Immediate prostaglandin E2 synthesis in rat 3Y1 fibroblasts following vasopressin V1a receptor stimulation.
Immediate prostaglandin E2 synthesis in rat 3Y1 fibroblasts following vasopressin V1a receptor stimulation.
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DOI：
10.1016/j.bbrc.2007.01.041
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发表时间：
2007-03
影响因子：
3.1
通讯作者：
Yoshihito Nakatani;Yuka Chin;S. Hara;I. Kudo
中科院分区：
文献类型：
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作者：
Yoshihito Nakatani;Yuka Chin;S. Hara;I. Kudo
精氨酸加压素(AVP)诱导大鼠3Y1成纤维细胞产生前列腺素E2(PGE2)。从几种抑制剂的作用来看，胞浆磷脂酶A2α(α)和环氧合酶-1(COX-1)主要参与了这一反应。V1a受体拮抗剂而不是V2受体拮抗剂抑制AVP诱导的PGE_2合成，提示AVP通过V1a受体激活cPLA2α。AVP处理3Y1细胞后，p44/42丝裂原活化蛋白激酶和cPLA2α被瞬时激活，而磷脂酰肌醇3-激酶(PI3K)抑制剂不仅阻断了AVP诱导的PGE2合成，也阻断了MAPK的激活，提示PI3K参与了AVP诱导的MAPK和cPLA2α的激活，从而启动了PGE2的产生。这些结果提示，AVP刺激产生的PGE_2可能对AVP的生理效应有调节作用。
Arginine vasopressin (AVP) induces immediate prostaglandin E2(PGE2) production in rat 3Y1 fibroblasts. Judging from effects of several inhibitors, cytosolic phospholipase A2α (cPLA2α) and cyclooxygenase-1 (COX-1) were mainly involved in this reaction. The antagonist of vasopressin receptor V1a, and not that of V2, inhibited the AVP-induced PGE2synthesis, indicating that AVP activates cPLA2α through V1a receptor. Treatment of 3Y1 cells with AVP resulted in transient activation of p44/42 mitogen-activated protein kinase (MAPK) and cPLA2α, and phosphatidylinositol 3-kinase (PI3K) inhibitor blocked not only AVP-induced PGE2synthesis but also MAPK activation, suggesting that PI3K is involved in the AVP-induced MAPK and cPLA2α activation, which initiates the production of PGE2. These results suggest that PGE2generated by the stimulation of AVP probably modulates the physiological effects of AVP.