本文選題：鳥苷酸交換因子　切入點：DOCK1　出處：《重慶醫(yī)科大學》2012年碩士論文　論文類型：學位論文

【摘要】：目的：探討鳥苷酸交換因子DOCK1對心肌細胞存活的影響。 方法：用重組真核質(zhì)粒pCXN2-Flag-hDOCK1（人DOCK1過表達質(zhì)粒），pCXN2-Flag（空質(zhì)粒）及空白試劑分別轉(zhuǎn)染大鼠源H9C2心肌細胞，并給予缺氧/復氧(H/R)干預。將心肌細胞分為空白組，空質(zhì)粒組，DOCK1過表達組，空白+H/R組，空質(zhì)粒+H/R組，DOCK1過表達+H/R組。用RT-PCR及Western bloting分別測定DOCK1mRNA及蛋白水平。流式細胞術(shù)、MTT分別測定細胞的凋亡率和增殖率。共聚焦激光掃描共焦顯微鏡觀察心肌細胞骨架的改變。 結(jié)果: DOCK1過表達組較空白組和空質(zhì)粒組，DOCK1過表達+H/R組較空白+H/R組和空質(zhì)粒+H/R組，人的DOCK1mRNA、DOCK1蛋白分別顯著增加、心肌細胞凋亡率分別顯著降低及增殖率分別顯著增加。較DOCK1過表達組，，DOCK1過表達+H/R組人的DOCK1mRNA顯著降低。較空白組、空質(zhì)粒組及DOCK1過表達組，空白+H/R組、空質(zhì)粒+H/R組及DOCK1過表達+H/R組大鼠的DOCK1mRNA、DOCK1蛋白分別顯著降低、心肌細胞凋亡率分別顯著增加及增殖率分別顯著降低（所有P0.05）。 結(jié)論: DOCK1可抑制細胞的凋亡，促進細胞骨架有序重排，促進細胞的增殖、存活；過表達DOCK1可抑制H/R誘導的心肌細胞凋亡增高、細胞骨架的排列紊亂、細胞增值、存活的降低。
[Abstract]:Objective: to investigate the effect of guanosine exchange factor DOCK1 on the survival of cardiac myocytes. Methods: rat H9C2 cardiomyocytes were transfected with recombinant eukaryotic plasmid pCXN2-Flag-hDOCK1 (human DOCK1 overexpression plasmid pCXN2-Flag1 (empty plasmid) and blank reagent respectively). The blank H / R group, The levels of DOCK1mRNA and protein were measured by RT-PCR and Western bloting. The apoptosis rate and proliferation rate were measured by flow cytometry. The cytoskeleton of cardiomyocytes was observed by confocal laser scanning confocal microscopy (confocal laser scanning confocal microscopy). Results: human DOCK1 mRNA-DOCK1 protein was significantly increased in DOCK1 overexpression group than that in blank H / R group and blank plasmid group. The apoptosis rate of cardiomyocytes was significantly decreased and the proliferation rate was significantly increased, compared with that of DOCK1 overexpression group, the human DOCK1mRNA was significantly decreased, compared with blank group, blank plasmid group and DOCK1 overexpression group, and blank H / R group. The expression of DOCK1 mRNA-DOCK1 protein in empty plasmid H / R group and DOCK1 overexpressed H / R group was significantly decreased, and the apoptosis rate and proliferation rate of cardiomyocytes were significantly increased (all P 0.05). Conclusion: DOCK1 can inhibit apoptosis, promote cytoskeleton rearrangement, promote cell proliferation and survival, and overexpression of DOCK1 can inhibit the increase of H / R induced cardiomyocyte apoptosis, the disorder of cytoskeleton arrangement, the increase of cell proliferation and the decrease of cell survival.
【學位授予單位】：重慶醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2012
【分類號】：R363

【參考文獻】

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