Control of dynamic cell behaviors during angiogenesis and anastomosis by Rasip1

Organ morphogenesis is driven by a wealth of tightly orchestrated cellular behaviors, which ensure proper organ assembly and function. Many of these cell activities involve cell-cell interactions and remodeling of the F-actin cytoskeleton. Here, we analyze the requirement for Rasip1 (Ras-interacting protein 1), an endothelial-specific regulator of junctional dynamics, during blood vessel formation. Phenotype analysis of rasip1 mutants in zebrafish embryos reveals distinct functions of Rasip1 during sprouting angiogenesis, anastomosis and lumen formation. During angiogenic sprouting, loss of Rasip1 causes cell pairing defects due to a destabilization of tricellular junctions, indicating that stable tricellular junctions are essential to maintain multicellular organization within the sprout. During anastomosis, Rasip1 is required to establish a stable apical membrane compartment; rasip1 mutants display ectopic, reticulated junctions and the apical compartment is frequently collapsed. Loss of Ccm1 and Heg1 function mimics the junctional defects of rasip1 mutants. Furthermore, downregulation of ccm1 and heg1 leads to a delocalization of Rasip1 at cell junctions, indicating that junctional tethering of Rasip1 is required for its function in junction formation and stabilization during sprouting angiogenesis

Rice ONAC106 inhibits leaf senescence and increases salt tolerance and tiller angle

NAM/ATAF1/ATAF2/CUC2 (NAC) is a plant-specific transcription factor (TF) family, and NACs participate in many diverse processes during the plant life cycle. Several Arabidopsis thaliana NACs have important roles in positively or negatively regulating leaf senescence, but in other plant species, including rice, the senescence-associated NACs (senNACs) remain largely unknown. Here we show that the rice senNAC TF ONAC106 negatively regulates leaf senescence. Leaves of onac106-1D (insertion of the 35S enhancer in the promoter region of the ONAC106 gene) mutants retained their green color under natural senescence and dark-induced senescence conditions. Genome-wide transcriptome analysis revealed that key senescence-associated genes (SGR, NYC1, OsNAC5, OsNAP, OsEIN3 and OsS3H) were differentially expressed in onac106-1D during dark-induced senescence. In addition to delayed senescence, onac106-1D also showed a salt stress-tolerant phenotype; key genes that down-regulate salt response signaling (OsNAC5, OsDREB2A, OsLEA3 and OsbZIP23) were rapidly up-regulated in onac106-1D under salt stress. Interestingly, onac106-1D also exhibited a wide tiller angle phenotype throughout development, and the tiller angle-related gene LPA1 was downregulated in onac106-1D. Using yeast one-hybrid assays, we found that ONAC106 binds to the promoter regions of SGR, NYC1, OsNAC5 and LPA1. Taking these results together, we propose that ONAC106 functions in leaf senescence, salt stress tolerance and plant architecture by modulating the expression of its target genes that function in each signaling pathway.OAIID:oai:osos.snu.ac.kr:snu2015-01/102/0000003606/12ADJUST_YN:NEMP_ID:A002118DEPT_CD:517CITE_RATE:4.931FILENAME:2015-13 onac106 (plant cell physiol)-sakuraba.pdfDEPT_NM:식물생산과학부SCOPUS_YN:YCONFIRM:

Study of enzyme-hydrolyzed soybean replacing fish meal and/or chicken meal on the growth of channel catfish (Ictalurus punctatus)

This study aimed to evaluate the effect of enzyme-hydrolyzed soybean (EHSB) to replace fish meal and chicken meal in channel catfish (Ictalurus punctatus) on the growth performance, serum biochemical indices and gastrointestinal structure of channel catfish. The channel catfish (initial weight: 21.25 ± 0.25 g) was fed four isonitrogenous, isolipidic and isophosphorous diets for 60 days. The control diet (CON group) contained 8% fish meal and 5% chicken meal. EHSB was used to replace fish meal (100%, RF group), chicken meal (100%, RC group), and 100% of fish meal and chicken meal (RFC group), respectively. The specific growth rate (SGR) and protein deposition rate (PR) of channel catfish in RF, RC and RFC groups were significantly increased compared to the control group and reached their peaks in RFC group (SGR: 2.92%, PR: 45.64%) (P  0.05). The catalase and alanine aminotransferase activities in serum were significantly decreased in replacement groups compared to the control group (P < 0.05). Besides, the activities of superoxide dismutase and aspartate aminotransferase in serum of channel catfish were remarkably increased in the RFC group (24.22 U/L and 193.00 U/L, respectively) (P < 0.05). The replacement of fish meal and chicken meal by EHSB, either alone or simultaneously, significantly increased the crude protein (51.68% in RC group) and crude lipid (31.27% in RFC group) in whole body of channel catfish (P < 0.05). The crude lipid in muscle of channel catfish was markedly increased in RF (16.31%, dry matter) and RFC groups (16.45%, dry matter) (P < 0.05). Replacement of fish meal and chicken meal by EHSB could significantly increase the intestinal villi length and intestinal wall thickness, thus improving the digestive capacity of channel catfish. The gastric epithelial cells in the RFC group were plumper and more structurally integrated than in the control group. In summary, replacing 100% of fish meal and 100% of chicken meal with EHSB could effectively improve the growth performance, antioxidation and digestive capacities of channel catfish

Inhibition of VEGF-C modulates distal lymphatic remodeling and secondary metastasis.

Tumor-associated lymphatics are postulated to provide a transit route for disseminating metastatic cells. This notion is supported by preclinical findings that inhibition of pro-lymphangiogenic signaling during tumor development reduces cell spread to sentinel lymph nodes (SLNs). However, it is unclear how lymphatics downstream of SLNs contribute to metastatic spread into distal organs, or if modulating distal lymph transport impacts disease progression. Utilizing murine models of metastasis, longitudinal in vivo imaging of lymph transport, and function blocking antibodies against two VEGF family members, we provide evidence that distal lymphatics undergo disease course-dependent up-regulation of lymph transport coincidental with structural remodeling. Inhibition of VEGF-C activity with antibodies against VEGF-C or NRP2 prevented these disease-associated changes. Furthermore, utilizing a novel model of adjuvant treatment, we demonstrate that antagonism of VEGF-C or NRP2 decreases post SLN metastasis. These data support a potential therapeutic strategy for inhibiting distant metastatic dissemination via targeting tumor-associated lymphatic remodeling

Characterization and Quantification of Luteolin-Metal Complexes in Aqueous Extract of Lonicerae Japonicae Flos and Huangshan Wild Chrysanthemum

Luteolin is a flavonoid compound widely found in vegetables, fruits, and medicinal plants. In this study, the reaction conditions for luteolin and five metal ions (Ca2+, Mg2+, Zn2+, Fe3+, and Cu2+) to form complexes in hot water were optimized, which was at a molar ratio of 1 : 1 for luteolin and metal ions at 90°C in a volume of 20 mL for 2 h, and the ability of luteolin to form complexes with Cu2+ was the strongest. The DPPH scavenging test showed that luteolin exerted a dose-dependent effect on the clearance of free radicals; luteolin-Cu2+ complexes and luteolin-Fe3+ complexes accentuated the clearance of free radicals. Furthermore, we used high performance liquid chromatography (HPLC) to analyze luteolin in samples from two medicinal plants, obtained from the dissolution of aqueous extracts in two different solvents. The results showed that the peak areas for luteolin in the samples dissolved in 20% formic acid-methanol were significantly larger than those from the samples dissolved in methanol alone, with increases in the peak area being 135.6% (Lonicerae Japonicae Flos), and 161.16% (Huangshan wild chrysanthemum). The aforementioned results indicate that complexes formed from organic compounds and metal ions are present in the decoction of a plant

Control of dynamic cell behaviors during angiogenesis and anastomosis by Rasip 1.

Organ morphogenesis is driven by a wealth of tightly orchestrated cellular behaviors, which ensure proper organ assembly and function. Many of these cell activities involve cell-cell interactions and remodeling of the F-actin cytoskeleton. Here, we analyze the requirement for Rasip1 (Ras-interacting protein 1), an endothelial-specific regulator of junctional dynamics, during blood vessel formation. Phenotype analysis of rasip1 mutants in zebrafish embryos reveal distinct functions of Rasip1 during sprouting angiogenesis, anastomosis and lumen formation. During angiogenic sprouting, loss of Rasip1 causes cell pairing defects due to a destabilization of tricellular junctions, indicating that stable tri-cellular junctions are essential to maintain multicellular organization within the sprout. During anastomosis, Rasip1 is required to establish a stable apical membrane compartment; rasip1 mutants display ectopic, reticulated junctions and the apical compartment is frequently collapsed. Loss of Ccm1 and Heg1 function mimics junctional defects of rasip1 mutants. Furthermore, downregulation of ccm1 and heg1 leads to a delocalization of Rasip1 at cell junctions, indicating that junctional tethering of Rasip1 is required for its function during junction formation and stabilization during sprouting angiogenesis

Control of dynamic cell behaviors during angiogenesis and anastomosis by Rasip1

Organ morphogenesis is driven by a wealth of tightly orchestrated cellular behaviors, which ensure proper organ assembly and function. Many of these cell activities involve cell-cell interactions and remodeling of the F-actin cytoskeleton. Here, we analyze the requirement for Rasip1 (Ras-interacting protein 1), an endothelial-specific regulator of junctional dynamics, during blood vessel formation. Phenotype analysis of rasip1 mutants in zebrafish embryos reveals distinct functions of Rasip1 during sprouting angiogenesis, anastomosis and lumen formation. During angiogenic sprouting, loss of Rasip1 causes cell pairing defects due to a destabilization of tricellular junctions, indicating that stable tricellular junctions are essential to maintain multicellular organization within the sprout. During anastomosis, Rasip1 is required to establish a stable apical membrane compartment; rasip1 mutants display ectopic, reticulated junctions and the apical compartment is frequently collapsed. Loss of Ccm1 and Heg1 function mimics the junctional defects of rasip1 mutants. Furthermore, downregulation of ccm1 and heg1 leads to a delocalization of Rasip1 at cell junctions, indicating that junctional tethering of Rasip1 is required for its function in junction formation and stabilization during sprouting angiogenesis

Hepatocytes express nerve growth factor during liver injury: evidence for paracrine regulation of hepatic stellate cell apoptosis

A key feature of recovery from liver fibrosis is hepatic stellate cell (HSC) apoptosis, which serves the dual function of removing the major source of neomatrix and tissue inhibitors of metalloproteinases thereby facilitating matrix degradation. The mechanisms regulating HSC apoptosis remain undefined but may include the interaction of nerve growth factor (NGF) with its receptor, p75, on HSC. In this study, by TaqMan polymerase chain reaction in situ hybridization and immunohistochemistry, we demonstrate that NGF is expressed by hepatocytes during fibrotic injury. Peak hepatocyte expression of NGF (48 hours after CCl4 injection) coincides with maximal rate of apoptosis of HSC by terminal dUTP nick-end labeling staining. Addition of recombinant NGF to HSC in tissue culture causes a dose-dependent increase in apoptosis. NGF regulates nuclear factor (NF)-?B activity, reducing p50/p65 binding detected by electromobility shift assay and reduced NF-?B CAT reporter activities from both basal unstimulated levels and after NF-?B induction by tumor necrosis factor. In each case, a relative reduction in NF-?B binding was associated with a significant increase in caspase 3 activity. These data provide evidence that NGF is expressed during fibrotic liver injury and may regulate number of activated HSCs via induction of apoptosis