PMID- 14722023
OWN - NLM
STAT- MEDLINE
DCOM- 20040625
LR  - 20220408
IS  - 0193-1849 (Print)
IS  - 0193-1849 (Linking)
VI  - 286
IP  - 6
DP  - 2004 Jun
TI  - Insulin-like growth factor I receptors are more abundant than insulin receptors 
      in human micro- and macrovascular endothelial cells.
PG  - E896-901
AB  - Micro- and macroangiopathy are major causes of morbidity and mortality in 
      patients with diabetes. Our aim was to characterize IGF-I receptor (IGF-IR) and 
      insulin receptor (IR) in human micro- and macrovascular endothelial cells. 
      Cultured human dermal microvascular endothelial cells (HMVEC) and human aortic 
      endothelial cells (HAEC) were used. Gene expression was measured by quantitative 
      real-time RT-PCR and receptor protein by ligand-binding assay. Phosphorylation of 
      IGF-IR beta-subunit was analyzed by immunoprecipitation and Western blot. Glucose 
      metabolism and DNA synthesis was assessed using [(3)H]glucose and [(3)H]thymidine 
      incorporation, respectively. We detected gene expression of IGF-IR and IR in HAEC 
      and HMVEC. IGF-IR gene expression was severalfold higher than that of IR. The 
      specific binding of (125)I-IGF-I was higher than that of (125)I-insulin in HAEC 
      and HMVEC. Insulin and the new, long-acting insulin analog glargine interacted 
      with the IGF-IR with thousand- and hundred-fold less potency than IGF-I itself. 
      Phosphorylation of the IGF-IR beta-subunit was shown in HAEC for IGF-I (10(-8) M) 
      and insulin (10(-6) M) and in HMVEC for IGF-I and glargine (10(-8) M, 10(-6) M). 
      IGF-I 10(-7) M stimulated incorporation of [(3)H]thymidine into DNA, and 
      10(-9)-10(-7) M also the incorporation of [(3)H]glucose in HMVEC, whereas 
      glargine and insulin had no significant effects at 10(-9)-10(-7) M. Human micro- 
      and macrovascular endothelial cells express more IGF-IR than IR. IGF-I and high 
      concentrations of glargine and insulin activates the IGF-IR. Glargine has a 
      higher affinity than insulin for the IGF-IR but probably has no effect on DNA 
      synthesis at concentrations reached in vivo.
FAU - Chisalita, Simona I
AU  - Chisalita SI
AD  - Division of Cell Biology, Department of Biomedicine and Surgery, Faculty of 
      Health Sciences, Linkoping University, Sweden.
FAU - Arnqvist, Hans J
AU  - Arnqvist HJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20040113
PL  - United States
TA  - Am J Physiol Endocrinol Metab
JT  - American journal of physiology. Endocrinology and metabolism
JID - 100901226
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (Insulin)
RN  - 0 (Iodine Radioisotopes)
RN  - 10028-17-8 (Tritium)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - EC 2.7.10.1 (Receptor, IGF Type 1)
RN  - EC 2.7.10.1 (Receptor, Insulin)
RN  - IY9XDZ35W2 (Glucose)
RN  - VC2W18DGKR (Thymidine)
SB  - IM
MH  - Aorta/cytology
MH  - Blotting, Western
MH  - Endothelium, Vascular/cytology/*metabolism
MH  - Gene Expression
MH  - Glucose/pharmacokinetics
MH  - Humans
MH  - Hypoglycemic Agents/metabolism/pharmacology
MH  - Insulin/metabolism/pharmacology
MH  - Insulin-Like Growth Factor I/metabolism/pharmacology
MH  - Iodine Radioisotopes
MH  - Microcirculation
MH  - Precipitin Tests
MH  - Radioligand Assay
MH  - Receptor, IGF Type 1/*genetics/*metabolism
MH  - Receptor, Insulin/*genetics/*metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Skin/blood supply
MH  - Thymidine/pharmacokinetics
MH  - Tritium
EDAT- 2004/01/15 05:00
MHDA- 2004/06/26 05:00
CRDT- 2004/01/15 05:00
PHST- 2004/01/15 05:00 [pubmed]
PHST- 2004/06/26 05:00 [medline]
PHST- 2004/01/15 05:00 [entrez]
AID - 00327.2003 [pii]
AID - 10.1152/ajpendo.00327.2003 [doi]
PST - ppublish
SO  - Am J Physiol Endocrinol Metab. 2004 Jun;286(6):E896-901. doi: 
      10.1152/ajpendo.00327.2003. Epub 2004 Jan 13.