Role of intercellular communication in the control of renin secretion

细胞间通讯在肾素分泌控制中的作用

• 批准号: 20590953
• 负责人: YAO Jian
• 金额: $ 2.91万
• 依托单位: University of Yamanashi
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2008
• 资助国家: 日本
• 起止时间: 2008 至 2010
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20590953/
• 关键词: 生理学; 腎臓; シグナル伝達; レニン; ギャップ結合; コネクシン; レニン分泌細胞; 細胞間コミュニケーション; cAMP; 傍糸球体装置; 腎臟

Renin plays an important role in the maintenance of blood pressure and renal blood flow. A lot paracrine factors such as neurotransmitters, vasoactive materials, growth factors and cytokines have been shown to be implicated in the control of renin. However, our understanding about the mechanisms of the gap junction-mediated direct intercellular communication in renin secretion is still lacking. Here, we investigated the role of gap junctions in the control of renin production in juxtaglomerular cells. Our results demonstrated that : 1) there are abundant connexins and functional gap junctions in renin-secreting cells ; 2) dysfunction of gap junctions with gap junction blockers stimulated the expression of COX_2, an important signal molecule implicated in the stimulation of renin synthesis and production ; and 3) the opening of gap junction hemichannls under low calcium conditions activated the renin-stimulating cAMP signaling pathway. Our results thus implicate gap junctions as an important regulator of renin secretion and production.

肾素在维持血压和肾血流量方面起着重要作用。许多旁分泌因子，如神经递质、血管活性物质、生长因子和细胞因子等已被证明与肾素的控制有关。然而，我们对缝隙连接介导的直接细胞间通讯在肾素分泌中的作用机制仍缺乏了解。在这里，我们研究了缝隙连接在肾小球旁细胞肾素生成控制中的作用。我们的结果表明：1)肾素分泌细胞中存在丰富的连接蛋白和功能缝隙连接；2)缝隙连接阻滞剂的功能障碍刺激了参与肾素合成和产生的重要信号分子COX_2的表达；3)低钙条件下缝隙连接半通道的开放激活了肾素刺激cAMP信号通路。因此，我们的结果表明缝隙连接是肾素分泌和产生的重要调节因子。

项目成果

Connexin43 hemichannels exaggerate cadmium-induced oxidative stress and cell injury in renal tubular epithelial cells.

Connexin43 半通道会加剧镉诱导的肾小管上皮细胞的氧化应激和细胞损伤。

• 发表时间: 2010
• 作者: Yao J Sun W;Huang T;Nakajima S;Kitamura M
• 通讯作者: Kitamura M

Pathophysiological roles of gap junction in renal microcirculation

间隙连接在肾微循环中的病理生理作用

• 发表时间: 2008
• 作者: N.Paragas;et al.;姚建
• 通讯作者: 姚建

Participation of gap junction in proteasome inhibition-induced cell damage.

间隙连接参与蛋白酶体抑制诱导的细胞损伤。

• 发表时间: 2008
• 作者: Huang T;Kitamura M;Yao J
• 通讯作者: Yao J

Gap junctional intercellular communication in the juxtaglomerular apparatus.

• DOI: 10.1152/ajprenal.90612.2008
• 发表时间: 2009-05
• 期刊: American journal of physiology. Renal physiology
• 作者: Jian Yao;T. Oite;M. Kitamura

Selective deletion of adipocytes, but not preadipocytes, by TNF-α via C/EBP- and PPARγ-mediated suppression of NF-κB.

TNF-α 通过 C/EBP 和 PPARγ 介导的 NF-κB 抑制选择性删除脂肪细胞，但不删除前脂肪细胞。

• 发表时间: 2010
• 期刊: Lab Invest 90
• 作者: Tamai M;Shimada T;Hiramatsu N;Hayakawa K;Okamura M;Tagawa Y;Takahashi S;Nakajima S;Yao J;Kitamura M
• 通讯作者: Kitamura M