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標題: 病毒感染所引起的細胞再分化暨胞器轉送的新蛋白傳輸系統
Virus-induced cell re-differentiation and a novel interorganelle protein transport pathway
作者: 姜淑芬
Chiang, Shu-Fen
關鍵字: phenotypic conversion;細胞再分化;SARS-CoV spike protein;interorganelle transport MAM;胞器轉送;蛋白傳輸系統
出版社: 獸醫微生物學研究所
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造血幹細胞透過不同生長因子、細胞(激)素或轉錄因子作用,可分化成不同種類的血球細胞。其中,B淋巴細胞與巨噬細胞雖然同屬抗原呈現細胞,卻是從兩種不同定向細胞譜系(committed lineage)分化而來,各自經由特異的轉錄因子調控其特有的基因表現。最近,在體外實驗中已證實經由改變轉錄因子的表現可以將B淋巴球再改造(reprogram)成巨噬細胞。本研究發現,昆蟲桿狀病毒(baculovirus)所表現嚴重急性呼吸道症候群冠狀病毒(SARS-CoV)的spike 蛋白可轉導(transduce)人類周邊白血球中B淋巴球與B淋巴癌細胞,並使其再分化成類巨噬細胞。這些類巨噬細胞不但變大且顆粒性增加,同時也會表現標記分子CD11b與CD68。此外,我們發現在極度缺氧時,也促使B淋巴癌細胞轉形成類巨噬細胞。這些現象和SARS病人的臨床表徵相似,如非典型肺炎的嚴重缺氧、肺部大量巨噬細胞浸潤、以及淋巴球低下。據此,我們合理推論嚴重急性呼吸道症候群冠狀病毒可能造成肺部發炎吸引B淋巴球到肺臟;然後B淋巴球受到病毒及缺氧影響,進而轉形成類巨噬細胞累積在受損的肺臟中。所以,未來亟待確定是否嚴重急性呼吸道症候群冠狀病毒具有促使B細胞再分化的能力。
粒線體功能已知與抗病毒的先天免疫功能有關。某些病毒蛋白會與粒線體作用,影響細胞的存活。粒線體中的蛋白,大部分由細胞核基因所編碼(encoded)。傳統上認為它們在細胞質製造,經由translocase輸送至粒線體中。然而,病毒蛋白可能干擾蛋白運輸。異常的蛋白運送會影響粒線體的活性,也會改變細胞的功能與存活能力。在本研究,我們發現粒線體蛋白AIF,係經由一條新的替代路徑。我們研究證實AIF在內質網合成,經由MAM及運送小泡(transport vesicle)運送至粒線體內。此運送路徑可能與運送磷脂質至粒線體之路徑相同,並且需要DRP1、Mfn-2、及ATAD3A三種蛋白。

Our studies included two subjects: (1) virus-induced cell re-differentiation; (2) a novel interorganelle protein transport pathway.
Hematopoietic stem cells (HSCs), through mediation by various growth factors, cytokines and transcription factors, can differentiate into different lineages of blood cells. Although B cells and macrophages are both antigen-presenting cells, they were descended from two distinctively committed lineages. Their respective differentiation was restricted by specific transcription factors, and exhibited diverse patterns of gene expression. Recently, B cells were shown to be reprogrammed into macrophages by way of altering expression of transcription factors. In this study, we found that human peripheral B cells and B lymphoma cell lines could be transduced by recombinant baculovirus-expressed Severe Acute Respiratory Syndrome- Coronavirus (SARS-CoV) spike protein, and re-differentiated into macrophage-like cells. These macrophage-like cells enlarged with increased granules, and expressed marker molecular, CD11b and CD68. Moreover, we found that severe hypoxia also triggered B lymphoma cells re-differentiated. These phenomena were similar to the clinical features observed in SARS patients, such as atypical pneumonia-induced severe hypoxia, massive macrophage infiltrates in the lungs, and lymphopenia. Hence, we suggested that B cells were recruited into inflammatory lungs upon SARS-CoV infection. They were subsequently reprogrammed into macrophage-like cells by virus and hypoxia, and accumulated in the afflicted lungs. In the future, it is imperative to determine whether SARS-CoV may have the ability to trigger B cell re-differentiation.
Function of mitochondria has been shown correlated with intracellular immunity. Certain viral proteins interact with mitochondrial proteins to affect cell survival. Most mitochondrial proteins are encoded by the nuclear genes. Traditionally, they were thought to be synthesized in the cytosol and imported into mitochondria through translocases. However, viral proteins may interfere with protein transport. Abnormal protein transport could hamper mitochondrial activities, and therefore influence cell function and viability. In this study, we found that mitochondrial protein apoptosis-inducing factor (AIF) was imported into mitochondria by a novel alternative transport pathway. We identified that AIF was synthesized in the endoplasmic reticulum (ER) and transported into mitochondria via mitochondria-associated membrane (MAM) and transport vesicle. This pathway may be similar to that for mitochondrial phospholipid transport, which requires three proteins: dynamin-related protein 1 (DRP1), mitofusin-2 (Mfn-2), and ATPase family AAA domain containing 3A (ATAD3A).
其他識別: U0005-1301201210175200
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