Differential pathways for calcium influx activated by concanavalin A and CD3 stimulation in Jurkat T cells
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- 作者：Bo Pang (1) (2)
Dong Hoon Shin (1)
Kyung Sun Park (3)
Yun Jeong Huh (1)
Joohan Woo (1)
Yin-Hua Zhang (1)
Tong Mook Kang (4)
Ki-Young Lee (5)
Sung Joon Kim (1) (6) - 关键词：Ca2+ influx ; Calcium signaling ; Lymphocyte ; Nonselective cation channel ; TRP channels
- 刊名：Pfl眉gers Archiv - European Journal of Physiology
- 出版年：2012
- 出版时间：February 2012
- 年：2012
- 卷：463
- 期：2
- 页码：309-318
- 全文大小：419KB
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Dong Hoon Shin (1)
Kyung Sun Park (3)
Yun Jeong Huh (1)
Joohan Woo (1)
Yin-Hua Zhang (1)
Tong Mook Kang (4)
Ki-Young Lee (5)
Sung Joon Kim (1) (6)
1. Department of Physiology, Seoul National University College of Medicine, 28 Yongon-dong, Chongro-gu, Seoul, 110-799, Republic of Korea
2. Key Laboratory of Hormones and Development, Ministry of Health Metabolic Diseases Hospital, Tianjin Medical University, Tianjin, 300070, China
3. Division of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, Pohang, 790-784, Republic of Korea
4. Department of Physiology, SBRI, Sungkyunkwan University School of Medicine, Suwon, 440-746, Republic of Korea
5. Department of Molecular Cell Biology, SBRI, Sungkyunkwan University School of Medicine, Suwon, 440-746, Republic of Korea
6. Ischemic/Hypoxic Disease Institute, Seoul National University College of Medicine, Seoul, 110-799, Republic of Korea - ISSN：1432-2013
文摘
Sustained increase in [Ca2+]c (Δ[Ca2+]c) is a critical early signal from T-cell receptor (TCR/CD3). In general, Ca2+-release activated Ca2+ channels (CRAC) are responsible for the Ca2+ influx and Δ[Ca2+]c after TCR/CD3 stimulation. However, T cells also express Ca2+-permeable nonselective cation channels such as TRPM2 and TRPC. Gd3+ is a relatively selective blocker for CRAC at micromolar concentrations. Here, Jurkat T cells were used to investigate the Gd3+-resistant Ca2+ influx (Δ[Ca2+]c,Gd) induced by concanavalin A (ConA, 1?μg/ml), a widely used mitogenic agent for T cells, or by anti-CD3 Ab (αCD3). αCD3-induced Δ[Ca2+]c was partly (~60%) inhibited by 1?μM Gd3+ while thapsigargin-induced Δ[Ca2+] was almost completely abolished. ConA-induced Δ[Ca2+] was mostly inhibited by 1?μM Gd3+ during the early phase (<30?s of ConA application) and became resistant during the late phase (>2?min). Induction of Δ[Ca2+]c,Gd by αCD3 and ConA was inhibited by 2-aminoethoxydiphenyl borate (2-APB) and by N-(p-amylcinnamoyl) anthranilic acid, indicating that TRPM2 and TRPC are involved in this process. Treatment with Pyr-3, a TRPC3-specific inhibitor, potently suppressed Δ[Ca2+]c,Gd by αCD3 (IC50, 0.16?μM). Patch clamp experiments demonstrated that the TRPM2 channels were activated by ConA, and the TRPC-like channels were activated by αCD3. Our present study suggests that TRPM2 and TRPC3 are activated by ConA and TCR/CD3, respectively, in Jurkat T cells and are responsible for the induction of Δ[Ca2+]c,Gd.