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Nucleus Near-Infrared (nNIR) Irradiation of Single A549 Cells Induces DNA Damage and Activates EGFR Leading to Mitochondrial Fission

為了解決318 cargo tracking的問題，作者MOMOH GBETUWA 這樣論述：

Abstract Background: There has been great interest in identifying the biological substrate for light-cell interaction and their relations to cancer treatment. In our study, a single cell nuclear NIR (nNIR) and cytosol exposed NIR has been used to determine for the first-time mitochondria fragmentat

ion count (MFC) to compare NIR effect on subcellular cells. Near infra-red (NIR) possesses less light scattering and absorption in biological tissues it has a biological window that bears a very small photodamage and thus possesses a deep tissue penetration depth. Aim: To evaluate near-infrared (NIR

) laser focused into the nucleus (nNIR) or cytoplasm (cNIR) of a single living cell by a high numerical aperture condenser to dissect the novel role of cell nucleus in mediating NIR effects on mitochondrial dynamics of A549 non-small cell lung cancer cells.Materials and Methods: Cultured 150 single

cell of A549 nucleus and cytosol were incubated with 0.3 μM mitotracker green for 30 min washed with PBS, imaged control cell then treated with 224.02 J/cm2 NIR for 10 s and cells imaged at different time points of 1, 5, 10, 15 and 20 min. A549 cells were treated with conjugated 100 nM FND-EGF and i

ncubated with PD153035, caffeine and cetuximab for 1 h, and imaged cells. Results: Our analysis showed nNIR, but not cNIR, triggered mitochondrial fission in 10 minutes. On the contrast, the fission/fusion balance of mitochondria directly exposed to cNIR does not change. While the same phenomenon is

also triggered by single molecular interactions between epidermal growth factor (EGF) and its receptor EGFR, pharmacological studies with cetuximab, PD153035 and caffeine suggest EGF signaling crosstalk to DNA damaging response to mediate rapid mitochondrial fission as a result of nNIR irradiation.

These results suggest that nuclear DNA integrity is a novel biological target for cellular response to NIR. Conclusions: These results suggest that nuclear DNA integrity is a novel biological target for cellular response to NIR. Keywords: Keywords: near infrared (NIR), epidermal growth factor recep

tor (EGFR), mitochondrial fragmentation count (MFC), mitochondrial dynamic, cetuximab, caffeine.

探討平衡核苷轉運蛋白3 (ENT3) 在亨丁頓氏症的小神經膠質細胞中所扮演的角色

為了解決318 cargo tracking的問題，作者呂瑩穗 這樣論述：

小神經膠質細胞是在中樞神經系統的常駐組織巨噬細胞，它們負責進行吞噬有害物質、蛋白累積、或是凋亡受損的細胞，因此在維持腦內的微環境恆定方面扮演著重要的角色。近年來也越來越多研究顯示在人或是老鼠的小神經膠質細胞對於神經退化性疾病的致病機轉處於至關重要的地位。平衡核苷轉運蛋白3 (ENT3)是由基因SLC29A3所編碼的蛋白，目前已被證明是主要的酸性pH依賴核苷轉運蛋白，會調控溶酶體和粒腺體中的核苷濃度的平衡。在先前研究我們已經證實缺乏ENT3將會影響周邊巨噬細胞中溶酶體的功能喪失以及有骨髓增生的表徵出現。在腦中我們發現ENT3高度表現在小神經膠質細胞，此外，ENT3在亨丁頓氏症(HD)的動物模型

及人類病人檢體的表現量顯著上升，這些結果顯示ENT3可能參與在神經退化性疾病HD中。本研究的目標為探討平衡核苷轉運蛋白3 (ENT3)在微膠細胞扮演的角色及其參與在神經退化性狀態的可能性。我們除了發現在ENT3缺失小鼠的腦內小神經膠質細胞數量顯著增加，並且伴隨著有抗發炎的表徵，進一步我們也利用亨丁頓氏症的動物模型R6/2小鼠研究ENT3對於HD疾病進展的影響。結果顯示將ENT3剔除之後，R6/2小鼠在體重、生命週期、四肢緊縮測試以及滾輪運動測試等行為測試皆具有惡化的現象，因此我們推測在疾病進程中ENT3在其中扮演保護性的角色。本研究的結果認為ENT3有對於調控小神經膠質細胞及腦內恆定的角色以及

參與在和緩亨丁頓氏症(HD)疾病進展的可能性。