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Gao Ran,Guo Wenjun,Fan Tianfei,Pang Junling,Hou Yangfeng,Feng Xiaohang,Li Bolun,Ge Weipeng,Fan Tianhui,Zhang Tiantian,Lu Jiakai,Jing He,Jin Mu,Yan Chen,Wang Jing 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Abdominal aortic aneurysm (AAA) is a permanent expansion of the abdominal aorta that has a high mortality but limited treatment options. Phosphodiesterase (PDE) 4 family members are cAMP-specific hydrolyzing enzymes and have four isoforms (PDE4A-PDE4D). Several pan-PDE4 inhibitors are used clinically. However, the regulation and function of PDE4 in AAA remain largely unknown. Herein, we showed that PDE4D expression is upregulated in human and angiotensin II-induced mouse AAA tissues using RT-PCR, western blotting, and immunohistochemical staining. Furthermore, smooth muscle cell (SMC)-specific Pde4d knockout mice showed significantly reduced vascular destabilization and AAA development in an experimental AAA model. The PDE4 inhibitor rolipram also suppressed vascular pathogenesis and AAA formation in mice. In addition, PDE4D deficiency inhibited caspase 3 cleavage and SMC apoptosis in vivo and in vitro, as shown by bulk RNA-seq, western blotting, flow cytometry and TUNEL staining. Mechanistic studies revealed that PDE4D promotes apoptosis by suppressing the activation of cAMP-activated protein kinase A (PKA) instead of the exchange protein directly activated by cAMP (Epac). Additionally, the phosphorylation of BCL2-antagonist of cell death (Bad) was reversed by PDE4D siRNA in vitro, which indicates that PDE4D regulates SMC apoptosis via the cAMP-PKA-pBad axis. Overall, these findings indicate that PDE4D upregulation in SMCs plays a causative role in AAA development and suggest that pharmacological inhibition of PDE4 may represent a potential therapeutic strategy.
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Tingting Zhang,Zihui Li,Ya Liu,Kangjia Ding,Yangfeng Guo,Yiyang Xu,Mengfan Sun,Dongfang Wang,Qian Li 한국섬유공학회 2023 Fibers and polymers Vol.24 No.12
Polytetrafluoroethylene (PTFE) nano-porous membrane has been widely used in various fields due to its excellent thermal stability and chemical stability. However, PTFE nanofiber membranes with simultaneous hydrophobic and oleophobic properties are essential to promote the application of PTFE. Here, based on inorganic/organic nanohybridization, we report a strategy for constructing nanostructures on fibers by adding nanoparticles, such as MOF and ZrO2. The results of FTIR and XRD confirmed MOF was synthesized successfully. At the same time, the SEM results showed UiO-66-(COOH)2 is spherical with an average diameter of 152 nm, and there is no agglomeration, which is suitable for electrospinning. Further, MOF and ZrO2 were payload into PTFE nanofibers. The results of SEM and AFM confirmed nanostructures will be more uniform and pronounced with the increase of UiO-66-(COOH)2 content, and nanostructures are most obvious when the content of UiO-66-(COOH)2 is 15%. The introduced nanostructures can increase the oil contact angle of the PTFE nano-porous membrane to 110° without introducing other groups, and further improve the water contact angle from 133° to 145°. Meanwhile, the introduction of a certain amount of hydrophilia groups can increase the oil contact angle to more than 120°. The simple strategy is of great significance to expand the application of PTFE fiber membrane in dealing with waste water treatment fields.
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Yang Feng,Zhiming Fu,Yajun Luo,Wang Tan,Zilin Liu,Pengcheng Ye,Fei Lu,Wanping Xiang,Linghan Tang,Lin Yao,Mengyun Song,Qingmei Huang,Yilun Liu,Jiangwei Xiao 대한독성 유전단백체 학회 2019 Molecular & cellular toxicology Vol.15 No.3
Backgrounds: The role of long non-coding RNAs (lncRNA) in gastric cancer (GC) has been highlighted in studies conducted over the past decade. However, the potential clinical value and the mechanisms of action of RP11-6O2.4 in GC have not been thoroughly elucidated to date. The specific aim of the present study was to assess RP11-6O2.4 and to explore its role in human GC. Methods: Quantitative real-time polymerase chain reaction (qPCR) was performed to analyze the expression levels of RP11-6O2.4 in GC tissues, paired adjacent noncancerous tissues (ANTs) and GC cell lines. In addition, the correlation between RP11-6O2.4 expression and the clinical characteristics and prognosis of patients with GC was statistically analyzed. The effects of RP11- 6O2.4 on the GC cell cycle transformation through the p38-MAPK signaling pathway were explored by flow cytometry, qPCR and Western blot analysis after treatment with SB203580, a p38MAPK specific inhibitor, in vitro. Results: The expression levels of RP11-6O2.4 in GC tissues were significantly lower than the paired ANTs (P<0.05). In addition, RP11-6O2.4 expression was significantly lower in cases with older age, longer maximum tumor diameter, higher ASA grade and deeper invasive depth (P<0.05). RP11-6O2.4 expression was significantly higher in cases with well/middle differentiation than poor/no differentiation; higher in cases without lymph node metastasis than in lymph node metastasis; and higher in cases in stage Ⅰ/Ⅱ than in stage Ⅲ/Ⅳ. An in vitro assay showed that RP11-6O2.4 induced G0/ G1 phase cell cycle arrest, likely by regulating the p38- MAPK signaling pathway. Conclusion: The above mentioned data suggested that RP11-6O2.4 was a tumor-suppressor gene in GC. RP11- 6O2.4 might play an important role in the cell cycle transformation by regulating the p38-MAPK signaling pathway, thereby representing a specific biomarker and a potential molecular target for the treatment of GC.
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