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- 저자 : Lingling Cui (검색결과 4 건)
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Xing, Qianguo,Wu, Lingling,Tian, Liqiao,Cui, Tingwei,Li, Lin,Kong, Fanzhou,Gao, Xuelu,Wu, Mengquan Elsevier 2018 Marine pollution bulletin Vol.133 No.-
<P><B>Abstract</B></P> <P>The world's largest green tide originated from the Jiangsu Shoal of the Yellow Sea was due to fast reproduction of floating green macroalgae (<I>Ulva prolifera</I>). It brought significant impacts on marine environment and ecosystem in the Yellow Sea. In this study, we examined the expansion of green tide from the Jiangsu Shoal during the period from 29 April to 25 June 2016. Using high-resolution satellite images, we revealed a declined growth rate during the northward drifting of early-stage green tide for the first time, i.e., the green tide had higher growth rate (up to 25% per day) in the turbid waters of the Jiangsu Shoal in May and a lower growth rate (low to 3% per day) in the relatively clear waters in the middle of the western Yellow Sea in June, which suggests that water clarity might not be the key factor controlling the growth rate of the floating macroalgae in the surface waters under natural conditions. The high growth rate led to shortened time windows for controlling the green tide by employing macroalgae collecting campaigns at the initial sites of the green tide, which was no more than 14 days in the 2016 case.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Using high-resolution satellite image for detecting early-stage green tide </LI> <LI> Found changing growth rate of green tide </LI> <LI> Assessed the countermeasure of collecting floating-macroalgae at the initial sites </LI> </UL> </P>
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Ru Sun,Xueqing Ba,Lingling Cui,Yan Xue,Xianlu Zeng 한국분자세포생물학회 2009 Molecules and cells Vol.27 No.4
Skeletal muscle regeneration is a highly orchestrated process initiated by activation of adult muscle satellite cells. Upon muscle injury, the inflammatory process is always accompanied by muscle regeneration. Leukotriene B4 is one of the essential inflammatory mediators. We isolated and cultured primary satellite cells. RT-PCR showed that myoblasts expressed mRNA for LTB4 receptors BLT1 and BLT2, and LTB4 promoted myoblast proliferation and fusion. Quantitative real-time PCR and immunoblotting showed that LTB4 treatment expedited the expression process of differentiation markers MyoD and M-cadherin. U-75302, a specific BLT1 inhibitor, but not LY2552833, a specific BLT2 inhibitor, blocked proliferation and differentiation of myoblasts induced by LTB4, which implies the involvement of the BLT1 pathway. Overall, the data suggest that LTB4 contributes to muscle regeneration by accelerating proliferation and differentiation of satellite cells.
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Zengli Yu,Xiaozhuan Liu,Zhan Gao,Zhitao Li,Jun Yin,Yuchang Tao,Lingling Cui,Zengli Yu 한국통합생물학회 2017 Animal cells and systems Vol.21 No.1
All-trans retinoic acid (atRA), the oxidative metabolite of retinoic acid (RA), is essential for palatogenesis. Overdose RA is capable of inducing cleft palate in mice and humans. Normal embryonic palatal mesenchymal (EPM) cell growth is crucial for shelf growth. Smad signaling is involved in many biological processes. However, it is not much clear if atRA could affect Smad signaling during EPM cells growth. In this study, the timed pregnant mice with maternal administration of 100 mg/kg body weight of RA by gastric intubation were cervical dislocation executed to evaluate growth changes of palatal shelves by hematoxylin and eosin (H&E) staining. At the same time, a primary mouse EPM (MEPM) cell culture model was also established. MEPM cells were treated with atRA (0.1, 0.5, 1, 5 and 10 μM) for 24, 48 and 72 h. The results indicated that the sizes of the shelves were smaller than those in control. AtRA inhibited MEPM cell growth with both increasing concentration and increasing incubation time, especially at 72 h in vitro. Moreover, atRA significantly increased the mRNA and protein expression levels of Smad7 (P < .05), but the mRNA and protein expression levels of PCNA were reduced (P < .05). We also found atRA inhibited phosphorylation of Smad2 compared with untreated group (P < .05). However, the protein and mRNA levels of Smad2 did not change both in atRA-treated and untreated group (P > .05). We demonstrated that RA induced inhibition of MEPM cell growth that could cause cleft palate partly by down-regulation of Smad pathway.
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