PMID- 21308740
OWN - NLM
STAT- MEDLINE
DCOM- 20110801
LR  - 20211020
IS  - 1097-4644 (Electronic)
IS  - 0730-2312 (Linking)
VI  - 112
IP  - 4
DP  - 2011 Apr
TI  - The presence of extracellular matrix alters the chondrocyte response to 
      endoplasmic reticulum stress.
PG  - 1118-29
LID - 10.1002/jcb.23025 [doi]
AB  - The objective of this study was to test the hypothesis that extracellular matrix 
      (ECM) would alter the endoplasmic reticulum (ER) stress response of chondrocytes. 
      Chondrocytes were isolated from calf knees and maintained in monolayer culture or 
      suspended in collagen I to form spot cultures (SCs). Our laboratory has shown 
      that bovine chondrocytes form cartilage with properties similar to native 
      cartilage after 2-4 weeks in SCs. Monolayer cultures treated with ER stressors 
      glucose withdrawal (-Glu), tunicamycin (TN), or thapsigargin (TG) up-regulated 
      Grp78 and Gadd153, demonstrating a complete ER stress response. SCs were grown at 
      specific times from 1 day to 6 weeks before treatment with ER stressors. 
      Additionally, SCs grown for 1, 2, or 6 weeks were treated with increasing 
      concentrations of TN or TG. Western blotting of SCs for Grp78 indicated that 
      increased ECM accumulation results in delayed expression; however, Grp78 mRNA is 
      up-regulated in response to ER stressors even after 6 weeks in culture. SCs 
      treated with ER stressors did not up-regulate Gadd153, suggesting that the cells 
      experienced ER stress but would not undergo apoptosis. In fact, SCs undergo 
      apoptosis upon ER stress treatment after 0-1 day of growth; however, after 4 days 
      and to 6 weeks, apoptosis in treated samples was not different than controls. 
      Pro-survival molecules Bcl-2 and Bag-1 were up-regulated upon ER stress in SCs. 
      These results suggest that presence of ECM confers protection from ER stressors. 
      Future studies involving chondrocyte physiology should focus on responses in 
      conditions more closely mimicking the in vivo cartilage environment.
CI  - Copyright (c) 2011 Wiley-Liss, Inc.
FAU - Nugent, Ashleigh E
AU  - Nugent AE
AD  - Department of Anatomy and Neurobiology, Northeastern Ohio Universities Colleges 
      of Medicine and Pharmacy, Rootstown, Ohio, USA. ashleigh.nugent@unibas.ch
FAU - McBurney, Denise L
AU  - McBurney DL
FAU - Horton, Walter E Jr
AU  - Horton WE Jr
LA  - eng
GR  - R15 AG029659/AG/NIA NIH HHS/United States
GR  - 1R15AG029659-01A1/AG/NIA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Cell Biochem
JT  - Journal of cellular biochemistry
JID - 8205768
RN  - 0 (BCL2-associated athanogene 1 protein)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Heat-Shock Proteins)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (Transcription Factors)
RN  - 11089-65-9 (Tunicamycin)
RN  - 67526-95-8 (Thapsigargin)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Blotting, Western
MH  - Cartilage, Articular/cytology
MH  - Cattle
MH  - Cells, Cultured
MH  - Chondrocytes/cytology/drug effects/*metabolism
MH  - DNA-Binding Proteins/genetics/metabolism
MH  - Dose-Response Relationship, Drug
MH  - Endoplasmic Reticulum/*metabolism
MH  - Extracellular Matrix/*metabolism
MH  - Glucose/pharmacology
MH  - Heat-Shock Proteins/genetics/metabolism
MH  - Proto-Oncogene Proteins c-bcl-2/genetics/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - *Stress, Physiological
MH  - Thapsigargin/pharmacology
MH  - Time Factors
MH  - Transcription Factors/genetics/metabolism
MH  - Tunicamycin/pharmacology
EDAT- 2011/02/11 06:00
MHDA- 2011/08/02 06:00
CRDT- 2011/02/11 06:00
PHST- 2011/02/11 06:00 [entrez]
PHST- 2011/02/11 06:00 [pubmed]
PHST- 2011/08/02 06:00 [medline]
AID - 10.1002/jcb.23025 [doi]
PST - ppublish
SO  - J Cell Biochem. 2011 Apr;112(4):1118-29. doi: 10.1002/jcb.23025.