PMID- 10559012
OWN - NLM
STAT- MEDLINE
DCOM- 19991130
LR  - 20190831
IS  - 1079-5642 (Print)
IS  - 1079-5642 (Linking)
VI  - 19
IP  - 11
DP  - 1999 Nov
TI  - Expression of LR11, a mosaic LDL receptor family member, is markedly increased in
      atherosclerotic lesions.
PG  - 2687-95
AB  - Receptors belonging to the LDL receptor (LDLR) family are thought to play key
      roles in lipoprotein metabolism in a variety of tissues, including the arterial
      wall. Here, we report that the expression of a 250-kDa mosaic LDLR family member,
      which we called LR11 for the presence of 11 ligand-binding repeats, is markedly
      induced during the process of atherogenesis in 2 animal models. Analysis by
      reverse transcription-polymerase chain reaction and RNase protection assays
      revealed that LR11 transcript levels rise in rabbit aortas displaying
      atheromatous lesions after the rabbits have been fed a high-cholesterol diet.
      Immunohistochemistry demonstrated that the highest induction of LR11 occurs in
      intimal smooth muscle cells (SMCs), followed by medial SMCs close to the intimal 
      border of the atheromatous lesions. Experimental intimal hyperplasia by
      endothelial denudation showed that LR11 mRNA levels were also increased in the
      arteries after balloon injury, with the transcripts localized primarily in the
      hyperplastic intimal layer. In agreement with the correlation of LR11 induction
      during increased cell proliferation, cultured SMCs showed an increase in LR11
      expression in the proliferative phase. Furthermore, Northern and Western blot
      analyses showed that medium conditioned by the monocyte-macrophage cell line
      THP-1 enhanced LR11 expression in cultured SMCs. These findings suggest that
      upregulation of LR11 might be contributing to the pathological roles of intimal
      and medial SMCs during arteriosclerotic lesion development and provide the first 
      insight into the as yet unknown functional significance of this intriguing LDLR
      family member.
FAU - Kanaki, T
AU  - Kanaki T
AD  - Second Department of Internal Medicine, School of Medicine, Chiba University,
      Japan.
FAU - Bujo, H
AU  - Bujo H
FAU - Hirayama, S
AU  - Hirayama S
FAU - Ishii, I
AU  - Ishii I
FAU - Morisaki, N
AU  - Morisaki N
FAU - Schneider, W J
AU  - Schneider WJ
FAU - Saito, Y
AU  - Saito Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Arterioscler Thromb Vasc Biol
JT  - Arteriosclerosis, thrombosis, and vascular biology
JID - 9505803
RN  - 0 (Cholesterol, Dietary)
RN  - 0 (Culture Media, Conditioned)
RN  - 0 (Membrane Transport Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, LDL)
RN  - 0 (Sorl1 protein, rat)
SB  - IM
MH  - Angioplasty, Balloon/adverse effects
MH  - Animals
MH  - Aorta/cytology
MH  - Arteriosclerosis/pathology/*physiopathology
MH  - Carotid Artery, Common/pathology/physiopathology
MH  - Cells, Cultured
MH  - Cholesterol, Dietary/pharmacology
MH  - Culture Media, Conditioned/pharmacology
MH  - Diet, Atherogenic
MH  - Disease Models, Animal
MH  - Endothelium, Vascular/pathology
MH  - Gene Expression/drug effects
MH  - In Situ Hybridization
MH  - Male
MH  - *Membrane Transport Proteins
MH  - Mosaicism
MH  - Muscle, Smooth, Vascular/*chemistry/injuries/*pathology
MH  - RNA, Messenger/analysis
MH  - Rabbits
MH  - Receptors, LDL/analysis/*genetics
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Transcription, Genetic
EDAT- 1999/11/13 00:00
MHDA- 1999/11/13 00:01
CRDT- 1999/11/13 00:00
PHST- 1999/11/13 00:00 [pubmed]
PHST- 1999/11/13 00:01 [medline]
PHST- 1999/11/13 00:00 [entrez]
AID - 10.1161/01.atv.19.11.2687 [doi]
PST - ppublish
SO  - Arterioscler Thromb Vasc Biol. 1999 Nov;19(11):2687-95. doi:
      10.1161/01.atv.19.11.2687.