodynamics during sepsis. This study investigated the production of VEGF by rat lung pericytes in response to LPS. LPS was found to enhance VEGF mRNA expression in a concentration-dependent manner peaking 2 h after stimulation in pericytes. Vascular endothelial growth factor protein levels in conditioned medium and in cell lysate also increased on increasing LPS and peaked after 24 to 48 h. LPS also significantly augmented iNOS expression in lung pericytes within 6 h. However, iNOS mRNA induction occurred later than LPS-induced VEGF mRNA increases. Interestingly, attempted inhibition with nuclear factor-kappaB or tyrosine kinase did not suppress LPS-induced augmented VEGF mRNA expression in lung pericytes, although both inhibitors markedly inhibited LPS-induced iNOS mRNA expression. SB203580, a p38 MAP kinase inhibitor, repressed LPS-induced VEGF mRNA expression. Furthermore, LPS stimulated a rapid and sustained phosphorylation of p38 MAP kinase. These results show that pericytes produce VEGF in response to LPS stimulation, and that this may be partly mediated by the p38 MAP kinase pathway. More research should be done to establish the regulation of capillary hemodynamics and identify mechanisms of their regulation.
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1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Myoung Soo(김명수)
Kim, June Myung(김준명)
Kim, Chang Oh(김창오) ORCID logo https://orcid.org/0000-0002-0773-5443
Song, Young Goo(송영구) ORCID logo https://orcid.org/0000-0002-0733-4156
Jeong, Su Jin(정수진) ORCID logo https://orcid.org/0000-0003-4025-4542
Chin, Bum Sik(진범식)
Choi, Suk Hoon(최석훈)
Choi, Jun Yong(최준용) ORCID logo https://orcid.org/0000-0002-2775-3315
Choi, Hee Kyoung(최희경)
Han, Sang Hoon(한상훈) ORCID logo https://orcid.org/0000-0002-4278-5198
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