Growth factor regulation of intracellular pH homeostasis under hypoxic conditions in isolated equine articular chondrocytes

2012 ◽  
Vol 31 (2) ◽  
pp. 197-203 ◽  
Author(s):  
Peter I. Milner ◽  
Hannah C. Smith ◽  
Rebecca Robinson ◽  
Robert J. Wilkins ◽  
John S. Gibson
2009 ◽  
Vol 284 (11) ◽  
pp. 6697-6704 ◽  
Author(s):  
Shuiliang Shi ◽  
Scott Mercer ◽  
George J. Eckert ◽  
Stephen B. Trippel

2015 ◽  
Vol 116 (7) ◽  
pp. 1391-1400 ◽  
Author(s):  
Shuiliang Shi ◽  
Congrong Wang ◽  
Anthony J. Acton ◽  
George J. Eckert ◽  
Stephen B. Trippel

2013 ◽  
Vol 32 (1) ◽  
pp. 54-60 ◽  
Author(s):  
Shuiliang Shi ◽  
Albert G. Chan ◽  
Scott Mercer ◽  
George J. Eckert ◽  
Stephen B. Trippel

1988 ◽  
Vol 263 (10) ◽  
pp. 4758-4763
Author(s):  
F Ghezzo ◽  
E Lauret ◽  
S Ferrari ◽  
R Baserga

Molecules ◽  
2021 ◽  
Vol 26 (4) ◽  
pp. 878
Author(s):  
Magdalena Kusaczuk ◽  
Monika Naumowicz ◽  
Rafał Krętowski ◽  
Bartosz Cukierman ◽  
Marzanna Cechowska-Pasko

Osteoarthritis (OA) is considered one of the most common arthritic diseases characterized by progressive degradation and abnormal remodeling of articular cartilage. Potential therapeutics for OA aim at restoring proper chondrocyte functioning and inhibiting apoptosis. Previous studies have demonstrated that tauroursodeoxycholic acid (TUDCA) showed anti-inflammatory and anti-apoptotic activity in many models of various diseases, acting mainly via alleviation of endoplasmic reticulum (ER) stress. However, little is known about cytoprotective effects of TUDCA on chondrocyte cells. The present study was designed to evaluate potential effects of TUDCA on interleukin-1β (IL-1β) and tunicamycin (TNC)-stimulated NHAC-kn chondrocytes cultured in normoxic and hypoxic conditions. Our results showed that TUDCA alleviated ER stress in TNC-treated chondrocytes, as demonstrated by reduced CHOP expression; however, it was not effective enough to prevent apoptosis of NHAC-kn cells in either normoxia nor hypoxia. However, co-treatment with TUDCA alleviated inflammatory response induced by IL-1β, as shown by down regulation of Il-1β, Il-6, Il-8 and Cox2, and increased the expression of antioxidant enzyme Sod2. Additionally, TUDCA enhanced Col IIα expression in IL-1β- and TNC-stimulated cells, but only in normoxic conditions. Altogether, these results suggest that although TUDCA may display chondoprotective potential in ER-stressed cells, further analyses are still necessary to fully confirm its possible recommendation as potential candidate in OA therapy.


2009 ◽  
Vol 285 (7) ◽  
pp. 5026-5039 ◽  
Author(s):  
Monica R. Walker ◽  
Sarah L. Brown ◽  
Terrence E. Riehl ◽  
William F. Stenson ◽  
Thaddeus S. Stappenbeck

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