PMID- 21161647
OWN - NLM
STAT- MEDLINE
DCOM- 20111118
LR  - 20211020
IS  - 1434-0879 (Electronic)
IS  - 0300-5623 (Print)
IS  - 0300-5623 (Linking)
VI  - 39
IP  - 4
DP  - 2011 Aug
TI  - Experimentally induced hyperoxaluria in MCP-1 null mice.
PG  - 253-8
LID - 10.1007/s00240-010-0345-7 [doi]
AB  - Experimental animal model studies suggest that calcium oxalate (CaOx) crystal 
      deposition in the kidneys is associated with the development of oxidative stress, 
      epithelial injury and inflammation. There is increased production of inflammatory 
      molecules including osteopontin (OPN), monocyte chemoattractant protein-1 (MCP-1) 
      and various subunits of inter-alpha-inhibitor such as bikunin. What does the 
      increased production of such molecules suggest? Is it a cause or consequence of 
      crystal deposition? We hypothesized that over-expression and increased production 
      of MCP-1 is a result of the interaction between renal epithelial cells and CaOx 
      crystals after their deposition in the renal tubules. We induced hyperoxaluria in 
      MCP-1 null as well as wild type mice and examined pathological changes in their 
      kidneys and urine. Both wild type and MCP-1 null male mice became hyperoxaluric 
      and demonstrated CaOx crystalluria. Neither of them developed crystal deposits in 
      their kidneys. Both showed some morphological changes in their renal proximal 
      tubules. Significant pathological changes such as cell death and increased 
      urinary excretion of LDH were not seen. Results suggest that at least in mice (1) 
      Increase in oxalate and decrease in citrate excretion can lead to CaOx 
      crystalluria but not CaOx nephrolithiasis; (2) MCP-1 does not play a role in 
      crystal retention within the kidneys; (3) Expression of OPN and MCP-1 is not 
      increased in the kidneys in the absence of crystal deposition; (4) Crystal 
      deposition is necessary for significant pathological changes and movement of 
      monocytes and macrophages into the interstitium.
FAU - Khan, Saeed R
AU  - Khan SR
AD  - Department of Pathology, Immunology and Laboratory Investigation, College of 
      Medicine, University of Florida, Box 100275, Gainesville, FL 32610, USA. 
      Khan@pathology.ufl.edu
FAU - Glenton, Patricia A
AU  - Glenton PA
LA  - eng
GR  - R01 DK078602/DK/NIDDK NIH HHS/United States
GR  - R01 DK078602-03/DK/NIDDK NIH HHS/United States
PT  - Journal Article
DEP - 20101216
PL  - Germany
TA  - Urol Res
JT  - Urological research
JID - 0364311
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 2612HC57YE (Calcium Oxalate)
SB  - IM
MH  - Animals
MH  - Calcium Oxalate/metabolism
MH  - Chemokine CCL2/genetics/*physiology
MH  - Crystallization
MH  - Disease Models, Animal
MH  - Female
MH  - Hyperoxaluria/*etiology/genetics
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Nephrolithiasis/*etiology/genetics
PMC - PMC3089659
MID - NIHMS265289
EDAT- 2010/12/17 06:00
MHDA- 2011/12/13 00:00
PMCR- 2012/08/01
CRDT- 2010/12/17 06:00
PHST- 2010/07/27 00:00 [received]
PHST- 2010/11/08 00:00 [accepted]
PHST- 2010/12/17 06:00 [entrez]
PHST- 2010/12/17 06:00 [pubmed]
PHST- 2011/12/13 00:00 [medline]
PHST- 2012/08/01 00:00 [pmc-release]
AID - 10.1007/s00240-010-0345-7 [doi]
PST - ppublish
SO  - Urol Res. 2011 Aug;39(4):253-8. doi: 10.1007/s00240-010-0345-7. Epub 2010 Dec 16.