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Articles by C. P Chen
Total Records ( 3 ) for C. P Chen
  Y. C Chiu , D. C Shieh , K. M Tong , C. P Chen , K. C Huang , P. C Chen , Y. C Fong , H. C Hsu and C. H. Tang
 

Chondrosarcoma is a type of highly malignant tumor with a capacity to invade locally and cause distant metastasis. Chondrosarcoma shows a predilection for metastasis to the lungs. Adiponectin is a protein hormone secreted predominantly by differentiated adipocytes and is involved in energy homeostasis. However, the effect of adiponectin on migration activity in human chondrosarcoma cells is mostly unknown. We found that adiponectin increased the migration and expression of 2β1 integrin in human chondrosarcoma cells. The protein and messenger RNA expression of adiponectin receptor (AdipoR1 and AdipoR2) in chondrosarcoma patients and chondrosarcoma cell lines were significantly higher than the normal cartilage. Moreover, primary chondrosarcoma and chondrosarcoma cell lines (SW1353 and JJ012) were more invasive than normal chondrocytes. Adiponectin-mediated migration and integrin expression was attenuated by 5'-adenosine monophosphate-activated protein kinase (AMPK) small interfering RNA and an AMPK inhibitor (Ara A and compound C). Activation of p38 and nuclear factor-kappa B (NF-B) pathways after adiponectin treatment was demonstrated, and adiponectin-induced expression of integrins and migration activity was inhibited by the specific inhibitor and mutant of p38 and NF-B cascades. This study showed for the first time that adiponectin mediates the migration of human chondrosarcoma cells. One mechanism underlying adiponectin-directed migration was transcriptional upregulation of 2β1 integrin and activation of AdipoR receptor, AMPK, p38 and NF-B pathways.

  H. L Hsieh , L. F Fan , C. P Chen , J. T Wu and W. C. Liu
 

We examined how tidal changes and which physical factors affected holo- and meroplankton assemblages in a subtropical estuary in Taiwan in February 1999. A factor analysis showed that during tidal flooding, the water mass properties changed from low salinity (5–16) and high particulate organic carbon (POC, 2.6–4.5 mg L–1) content to increasing salinity and high total suspended matter content (29.0–104.5 mg L–1). With a receding tide, the water became more saline again, and its velocity increased (from non-detectable to 0.67 m s–1). One-way ANOVA showed that the distributions of four dominant taxa were affected by the ebb tide and exhibited two distinct groups. The first group consisted of non-motile invertebrate eggs and weakly swimming polychaete sabellid embryos and larvae (at densities of 1.25–1.40 ind. L–1), while the second consisted of better-swimming copepods and polychaete spionid larvae (at densities of 0.70–1.65 ind. L–1). A canonical correlation analysis demonstrated that the former group occurred at sites with greater freshwater input, higher POC content and greater depth, whereas the latter group was significantly associated with sites subject to seawater and faster flows. We propose that a two-layered circulation process and tidally induced oscillations in water movements might account for the distributional differences between these two groups.

  M. H Chiang , F. Y Liang , C. P Chen , C. W Chang , M. L Cheong , L. J Wang , C. Y Liang , F. Y Lin , C. C Chou and H. Chen
 

Preeclampsia is a major pregnancy-specific disorder affecting 5–7% of pregnancies worldwide. Although hypoxia caused by incomplete trophoblast invasion and impaired spiral arterial remodeling is thought to be a major cause of preeclampsia, how hypoxia affects placental development remains uncertain. GCM1 (glial cells missing homolog 1) is a transcription factor critical for placental development. In preeclampsia, GCM1 and its target genes syncytin 1 and placental growth factor, important for syncytiotrophoblast formation and placental vasculogenesis, are all decreased. Here we present evidence that GCM1 is a major target of hypoxia associated with preeclampsia. We show that hypoxia triggers GCM1 degradation by suppressing the phosphatidylinositol 3-kinase-Akt signaling pathway, leading to GSK-3β activation. Activated GSK-3β phosphorylates GCM1 on Ser322, which in turn recruits the F-box protein FBW2, leading to GCM1 ubiquitination and degradation. Importantly, the GSK-3β inhibitor LiCl prevented hypoxia-induced GCM1 degradation. Our study identifies a molecular basis for the disrupted GCM1 transcription network in preeclampsia and provides a potential avenue for therapeutic intervention.

 
 
 
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