Mechanotransduction and intracellular signaling mechanisms of stretch-induced remodeling in endothelial cells

被引:0
|
作者
Sokabe, M [1 ]
Naruse, K [1 ]
Sai, S [1 ]
Yamada, T [1 ]
Kawakami, K [1 ]
Inoue, M [1 ]
Murase, K [1 ]
Miyazu, M [1 ]
机构
[1] Nagoya Univ, Sch Med, Dept Physiol, Nagoya, Aichi 466, Japan
关键词
stretch activated channel; remodeling; endothelial cell; Ca2+](i); tyrosine kinase;
D O I
暂无
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
We investigated the signaling mechanism of stretch-induced cell remodeling in human umbilical vein endothelial cells (HUVECs). Freshly dissociated HUVECs were cultured on an elastic silicon membrane and subjected to uniaxial cyclic stretch (20% in length, 1Hz). The cells started to change their morphology as early as 15 min after stretch onset, and most cells eventually aligned perpendicularly to the stretch axis within Ih. This remodeling was dependent on the increase in intracellular calcium concentration ([Ca2+](i)) via a Ca2+-permeable stretch-activated (SA) channel. During the process of remodeling, extensive rearrangement of stress fibers and focal adhesions was observed, which may be close to the final step in the intracellular signaling cascade. This event was [Ca2+](i)-dependent, suggesting the existence of a Ca2+-dependent intermediate cascade that links [Ca2+](i) to the rearrangement of cytoskeletons and focal adhesions. We found that some proteins, including pp125(FAK) (focal adhesion kinase) and paxillin, were tyrosine phosphorylated during cyclic stretch in a Ca2+-dependent manner. Inhibition of this tyrosine phosphorylation prohibited the stretch-dependent rearrangement of cytoskeletons and focal adhesions as well as the remodeling. Finally the tyrosine kinase src, which could phosphorylate pp125(FAK), was found to be activated in a [Ca2+](i)-dependent way during stretch. All of the above molecular events were consistently Ca2+-dependent, which led us to propose the signaling cascade: SA channel activation --> [Ca2+](i) increase --> src activation --> protein tyrosine phosphorylation --> rearrangement of cytoskeletons and focal adhesions --> cell remodeling.
引用
收藏
页码:191 / 193
页数:3
相关论文
共 50 条
  • [1] Stretch-induced intracellular calcium releases in endothelial cells.
    Murase, K
    Okumura, K
    Naruse, K
    Sokabe, M
    [J]. BIOPHYSICAL JOURNAL, 2000, 78 (01) : 472A - 472A
  • [3] Quantification of stretch-induced cytoskeletal remodeling in vascular endothelial cells by image processing
    Yoshigi, M
    Clark, EB
    Yost, HJ
    [J]. CYTOMETRY PART A, 2003, 55A (02): : 109 - 118
  • [4] Quantitative analysis of stretch-induced cytoskeletal remodeling in the human umbilical vein endothelial cells
    Yoshigi, M
    Yasuda, K
    Clark, EB
    Yost, HJ
    [J]. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2002, 22 (05) : A72 - A72
  • [5] MECHANOTRANSDUCTION IN STRETCH-INDUCED HYPERTROPHY OF CARDIAC MYOCYTES
    SADOSHIMA, J
    IZUMO, S
    [J]. JOURNAL OF RECEPTOR RESEARCH, 1993, 13 (1-4): : 777 - 794
  • [6] REGULATION OF STRETCH-INDUCED MECHANOTRANSDUCTION BY CYTOSKELETAL TENSION
    Hsu, Hui-Ju
    Locke, Andrea K.
    Vanderzyl, Susan O.
    Lee, Chin-Fu
    Kaunas, Roland
    [J]. PROCEEDINGS OF THE ASME SUMMER BIOENGINEERING CONFERENCE, 2010, 2010, : 347 - 348
  • [7] Mechanotransduction of stretch-induced prostanoid release by fetal lung epithelial cells
    Copland, Ian B.
    Reynaud, Denis
    Pace-Asciak, Cecil
    Post, Martin
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 2006, 291 (03) : L487 - L495
  • [8] Stretch-induced morphological response in endothelial cells.
    Sokabe, M
    Kawakami, K
    Naruse, K
    [J]. JOURNAL OF PHARMACOLOGICAL SCIENCES, 2003, 91 : 66P - 66P
  • [9] Mechanisms of stretch-induced electro-anatomical remodeling and atrial arrhythmogenesis
    Medvedev, Roman Y.
    Afolabi, Saheed O.
    Turner, Daniel G. P.
    Glukhov, Alexey V.
    [J]. JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2024, 193 : 11 - 24
  • [10] Blocking stretch-induced myocardial remodeling
    Margulies, KB
    [J]. CIRCULATION RESEARCH, 2003, 93 (11) : 1020 - 1022