PMID- 16830205
OWN - NLM
STAT- MEDLINE
DCOM- 20060905
LR  - 20220321
IS  - 0171-967X (Print)
IS  - 0171-967X (Linking)
VI  - 78
IP  - 6
DP  - 2006 Jun
TI  - Bone biomechanical properties in EP4 knockout mice.
PG  - 357-62
AB  - Among the four prostaglandin E receptor subtypes, EP(4) has been implicated as an 
      important regulator of both bone formation and bone resorption; however, the 
      integrated activities of this receptor on bone biomechanical properties have not 
      been examined previously. This study compared the bone biomechanical properties 
      of EP(4) knockout (KO) transgenic mice to strain-matched wild-type (WT) controls. 
      We examined two groups of adult female mice: WT (n = 12) and EP(4) KO (n = 12). 
      Femurs were tested in three-point bending and the lumbar-4 (L4) vertebral body by 
      compression. Distal femur and vertebral body trabecular bone architecture were 
      quantified using micro-computed tomography. Biomechanical structural parameters 
      (ultimate/yield load, stiffness) were measured and apparent material parameters 
      (ultimate/yield stress, modulus) calculated. Body weights and bone sizes were not 
      different between EP(4) KO and WT mice (P > 0.05, Student's t-test). EP(4) KO 
      mice exhibited reduced structural (ultimate/yield load) and apparent material 
      (ultimate/yield stress) strength in the femoral shaft and vertebral body compared 
      to WT (P < 0.05). Vertebral body stiffness and femoral neck ultimate load 
      (structural strength) were marginally lower in EP(4) KO than that in WT mice (P < 
      0.1). In addition, EP(4) KO mice have smaller distal femur and vertebral bone 
      volume to total volume (BV/TV) trabecular thickness than WT mice (P < 0.05). 
      These results suggest that the prostaglandin receptor EP(4) has an important role 
      in determining biomechanical competence in the mouse skeleton. Despite similar 
      bone size, the absence of an EP(4) receptor may have removed a necessary link for 
      bone adaptation pathways, which resulted in relatively weaker bone properties.
FAU - Akhter, M P
AU  - Akhter MP
AD  - Osteoporosis Research Center, Creighton University, Omaha, NE, USA. 
      akhtermp@creighton.edu
FAU - Cullen, D M
AU  - Cullen DM
FAU - Pan, L C
AU  - Pan LC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20060621
PL  - United States
TA  - Calcif Tissue Int
JT  - Calcified tissue international
JID - 7905481
RN  - 0 (Ptger4 protein, mouse)
RN  - 0 (Receptors, Prostaglandin E)
RN  - 0 (Receptors, Prostaglandin E, EP4 Subtype)
SB  - IM
MH  - Animals
MH  - Biomechanical Phenomena
MH  - Bone and Bones/anatomy & histology/*physiology
MH  - Female
MH  - Femur/anatomy & histology/physiology
MH  - Gene Expression Regulation
MH  - Homeostasis/physiology
MH  - Lumbar Vertebrae/anatomy & histology/physiology
MH  - Male
MH  - Mice
MH  - Mice, Knockout
MH  - Mice, Transgenic
MH  - Osteogenesis/genetics/*physiology
MH  - Receptors, Prostaglandin E/genetics/*physiology
MH  - Receptors, Prostaglandin E, EP4 Subtype
MH  - Weight-Bearing/physiology
EDAT- 2006/07/11 09:00
MHDA- 2006/09/06 09:00
CRDT- 2006/07/11 09:00
PHST- 2005/07/22 00:00 [received]
PHST- 2006/02/23 00:00 [accepted]
PHST- 2006/07/11 09:00 [pubmed]
PHST- 2006/09/06 09:00 [medline]
PHST- 2006/07/11 09:00 [entrez]
AID - 10.1007/s00223-005-0186-5 [doi]
PST - ppublish
SO  - Calcif Tissue Int. 2006 Jun;78(6):357-62. doi: 10.1007/s00223-005-0186-5. Epub 
      2006 Jun 21.