PMID- 20008269
OWN - NLM
STAT- MEDLINE
DCOM- 20100402
LR  - 20211020
IS  - 1522-1539 (Electronic)
IS  - 0363-6135 (Print)
IS  - 0363-6135 (Linking)
VI  - 298
IP  - 3
DP  - 2010 Mar
TI  - Diabetic conditions promote binding of monocytes to vascular smooth muscle cells 
      and their subsequent differentiation.
PG  - H736-45
LID - 10.1152/ajpheart.00935.2009 [doi]
AB  - Diabetes is associated with significantly accelerated rates of atherosclerosis, 
      key features of which include the presence of excessive macrophage-derived foam 
      cells in the subendothelial space. We examined the hypothesis that enhanced 
      monocyte-vascular smooth muscle cell (VSMC) interactions leading to 
      subendothelial monocyte retention and differentiation to macrophages under 
      diabetic conditions may be underlying mechanisms. Human aortic VSMCs (HVSMCs) 
      treated with diabetic stimuli high glucose (HG) or S100B, a ligand of the 
      receptor for advanced glycation end products, exhibited significantly increased 
      binding of THP-1 monocytic cells. Diabetic stimuli increased the expression of 
      the adhesive chemokine fractalkine (FKN) in HVSMCs. Pretreatment of HVSMCs with 
      FKN or monocyte chemoattractant protein-1 (MCP-1) neutralizing antibodies 
      significantly inhibited monocyte-VSMC binding, whereas monocytes treated with FKN 
      showed enhanced binding to VSMC. Mouse aortic VSMCs (MVSMCs) derived from type 2 
      diabetic db/db mice exhibited significantly increased FKN levels and binding to 
      mouse WEHI78/24 monocytic cells relative to nondiabetic control db/+ cells. The 
      enhanced monocyte binding in db/db cells was abolished by both FKN and MCP-1 
      antibodies. Endothelium-denuded aortas from db/db mice and streptozotocin-induced 
      diabetic mice also exhibited enhanced FKN expression and monocyte binding, 
      relative to respective controls. Coculture with HVSMCs increased CD36 expression 
      in THP-1 cells, and this was significantly augmented by treatment of HVSMCs with 
      S100B or HG. CD36 mRNA and protein levels were also significantly increased in 
      WEHI78/24 cells after coincubation with db/db MVSMCs relative to control MVSMCs. 
      These results demonstrate that diabetic conditions may accelerate atherosclerosis 
      by inducing key chemokines in the vasculature that promote VSMC-monocyte 
      interactions, subendothelial monocyte retention, and differentiation.
FAU - Meng, Li
AU  - Meng L
AD  - Department of Diabetes, Beckman Research Institute of City of Hope, Duarte, 
      California 91010, USA.
FAU - Park, Jehyun
AU  - Park J
FAU - Cai, Qiangjun
AU  - Cai Q
FAU - Lanting, Linda
AU  - Lanting L
FAU - Reddy, Marpadga A
AU  - Reddy MA
FAU - Natarajan, Rama
AU  - Natarajan R
LA  - eng
GR  - R01 DK065073/DK/NIDDK NIH HHS/United States
GR  - R01 HL087864/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20091211
PL  - United States
TA  - Am J Physiol Heart Circ Physiol
JT  - American journal of physiology. Heart and circulatory physiology
JID - 100901228
RN  - 0 (CD36 Antigens)
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CX3CL1)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (S100 Calcium Binding Protein beta Subunit)
RN  - 0 (S100 Proteins)
RN  - 0 (S100B protein, human)
RN  - 0 (S100b protein, mouse)
RN  - 5W494URQ81 (Streptozocin)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
CIN - Am J Physiol Heart Circ Physiol. 2010 Mar;298(3):H731-3. PMID: 20023118
MH  - Animals
MH  - CD36 Antigens/metabolism
MH  - Cell Adhesion
MH  - *Cell Communication
MH  - *Cell Differentiation
MH  - Cells, Cultured
MH  - Chemokine CCL2/metabolism/pharmacology
MH  - Chemokine CX3CL1/metabolism/pharmacology
MH  - Diabetes Mellitus, Experimental/metabolism/*pathology
MH  - Disease Models, Animal
MH  - Glucose/pharmacology
MH  - Humans
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Inbred Strains
MH  - Monocytes/metabolism/*pathology
MH  - Muscle, Smooth, Vascular/drug effects/metabolism/*pathology
MH  - Nerve Growth Factors/pharmacology
MH  - S100 Calcium Binding Protein beta Subunit
MH  - S100 Proteins/pharmacology
MH  - Streptozocin
PMC - PMC2838549
EDAT- 2009/12/17 06:00
MHDA- 2010/04/03 06:00
PMCR- 2011/03/01
CRDT- 2009/12/17 06:00
PHST- 2009/12/17 06:00 [entrez]
PHST- 2009/12/17 06:00 [pubmed]
PHST- 2010/04/03 06:00 [medline]
PHST- 2011/03/01 00:00 [pmc-release]
AID - 00935.2009 [pii]
AID - H-00935-2009 [pii]
AID - 10.1152/ajpheart.00935.2009 [doi]
PST - ppublish
SO  - Am J Physiol Heart Circ Physiol. 2010 Mar;298(3):H736-45. doi: 
      10.1152/ajpheart.00935.2009. Epub 2009 Dec 11.