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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Lee, H. Wright, M. O. Salter, D. M. Millward-sadler, S. J. Nuki, G. Nishida, K. Caldwell, H. |
| Description | Author Affiliation: Millward-Sadler SJ ( Department of Pathology, University of Edinburgh Medical School, Edinburgh, United Kingdom EH8 9AG.) |
| Abstract | Chondrocyte function is regulated partly by mechanical stimulation. Optimal mechanical stimulation maintains articular cartilage integrity, whereas abnormal mechanical stimulation results in development and progression of osteoarthritis (OA). The responses of signal transduction pathways in human articular chondrocytes (HAC) to mechanical stimuli remain unclear. Previous work has shown the involvement of integrins and integrin-associated signaling pathways in activation of plasma membrane apamin-sensitive $Ca^{2+}-activated$ $K^{+}$ channels that results in membrane hyperpolarization of HAC after 0.33 Hz cyclical mechanical stimulation. To further investigate mechanotransduction pathways in HAC and show that the hyperpolarization response to mechanical stimulation is a result of an integrin-dependent release of a transferable secreted factor, we used this response. Neutralizing antibodies to interleukin 4 (IL-4) and IL-4 receptor α inhibit mechanically induced membrane hyperpolarization and anti–IL-4 antibodies neutralize the hyperpolarizing activity of medium from mechanically stimulated cells. Antibodies to interleukin 1β (IL-1β) and cytokine receptors, interleukin 1 receptor type I and the common γ chain/CD132 (γ) have no effect on me- chanically induced membrane hyperpolarization. Chondrocytes from IL-4 knockout mice fail to show a membrane hyperpolarization response to cyclical mechanical stimulation. Mechanically induced release of the chondroprotective cytokine IL-4 from HAC with subsequent autocrine/paracrine activity is likely to be an important regulatory pathway in the maintenance of articular cartilage structure and function. Finally, dysfunction of this pathway may be implicated in OA. |
| ISSN | 00219525 |
| e-ISSN | 15408140 |
| Journal | The Journal of Cell Biology |
| Issue Number | 1 |
| Volume Number | 145 |
| Language | English |
| Publisher | Rockefeller University Press (United States) |
| Publisher Date | 1999-04-05 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Cartilage, Articular Physiology Interleukin-4 Secretion Stress, Mechanical Animals Antigens, CD29 Apamin Pharmacology Calcium Cytology Flunarizine Gadolinium Genistein Deficiency Genetics Ion Channel Gating Drug Effects Ion Transport Membrane Potentials Mice Mice, Knockout Neomycin Phosphatidylinositol Diacylglycerol-Lyase Potassium Channels Receptors, Interleukin-4 Biosynthesis Reverse Transcriptase Polymerase Chain Reaction Signal Transduction Type C Phospholipases Research Support, Non-U.S. Gov't Cell Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Medicine |
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