@article{GaoWangZhangetal.2018,
  author    = {Gao, Lin-rui and Wang, Guang and Zhang, Jing and Li, Shuai and Chuai, Manli and Bao, Yongping and Hocher, Berthold and Yang, Xuesong},
  title     = {High salt-induced excess reactive oxygen species production resulted in heart tube malformation during gastrulation},
  series = {Journal of Cellular Physiology},
  volume    = {233},
  journal   = {Journal of Cellular Physiology},
  number    = {9},
  publisher = {Wiley},
  address   = {Hoboken},
  issn      = {0021-9541},
  doi       = {10.1002/jcp.26528},
  pages     = {7120 -- 7133},
  year      = {2018},
  abstract  = {An association has been proved between high salt consumption and cardiovascular mortality. In vertebrates, the heart is the first functional organ to be formed. However, it is not clear whether high-salt exposure has an adverse impact on cardiogenesis. Here we report high-salt exposure inhibited basement membrane breakdown by affecting RhoA, thus disturbing the expression of Slug/E-cadherin/N-cadherin/Laminin and interfering with mesoderm formation during the epithelial-mesenchymal transition(EMT). Furthermore, the DiI(+) cell migration trajectory in vivo and scratch wound assays in vitro indicated that high-salt exposure restricted cell migration of cardiac progenitors, which was caused by the weaker cytoskeleton structure and unaltered corresponding adhesion junctions at HH7. Besides, down-regulation of GATA4/5/6, Nkx2.5, TBX5, and Mef2c and up-regulation of Wnt3a/-catenin caused aberrant cardiomyocyte differentiation at HH7 and HH10. High-salt exposure also inhibited cell proliferation and promoted apoptosis. Most importantly, our study revealed that excessive reactive oxygen species(ROS)generated by high salt disturbed the expression of cardiac-related genes, detrimentally affecting the above process including EMT, cell migration, differentiation, cell proliferation and apoptosis, which is the major cause of malformation of heart tubes.},
  language  = {en}
}
@article{ZhangHuYangetal.2022,
  author    = {Zhang, Kai and Hu, Jiege and Yang, Shuai and Xu, Wei and Wang, Zhichao and Zhuang, Peiwen and Grossart, Hans-Peter and Luo, Zhuhua},
  title     = {Biodegradation of polyester polyurethane by the marine fungus Cladosporium halotolerans 6UPA1},
  series = {Journal of hazardous materials},
  volume    = {437},
  journal   = {Journal of hazardous materials},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {0304-3894},
  doi       = {10.1016/j.jhazmat.2022.129406},
  pages     = {10},
  year      = {2022},
  abstract  = {Lack of degradability and the accumulation of polymeric wastes increase the risk for the health of the environment. Recently, recycling of polymeric waste materials becomes increasingly important as raw materials for polymer synthesis are in short supply due to the rise in price and supply chain disruptions. As an important polymer, polyurethane (PU) is widely used in modern life, therefore, PU biodegradation is desirable to avoid its accumulation in the environment. In this study, we isolated a fungal strain Cladosporium halotolerans from the deep sea which can grow in mineral medium with a polyester PU (Impranil DLN) as a sole carbon source. Further, we demonstrate that it can degrade up to 80\% of Impranil PU after 3 days of incubation at 28 celcius by breaking the carbonyl groups (1732 cm(-1)) and C-N-H bonds (1532 cm(-1) and 1247 cm(-1)) as confirmed by Fourier-transform infrared (FTIR) spectroscopy analysis. Gas chromatography-mass spectrometry (GC-MS) analysis revealed polyols and alkanes as PU degradation intermediates, indicating the hydrolysis of ester and urethane bonds. Esterase and urease activities were detected in 7 days-old cultures with PU as a carbon source. Transcriptome analysis showed a number of extracellular protein genes coding for enzymes such as cutinase, lipase, peroxidase and hydrophobic surface binding proteins A (HsbA) were expressed when cultivated on Impranil PU. The yeast two-hybrid assay revealed that the hydrophobic surface binding protein ChHsbA1 directly interacts with inducible esterases, ChLip1 (lipase) and ChCut1 (cutinase). Further, the KEGG pathway for "fatty acid degradation " was significantly enriched in Impranil PU inducible genes, indicating that the fungus may use the degradation intermediates to generate energy via this pathway. Taken together, our data indicates secretion of both esterase and hydrophobic surface binding proteins by C. halotolerans plays an important role in Impranil PU absorption and subsequent degradation. Our study provides a mechanistic insight into Impranil PU biodegradation by deep sea fungi and provides the basis for future development of biotechnological PU recycling.},
  language  = {en}
}