Physical memory of astrocytes
Physical memory of astrocytes
复制标题
星形胶质细胞的物理记忆
DOI：
10.1016/j.brainres.2022.148076
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发表时间：
2022
期刊：
影响因子：
2.9
通讯作者：
Hua, Susan Z.
中科院分区：
文献类型：
--
作者：
Shireen, Tasnim;Sachs, Frederick;Hua, Susan Z.
创伤性脑损伤（TBI）是日后发生神经退行性疾病的主要危险因素。短暂、重复的机械冲击可能导致几天或几个月后出现的病变。细胞对机械事件具有物理“记忆”。这种记忆的起源不得而知。为了研究这种记忆的特性，我们使用微流控芯片将程序化的流体剪切脉冲施加到粘附的成年大鼠星形胶质细胞上。这些引起细胞内Ca2+的瞬时升高。在重复的刺激，6至24小时间隔，Ca 2+反应增加。这种效应持续超过24小时。Ca2+反应的重复次数比刺激之间的休息时间更敏感。我们发现，抑制条件刺激过程中的Ca 2+内流并没有消除应力增强，这表明在初级损伤的机械变形是负责后来的反应。触发这种长期“记忆”的机械机制可能通过细胞骨架的塑性变形起作用。
Traumatic brain injury (TBI) is a major risk factor for development of neurodegenerative disorders later in life. Short, repetitive, mechanical impacts can lead to pathology that appears days or months later. The cells have a physical “memory” of mechanical events. The origin of this memory is not known. To examine the properties of this memory, we used a microfluidic chip to apply programmed fluid shear pulses to adherent adult rat astrocytes. These caused a transient rise in intracellular Ca2+. In response to repeated stimuli, 6 to 24 hrs apart, the Ca2+response increased. This effect lasted longer than 24 hrs. The Ca2+responses were more sensitive to the number of repetitions than to the rest time between stimuli. We found that inhibiting the Ca2+influx during conditioning stimulus did not eliminate the stress potentiation, suggesting that mechanical deformation during the primary injury is accountable for the later response. The mechanical mechanism that triggers this long term “memory” may act by plastic deformation of the cytoskeleton.
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影响因子：
4.2
作者：
Maneshi, Mohammad Mehdi;Sachs, Frederick;Hua, Susan Z.
通讯作者：
Hua, Susan Z.
酪氨酸激酶信号传导参与谷氨酸诱导的星形胶质细胞增殖
影响因子：
1.7
作者：
Su;Chun
通讯作者：
Chun
影响因子：
5.7
作者：
Mills, LR;Velumian, AA;Fehlings, MG
通讯作者：
Fehlings, MG
影响因子：
4.6
作者：
Maneshi MM;Maki B;Gnanasambandam R;Belin S;Popescu GK;Sachs F;Hua SZ
通讯作者：
Hua SZ
DOI：
10.1073/pnas.88.7.2951
发表时间：
1991-04-01
影响因子：
11.1
作者：
DANOFF, SK;FERRIS, CD;ROSS, CA
通讯作者：
ROSS, CA