PMID- 19010548
OWN - NLM
STAT- MEDLINE
DCOM- 20090622
LR  - 20131121
IS  - 1872-9142 (Electronic)
IS  - 0161-5890 (Linking)
VI  - 46
IP  - 6
DP  - 2009 Mar
TI  - The presence and activity of SP-D in porcine coronary endothelial cells depend on 
      Akt/PI3K, Erk and nitric oxide and decrease after multiple passaging.
PG  - 1050-7
LID - 10.1016/j.molimm.2008.09.027 [doi]
AB  - Surfactant protein D (SP-D) mediates clearance of microorganisms and modulates 
      inflammation in response to cytotoxic stimulation. It is present in various 
      epithelia, but also in vascular smooth muscle and endothelial cells. Experiments 
      were designed to determine whether or not SP-D is present in porcine coronary 
      arterial endothelial cells and if so, to investigate the molecular mechanisms 
      underlying this presence. The expression of SP-D, NO synthase, Akt 1/2 and Erk 
      1/2 proteins was determined in cultures at passages 1 (#1) and 4 (#4). SP-D in 
      primary cells existed in three isoforms (37-38 kDa and 50 kDa). The 37-38 kDa 
      SP-D forms were the dominant isoforms in the porcine endothelium and were 
      prominent at #1 but partially lost at #4. Tumor necrosis factor-alpha (TNF-alpha) 
      significantly augmented the level of SP-D expression at #1 but not at #4. The 
      basal level of 37-38 kDa SP-D isoforms at #1 was reduced by L-NAME, wortmannin 
      and PD 98059. The low basal expression at #4 could be increased by DETA NONOate 
      (donor of NO) or insulin (activator of PI(3)K/Akt). The presence of nitric oxide 
      synthase was reduced while that of Akt 1/2 and Erk 1/2 was increased at #4. In 
      cells both at passages 1 and 4, TNF-alpha downregulated NO synthase and 
      up-regulated p-Erk 1/2 protein. The present findings demonstrate the presence of 
      SP-D in endothelial cells which is NO-, PI(3)K/Akt- and Erk-dependent. They 
      suggest a protective role of SP-D in these cells.
FAU - Lee, Mary Y K
AU  - Lee MY
AD  - Department of Pharmacology, Li Ka Shing Faculty of Medicine, The University of 
      Hong Kong, L2-48, Laboratory Block, 21 Sassoon Road, Pokfulam, Hong Kong.
FAU - Sorensen, Grith L
AU  - Sorensen GL
FAU - Holmskov, Uffe
AU  - Holmskov U
FAU - Vanhoutte, Paul M
AU  - Vanhoutte PM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20081117
PL  - England
TA  - Mol Immunol
JT  - Molecular immunology
JID - 7905289
RN  - 0 (Protein Isoforms)
RN  - 0 (Pulmonary Surfactant-Associated Protein D)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Coronary Vessels/cytology/metabolism
MH  - Culture Techniques
MH  - Endothelial Cells/*metabolism
MH  - Endothelium, Vascular/cytology/*metabolism
MH  - Extracellular Signal-Regulated MAP Kinases/*metabolism
MH  - Gene Expression Regulation
MH  - Nitric Oxide/*metabolism
MH  - Nitric Oxide Synthase Type III/metabolism
MH  - Protein Isoforms/metabolism
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - Pulmonary Surfactant-Associated Protein D/genetics/*physiology
MH  - Swine
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2008/11/18 09:00
MHDA- 2009/06/23 09:00
CRDT- 2008/11/18 09:00
PHST- 2008/09/02 00:00 [received]
PHST- 2008/09/24 00:00 [accepted]
PHST- 2008/11/18 09:00 [pubmed]
PHST- 2009/06/23 09:00 [medline]
PHST- 2008/11/18 09:00 [entrez]
AID - S0161-5890(08)00699-8 [pii]
AID - 10.1016/j.molimm.2008.09.027 [doi]
PST - ppublish
SO  - Mol Immunol. 2009 Mar;46(6):1050-7. doi: 10.1016/j.molimm.2008.09.027. Epub 2008 
      Nov 17.