Koolpe M, Pearson D, Benton H P
University of California, Davis 95616, USA.
Arthritis Rheum. 1999 Feb;42(2):258-67. doi: 10.1002/1529-0131(199902)42:2<258::AID-ANR7>3.0.CO;2-O.
To assess the expression and function of purine receptors in articular chondrocytes.
Reverse transcriptase-polymerase chain reaction (RT-PCR) was used to screen human chondrocyte RNA for expression of P1 and P2 purine receptor subtypes. Purine-stimulated prostaglandin E2 (PGE2) release from chondrocytes, untreated or treated with recombinant human interleukin-1alpha (rHuIL-1alpha), was assessed by radioimmunoassay.
RT-PCR demonstrated that human articular chondrocytes transcribe messenger RNA for the P1 receptor subtypes A2a and A2b and the P2 receptor subtype P2Y2, but not for the P1 receptor subtypes A1 and A3. The P1 receptor agonists adenosine and 5'-N-ethylcarboxamidoadenosine did not change PGE2 release from chondrocytes. The P2Y2 agonists ATP and UTP stimulated a small release of PGE2 that was potentiated after pretreatment with rHuIL-1alpha. PGE2 release in response to ATP and UTP cotreatment was not additive, but release in response to coaddition of ATP and bradykinin (BK) or UTP and BK was additive, consistent with ATP and UTP competition for the same receptor site. The potentiation of PGE2 release in response to ATP and UTP after rHuIL-1alpha pretreatment was mimicked by phorbol myristate acetate.
Human chondrocytes express both P1 and P2 purine receptor subtypes. The function of the P1 receptor subtype is not yet known, but stimulation of the P2Y2 receptor increases IL-1-mediated PGE2 release.
评估嘌呤受体在关节软骨细胞中的表达及功能。
采用逆转录聚合酶链反应（RT-PCR）筛选人软骨细胞RNA中P1和P2嘌呤受体亚型的表达。通过放射免疫分析法评估嘌呤刺激软骨细胞释放前列腺素E2（PGE2）的情况，软骨细胞未处理或经重组人白细胞介素-1α（rHuIL-1α）处理。
RT-PCR表明，人关节软骨细胞转录P1受体亚型A2a和A2b以及P2受体亚型P2Y2的信使RNA，但不转录P1受体亚型A1和A3的信使RNA。P1受体激动剂腺苷和5'-N-乙基羧酰胺腺苷未改变软骨细胞释放PGE2的情况。P2Y2激动剂ATP和UTP刺激了少量PGE2释放，rHuIL-1α预处理后这种释放增强。ATP和UTP联合处理时PGE2的释放无叠加效应，但ATP与缓激肽（BK）或UTP与BK联合添加时PGE2的释放有叠加效应，这与ATP和UTP竞争同一受体位点一致。佛波酯可模拟rHuIL-1α预处理后ATP和UTP诱导的PGE2释放增强。
人软骨细胞表达P1和P2嘌呤受体亚型。P1受体亚型的功能尚不清楚，但刺激P2Y2受体可增加IL-1介导的PGE2释放。
