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肝癌細胞線粒體在ROS生成下HSP60介導並調控MAPK信號傳遞的分子機制

為了解決3m mb45前檔的問題，作者JayaPrakash Mandal 這樣論述：

Our previous studies showed that mitogen-activated protein kinases (MAPKs) are activated by the interaction of protein kinase C (PKC) and reactive oxygen species (ROS) for hepatocellular carcinoma (HCC) progression. However, the relevant mechanisms remained to be clarified in more detail. In this s

tudy, we used two hepatoma cell lines HepG2 and HCC340 as models to investigate the comprehensive ROS-PKC signaling triggered by tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA). Since mitochondria-derived reactive oxygen species (mtROS) signaling is well known to be involved in tumor prog

ression, we examined whether TPA triggers the generation of mtROS that can crosstalk with PKC. By mtROS assay, TPA maximally induced mtROS generation at 10 min, which could be prevented by the mitochondria-specific scavenger of mtROS, MitoTEMPO. By western blot, we observed TPA induced transient pho

sphorylation of ERK/JNK and expression of transcriptional factors c-jun/c-fos. Using inhibitors of PKC isozymes and mitoTEMPO, the signal pathway was proved to be transmitted in mtROS/PCK-dependent manner. By BIAM-labeling coupled with LC-MS/MS, heat shock protein 60 (HSP60) was identified as the m

ajor oxidative target. Moreover, suppression of HSP60 by HSP60shRNA, HSP60 inhibitor mizoribine, and expression of dominant-negative HSP60 Cys-mutant prevented TPA-induced phosphorylation of MAPKs and expression of c-jun. In the mechanistic study, for oxidation of HSP60 leading to MAPK activation, w

e found Raf kinase inhibitor protein (RKIP), a negative regulator of MAPK and well-known metastatic suppressor, was involved. Using immunoprecipitation (IP)/Western blot analysis, we found TPA induced the dissociation RKIP from HSP60 within 30 min in both HCCs which can be attenuated by inhibitor of

PKC delta, mtROS scavenger and HSP60 Cys-mutant. At the same time, translocation of HSP60 coupled with MAPK from mitochondria to cytosol was observed. These were closely associated with the robust phosphorylation of MAPKs in the cytosol. By transwell migration assay and cell cycle analysis, TPA ind

uced G1 cell cycle arrest and cell migration, respectively, two dichotomous phenotypical changes of HCCs. Such phenotypes were prevented by the inhibitor of mtROS and knockdown of PKC and HSP60. Several migratory genes such as MMP1/3 (matrix metalloproteinase), LAMC2 (laminin????2), Hic-5 (hydrogen

peroxide inducible clone-5), and a miR-6134, targeting CCNE1 (cyclin E1) were upregulated by TPA. In addition, transcriptional system AP-1 (c-jun/c-fos) regulated TPA-induced migratory genes and miR-6134.In conclusion, we established TPA-induced PKC-mtROS-HSP60 (RKIP)-MAPK-(AP-1) signal axis requi

red for regulating gene expressions triggering dichotomous phenotype in HCCs. Several key players in this pathway such as PKCδ, RKIP, and HSP60 are promising candidates for targeted therapy to prevent HCC progression.

多層奈米纖維於抑菌光動力治療之傷口敷料評估

為了解決3m mb45前檔的問題，作者鄧如婷 這樣論述：

本研究所設計的多層靜電紡絲奈米纖維膜(Three layers-3SB)，外層由熱塑性聚氨酯彈性橡膠(thermoplastic polyurethane, TPU)組成；中間吸水層由[2-(methacryloyloxy)ethyl] dimethyl-(3-sulfopropyl) ammonium hydroxide (SBMA) 與具有化學交聯反應的單體N-methylol acrylamide (NMA)以自由基聚合法合成poly(SBMA-co-NMA)共聚高分子組成；內層由chitosan (CS)、poly(vinyl alcohol) (PVA)與親水性光敏劑methyle

ne blue (MB)組成。Three layers-3SB水分吸收率可達到1100%以上，保水效果在12小時仍維持近14%的水分，水氣滲透率為2223.8 g/m2 ∙ day，敷料性質測試結果優於商用敷料3M Tegaderm與AQUACEL® Ag Foam。添加光敏劑MB之多層奈米纖維膜(3S-3MB與3S-5MB)都具有高封裝效率且藥物釋放效率可達到80%以上。藉由2,7-dichlorofluorescin diacetate (DCFH-DA)指示劑來檢測ROS生成效率，結果顯示出3S-5MB具有較高的ROS生成效率。在體外細胞實驗結果顯示出3S-3MB與3S-5MB對於纖維母

細胞(L929)具有生物相容性。3S-5MB在照光前大腸桿菌(E. coli)存活率為2.75%，照光後下降至0.24%，在金黃色葡萄球菌(S. aureus)未照光存活率為0.04%，照光後下降到0.004%，因MB暗毒性使3S-5MB在未照光時對於兩種菌即具有抑制效果，3S-5MB在照光後產生光動力作用對於金黃色葡萄球菌抑菌生長較為顯著。由抑菌圈與細菌存活率實驗結果顯示3S-5MB在照光對於金黃色葡萄球菌或大腸桿菌抑菌效果都比商用銀離子敷料AQUACEL® Ag Foam更好。綜合以上結果，3S-5MB具有吸濕性、保濕性、透氣性以及良好的機械性質，並且具備光動力抗菌的特性，可作為新型抗菌傷

口敷料的潛力。