Heat shock-induced cardioprotection activates cytoskeletal-based cell survival pathways.
Heat shock-induced cardioprotection activates cytoskeletal-based cell survival pathways.
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热休克诱导的心脏保护作用激活基于细胞骨架的细胞存活途径。
DOI：
10.1152/ajpheart.00144.2006
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发表时间：
2006
期刊：
影响因子：
--
通讯作者：
VanderHeide,RichardS
中科院分区：
文献类型：
--
作者：
Wei,Hongguang;Campbell,Wendy;VanderHeide,RichardS
为了更好地阐明热休克(HS)诱导的心肌保护的亚细胞机制，我们研究了HS以及选择性表达HS蛋白(HSPs)对新生大鼠心室肌细胞(NRVM)细胞损伤的影响。在NRVM中，快速升温至42℃20min，然后在37℃下恢复20-24小时，诱导HS。其他NRVM感染编码HSP27或HSP70的复制缺陷型腺病毒。同日，所有组均接受代谢抑制(MI)。测定细胞总乳酸脱氢酶释放百分率、台盼蓝染色细胞百分率或TdT介导的dUTP缺口末端标记法检测细胞损伤，免疫印迹分析和免疫共沉淀法检测细胞信号转导。在心肌梗死前，所有处理组的存活率与对照组无显著差异。HS导致HSP70和HSP27表达显著增加。与对照NRVM相比，感染这两种病毒的NRVM细胞选择性HSP含量均显著增加。HS保护NRVM免受损伤。单独选择性表达HSP27或HSP70对NRVM无保护作用，但两种病毒载体(HSP27+HSP70)联合感染对NRVM有保护作用。与对照NRVM相比，HS和HSP27+HSP70的表达增加了PX在膜组分中的定位，这种定位持续存在于MI后。HS增加了整合素-帕西林-粘着斑激酶的相互作用，而靶向抑制粘着斑激酶活性则取消了整合素-帕西林的结合，导致细胞死亡增加。HS和HSP27+HSP70的表达增加了局部黏附复合体成员之间的联系，保护了NRVM免受不可逆转的损伤。粘着斑处以细胞骨架为基础的信号通路可能是一种独特的心脏保护途径。
To define better the subcellular mechanism of heat shock (HS)-induced cardioprotection, we examined the effect of HS, as well as selective expression of individual HS proteins (HSPs), on cell injury in neonatal rat ventricular myocytes (NRVM). HS was induced in NRVM by a rapid elevation of temperature to 42°C for 20 min followed by 20–24 h of recovery at 37°C. Other NRVM were infected with a replication-deficient adenovirus encoding HSP27 or HSP70. On the same day, all groups were subjected to metabolic inhibition (MI). Cell injury was assayed by measurement of the percentage of total lactate dehydrogenase released, the percentage of cells staining with trypan blue, or TdT-mediated dUTP nick-end labeling, whereas cell signaling was assayed by immunoblot analysis and coimmunoprecipitation. Before MI, the viability of all treated groups did not differ significantly from control NRVM. HS resulted in a significant increase in HSP70 and HSP27 expression. Infection with either virus caused a significant increase in selective HSP content compared with control NRVM. HS protected NRVM from injury. Selective expression of HSP27 or HSP70 alone was not protective in NRVM, but dual infection with both viral vectors (HSP27 + HSP70) was protective. HS and HSP27 + HSP70 expression caused increased paxillin localization in the membrane fraction, which persisted in response to MI, compared with control NRVM. HS increased the integrin-paxillin-focal adhesion kinase interaction, whereas targeted inhibition of focal adhesion kinase activity abolished the integrin-paxillin association and resulted in an increase in cell death. HS and HSP27 + HSP70 expression increased the association of members of the focal adhesion complex and protected NRVM against irreversible injury. Cytoskeletal-based signaling pathways at focal adhesion junctions may represent a unique pathway of cardioprotection.
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通过对扩增的基因组 DNA 进行直接测序来表征因子 VIII 基因的突变。
影响因子：
4.4
作者：
M. Higuchi;C. Wong;L. Kochhan;K. Olek;S. Aronis;C. Kasper;H. Kazazian;S. Antonarakis
通讯作者：
S. Antonarakis
III 型前胶原基因 (COL3A1) 的三个不同内含子中相同的 G 1 到 A 突变在埃勒斯-当洛斯综合征的三种变体中产生不同的 RNA 剪接模式。
DOI：
--
发表时间：
1990
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Kuivaniemi,H;Kontusaari,S;Tromp,G;Zhao,MJ;Sabol,C;Prockop,DJ
通讯作者：
Prockop,DJ
影响因子：
39.2
作者：
Uitto,J;Murray,LW;Blumberg,B;Shamban,A
通讯作者：
Shamban,A
DOI：
10.1073/pnas.86.6.1919
发表时间：
1989-03-01
影响因子：
11.1
作者：
GIBBS, RA;NGUYEN, PN;CASKEY, CT
通讯作者：
CASKEY, CT
家族性腹主动脉瘤有何不同？
影响因子：
4.3
作者：
R. Darling;D. Brewster;R. Darling;G. LaMuraglia;A. Moncure;R. Cambria;W. Abbott
通讯作者：
W. Abbott