Rele of the interaction between arterial smooth muscle cellsand endothelial cell or macrophages in foam cell formation.

泡沫细胞形成中动脉平滑肌细胞与内皮细胞或巨噬细胞之间相互作用的关系。

• 批准号: 61570300
• 负责人: SAITO Yasushi
• 金额: $ 1.47万
• 依托单位: The 2nd Department of Internal Meicine, School of Medicine, Chiba University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1986
• 资助国家: 日本
• 起止时间: 1986 至 1987
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-61570300/
• 关键词: Cell to cell interaction; Intimal smooth muscle cell; Medial smooth muscle cell; Macrophage; Endothelial cell,; 実質細胞; 細胞相互間作用; LDL受容体

1 Interaction between macrophages and smooth muscle cells (SMC):<beta>-VLDL ([^3H]cholesterol ester labeled ) was incubated with macrophages and the conditioned medium was added to the smooth muscle cells. The incorporated radioactivities into SMC were increased by incubation with <beta>-VLDL containing medium conditioned with macrophages, comparing to those conditioned without macrophages. The increase in incorporated radioactivities into SMC was also obseryed with IDL containing medium conditioned with macrophage. Conditioning of <beta>-VLDL or IDL with macrophages produced lipid-protein particles (d = 1.19, <beta>-mobility). These results suggest that macrophage-SMC interaction might promote the foam cell formation with <beta>-VLDL.or IDL.2. Interaction between endothelial cells and smooth muscle cells:Medial SMC was cultured from aortic media and intimal SMC was cultured from canulated aortic intima. The intiaml SMC proliferation increased comparing to that of medial SMC. By co-culturing of these SMC with endothelial cells, the proliferation of medial SMC was inhibited, but proliferation of intimal SMC was bit inhibited. These results suggest that SMC proliferation was regulated by endothelial cells, and loss of endothelial cell may promote proliferation of medial SMC.

1巨噬细胞与平滑肌细胞（SMC）的相互作用：<beta>-VLDL（[^3H]胆固醇酯标记）与巨噬细胞孵育，并将条件培养基加入平滑肌细胞。与<beta>无巨噬细胞的条件相比，用含有巨噬细胞的-VLDL的培养基孵育增加了SMC的放射性。用含IDL的巨噬细胞条件培养基也可观察到SMC中掺入放射性的增加。条件<beta>-VLDL或IDL与巨噬细胞产生的脂质蛋白颗粒（d = 1.19<beta>，流动性）。这些结果提示巨噬细胞与SMC的相互作用可能促进泡沫细胞的形成<beta>.内皮细胞和平滑肌细胞之间的相互作用：从主动脉中膜培养中膜SMC，从插管的主动脉内膜培养内膜SMC。内膜平滑肌细胞增殖明显高于中膜平滑肌细胞。与内皮细胞共培养，中膜平滑肌细胞的增殖受到抑制，内膜平滑肌细胞的增殖受到一定的抑制。提示平滑肌细胞的增殖受内皮细胞的调控，内皮细胞的缺失可促进中膜平滑肌细胞的增殖。

项目成果

Saito,Y.;Bujo,H.;Morisaki,N.;Shirai,K. and Yoshida,S.: Atherosclerosis. 69. 161-164 (1988)

Saito，Y.；Bujo，H.；Morisaki，N.；Shirai，K.

Saito,Y.;Shiki,Y.;Shirai,K. and Yoshida,S.: Arzneim-Forsch/Drug Res.38(I)Nr.2. 251-253 (1988)

齐藤，Y.；志木，Y.；白井，K.

Morisaki,N.;Saito,Y.;ed al.: American Journal of Kidney Diseases. 【VII】(1). 41-46 (1986)

Morisaki，N.；Saito，Y. 等人：《美国肾脏疾病杂志》[VII] (1)。

Matsuoka,N.;Saito,Y.;Yoshida,S.: Tohoku J.exp.Med.149. 61-66 (1986)

松冈，N.；斋藤，Y.；吉田，S.：东北 J.exp.Med.149。

神崎哲人,森崎信尋,斎藤康,吉田尚: 動脈硬化. 14(3). 767-773 (1986)

Tetsuto Kanzaki、Nobuhiro Morisaki、Yasushi Saito、Hisashi Yoshida：动脉硬化。