Journal article
Acid-sensing ion channel 3 expressed in type B synoviocytes and chondrocytes modulates hyaluronan expression and release
Annals of the rheumatic diseases, Vol.69(5), pp.903-909
2010
DOI: 10.1136/ard.2009.117168
PMCID: PMC3476728
PMID: 19933746
Abstract
Background: Rheumatoid arthritis is an inflammatory disease marked by intra-articular decreases in pH, aberrant hyaluronan regulation and destruction of bone and cartilage. Acid-sensing ion channels (ASICs) are the primary acid sensors in the nervous system, particularly in sensory neurons and are important in nociception. ASIC3 was recently discovered in synoviocytes, non-neuronal joint cells critical to the inflammatory process.
Objectives: To investigate the role of ASIC3 in joint tissue, specifically the relationship between ASIC3 and hyaluronan and the response to decreased pH.
Methods: Histochemical methods were used to compare morphology, hyaluronan expression and ASIC3 expression in ASIC3+/+ and ASIC3-/- mouse knee joints. Isolated fibroblast-like synoviocytes (FLS) were used to examine hyaluronan release and intracellular calcium in response to decreases in pH.
Results: In tissue sections from ASIC3+/+ mice, ASIC3 localised to articular cartilage, growth plate, meniscus and type B synoviocytes. In cultured FLS, ASIC3 mRNA and protein was also expressed. In FLS cultures, pH 5.5 increased hyaluronan release in ASIC3+/+ FLS, but not ASIC3-/- FLS. In FLS from ASIC3+/+ mice, approximately 50% of cells (25/53) increased intracellular calcium while only 24% (14/59) showed an increase in ASIC3-/- FLS. Of the cells that responded to pH 5.5, there was significantly less intracellular calcium increases in ASIC3-/- FLS compared to ASIC3+/+ FLS.
Conclusion: ASIC3 may serve as a pH sensor in synoviocytes and be important for modulation of expression of hyaluronan within joint tissue.
Details
- Title: Subtitle
- Acid-sensing ion channel 3 expressed in type B synoviocytes and chondrocytes modulates hyaluronan expression and release
- Creators
- S. J KOLKER - Graduate Program in Physical Therapy and Rehabilitation Science, Pain Research Program, University of Iowa, Iowa, United StatesR. Y WALDER - Graduate Program in Physical Therapy and Rehabilitation Science, Pain Research Program, University of Iowa, Iowa, United StatesY USACHEV - Department of Pharmacology, Pain Research Program, University of Iowa, Iowa, United StatesJ HILLMAN - Division of Rheumatology, Allergy and Immunology, University of California, San Diego School of Medicine, La Jolla, California, United StatesD. L BOYLE - Division of Rheumatology, Allergy and Immunology, University of California, San Diego School of Medicine, La Jolla, California, United StatesG. S FIRESTEIN - Division of Rheumatology, Allergy and Immunology, University of California, San Diego School of Medicine, La Jolla, California, United StatesK. A SLUKA - Graduate Program in Physical Therapy and Rehabilitation Science, Pain Research Program, University of Iowa, Iowa, United States
- Resource Type
- Journal article
- Publication Details
- Annals of the rheumatic diseases, Vol.69(5), pp.903-909
- DOI
- 10.1136/ard.2009.117168
- PMID
- 19933746
- PMCID
- PMC3476728
- NLM abbreviation
- Ann Rheum Dis
- ISSN
- 0003-4967
- eISSN
- 1468-2060
- Publisher
- BMJ Publishing Group; London
- Language
- English
- Date published
- 2010
- Academic Unit
- Iowa Neuroscience Institute; Nursing; Anesthesia; Physical Therapy and Rehabilitation Science; Fraternal Order of Eagles Diabetes Research Center; Neuroscience and Pharmacology
- Record Identifier
- 9984040275002771
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