L-Threonine induces heat shock protein expression and decreases apoptosis in heat-stressed intestinal epithelial cells.
L-Threonine induces heat shock protein expression and decreases apoptosis in heat-stressed intestinal epithelial cells.
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DOI：
10.1016/j.nut.2013.05.017
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发表时间：
2013-11
期刊：
影响因子：
--
通讯作者：
Wischmeyer PE
中科院分区：
文献类型：
--
作者：
Baird CH;Niederlechner S;Beck R;Kallweit AR;Wischmeyer PE
渗透作用氨基酸在损伤后具有细胞保护作用。由于苏氨酸（THR）诱导渗透性细胞肿胀，我们的目的是研究THR在肠上皮细胞中诱导细胞保护的潜力，并评估可能的保护机制。用一定剂量的THR处理的细胞在热应激（HS）损伤后进行评估。α -氨基异丁酸（AIB），一种非代谢氨基酸类似物，被用作渗透控制。MTS法测定细胞存活率。western blot检测热休克蛋白（HSP）和裂解caspase-3 （CC3）的表达。通过显微镜观察细胞形态和细胞大小。在HS后，THR处理与CT相比，以剂量依赖性的方式增加了5至20 mM的细胞活力。非代谢氨基酸类似物α -氨基异丁酸（AIB）也比HS-CT增加了HS细胞的细胞存活率。与HS-CT相比，THR和AIB治疗后HSP70和HSP25表达增加。THR也增加了非应激细胞的HSP25。镜检结果显示，与HS-CT相比，THR和AIB均能保持HS-CT细胞肌动蛋白骨架的结构完整性。THR增强HSP25在HS中的核易位，而AIB没有。这种核易位与THR引起的HS细胞凋亡减少60%有关。AIB无抗凋亡作用。这是第一次证明THR增加HSP70和hsp25并保护细胞免受HS。THR的保护机制可能包括细胞骨架稳定、HSP上调和核易位以及减少细胞凋亡。THR的保护似乎涉及细胞肿胀依赖和独立的过程。
Osmotically acting amino acids can be cytoprotective following injury. As threonine (THR) induces osmotic cell-swelling, our aim was to investigate the potential for THR to induce cellular protection in intestinal epithelial cells and evaluate possible mechanisms of protection. Cells treated with a range of THR doses were evaluated following heat stress (HS) injury. Alpha-aminoisobutyric acid (AIB), a non-metabolizable amino acid analog, was used as an osmotic control. MTS assays were used to assess cell survival. Heat shock protein (HSP) expression and cleaved caspase-3 (CC3) were evaluated via western blot. Cell morphology and cell size sanalyzed via microscopy. Following HS, THR treatment increased cell viability versus CT in a dose-dependent fashion from 5 to 20 mM. The non-metabolized amino acid analogue, Alpha-aminoisobutyric acid (AIB) also increased cell survival in HS cells versus HS-CT. HSP70 and HSP25 expression increased with THR and AIB treatment versus HS-CT. THR also increased HSP25 in non-stressed cells. Microscopic evaluation revealed both THR and AIB preserved structural integrity of the actin cytoskeleton in HS-cells versus HS-CT. THR, but not AIB, enhanced nuclear translocation of HSP25 during HS. This nuclear translocation, was associated with a 60% decrease in apoptosis in HS cells with THR. No anti-apoptotic effect was observed with AIB. This is the first demonstration THR increases HSP70 and HSP 25 and protects cells from HS. THR’s mechanism of protection may involve cytoskeletal stabilization, HSP up-regulation and nuclear translocation, and decreased apoptosis. THR’s protection appears to involve both cell swelling-dependent and independent processes.
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影响因子：
3.7
作者：
Niederlechner S;Klawitter J;Baird C;Kallweit AR;Christians U;Wischmeyer PE
通讯作者：
Wischmeyer PE
影响因子：
3.3
作者：
Wischmeyer, PE;Kahana, M;Chang, EB
通讯作者：
Chang, EB
影响因子：
7.7
作者：
Shim, EH;Kim, JI;Seo, JS
通讯作者：
Seo, JS
影响因子：
4.1
作者：
Caruccio, L;Bae, SW;Chen, KY
通讯作者：
Chen, KY
DOI：
10.1097/mco.0b013e32830a4c6e
发表时间：
2008-09-01
影响因子：
3.1
作者：
Sandek, Anja;Rauchhaus, Mathias;von Haehling, Stephan
通讯作者：
von Haehling, Stephan