## Abstract ## Objective To elucidate the mechanism of basic calcium phosphate (BCP) crystal–induced prostaglandin E~2~ (PGE~2~) production in human foreskin fibroblasts (HFFs), to identify the signaling pathway involved in the induction of cyclooxygenase 2 (COX‐2) messenger RNA (mRNA) by BCP crys
Expression of interleukin-1β, cyclooxygenase-2, and prostaglandin E2 in a rotator cuff tear in rabbits
✍ Scribed by Hiroshi Koshima; Seiji Kondo; Shinji Mishima; Ho-Rim Choi; Hisashi Shimpo; Tadahiro Sakai; Naoki Ishiguro
- Book ID
- 102395514
- Publisher
- Elsevier Science
- Year
- 2006
- Tongue
- English
- Weight
- 206 KB
- Volume
- 25
- Category
- Article
- ISSN
- 0736-0266
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✦ Synopsis
Abstract
We investigated the specific factors related to shoulder pain due to a rotator cuff tear using a model in rabbits. A rotator cuff tear was surgically created, and the expression of interleukin‐1β (IL‐1β), prostaglandin E2 (PGE2), and cyclooxygenase‐2 (COX‐2) was analyzed. In the supernatant of the tissue culture of the torn tendon, IL‐1β production was detected. The amount of IL‐1β was highest 1 day after injury, and then decreased gradually to 21 days. PGE2, the mediator of pain and the product of COX‐2, was also detected in the supernatant of the tissue culture. The production of PGE2 significantly increased to 7 days after injury, and then decreased to 21 days. RT‐PCR analysis confirmed the mRNA expression of IL‐1β and COX‐2 in the torn tendon. Immunohistochemical study demonstrated that cells in the tendon stump were immunopositive for IL‐1β and COX‐2. Furthermore, in the affected joint, articular chondrocytes in the remote area from the tear expressed COX‐2 strongly. When the rotator cuff is torn, IL‐1β is produced in the torn tendon, and stimulates the expression of COX‐2 in not only the torn tendon but also in articular chondrocytes. The COX‐2 then produces PGE2, which would mediate shoulder pain. © 2006 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 25:92–97, 2007
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