Fig. 3. LTB4 exhibits concentration-dependent effects on HLEC lymphangiogenesis and survival. LTB4 exhibits concentration-dependent effects on HLEC lymphangiogenesis.

Slides:

Advertisements

Similar presentations

From: Administration of Menadione, Vitamin K3, Ameliorates Off-Target Effects on Corneal Epithelial Wound Healing Due to Receptor Tyrosine Kinase Inhibition.

Advertisements

MicroRNA-101 Inhibits Growth, Proliferation and Migration and Induces Apoptosis of Breast Cancer Cells by Targeting Sex-Determining Region Y-Box 2 Cell.

Molecular Therapy - Nucleic Acids

Journal of Ginseng Research

Volume 18, Issue 6, Pages (December 2010)

Interleukin-33 induces angiogenesis and vascular permeability through ST2/TRAF6-mediated endothelial nitric oxide production by Yeon-Sook Choi, Hyun-Jung.

LTB4 production is elevated in preclinical and clinical lymphedema

Fig. 4. Primary human metastatic melanomas contain CCL21-expressing LECs, and expression of VEGFC positively correlates with hallmarks of tumor inflammation.

Sphingosine-1-phosphate promotes lymphangiogenesis by stimulating S1P1/Gi/PLC/Ca2+ signaling pathways by Chang Min Yoon, Bok Sil Hong, Hyung Geun Moon,

Fig. 1. Potent and selective down-regulation of KRAS mRNA and protein by AZD4785 in vitro and in vivo. Potent and selective down-regulation of KRAS mRNA.

Fig. 5. Blocking LTB4 during initial lymphangiogenesis period abrogates the therapeutic benefit of LTB4 antagonism. Blocking LTB4 during initial lymphangiogenesis.

Fig. 5. Circulating PPi concentration does not correlate with severity of calcification phenotype in mice. Circulating PPi concentration does not correlate.

Fig. 4. Intramuscular injection of AAV9-Cas9/sgRNA-51 corrects dystrophin expression. Intramuscular injection of AAV9-Cas9/sgRNA-51 corrects dystrophin.

A FOXO3a-BIM cascade mediates sensitivity to PARP and MEK inhibition

Fig. 2. Bestatin treatment improves tail anatomy and restores lymphatic function. Bestatin treatment improves tail anatomy and restores lymphatic function.

Fig. 4. Bexarotene promotes PPARδ activation of target genes in mouse brain and muscle. Bexarotene promotes PPARδ activation of target genes in mouse brain.

Fig. 2. Mechanism of PD-L1 down-regulation in NOD HSPCs.

Fig. 1. Ketoprofen efficacy in a preclinical model of lymphedema can be attributed to its inhibition of LTB4. Ketoprofen efficacy in a preclinical model.

Fig. 1. BCAS1 expression identifies newly generated oligodendrocytes.

Functions of Rhomboid Family Protease RHBDL2 and Thrombomodulin in Wound Healing Tsung-Lin Cheng, Yu-Ting Wu, Hung-Yu Lin, Fu-Chih Hsu, Shi-Kai Liu,

Fig. 6. Combinatorial VCPI and OV M1 treatment is efficacious in vivo and ex vivo. Combinatorial VCPI and OV M1 treatment is efficacious in vivo and ex.

Fig. 4. Biomechanical properties of treated tibiae.

Synergistic effect of S63845 with lapatinib, trastuzumab, or docetaxel

Fig. 8. In vivo suppression of MM by CMLD

Fig. 3. BET inhibition reduces homologous recombination.

Fig. 3. A circadian rhythm in fibroblast wound-healing response.

MRSA virulence proteins cause LMC death and diminished CLV function

Fig. 8. mRIPO elicits neutrophil influx followed by DC and T cell infiltration into tumors. mRIPO elicits neutrophil influx followed by DC and T cell infiltration.

Fig. 4 Infection-induced CLV dysfunction is associated with decreased LMC coverage. Infection-induced CLV dysfunction is associated with decreased LMC.

Volume 18, Issue 6, Pages (December 2010)

Fig. 5. Antitumor efficacy of ERY974 in immunocompetent human CD3 transgenic mice. Antitumor efficacy of ERY974 in immunocompetent human CD3 transgenic.

Fig. 3. Wisper controls CF behavior and survival.

Fig. 1 Chemical inactivation of BPL kills Mtb and prevents growth in mouse macrophages. Chemical inactivation of BPL kills Mtb and prevents growth in mouse.

Fig. 4. Antitumor efficacy of ERY974 against various cancer types.

Fig. 3 Biological function of TG2 and the interaction with MT-2.

Fig. 5. Remnants of PS+ platelets induce neutrophil macroaggregation.

Fig. 7 Gel scaffold for inhibition of postsurgical recurrence of B16F10 tumors. Gel scaffold for inhibition of postsurgical recurrence of B16F10 tumors.

Fig. 6. A circadian rhythm in keratinocyte wound healing and a diurnal variation in human burn healing outcome. A circadian rhythm in keratinocyte wound.

Fig. 1. Muscles of LAMA2 MD patients and dyW/dyW mice contain high amounts of laminin-α4 and show deficits in BM. Muscles of LAMA2 MD patients and dyW/dyW.

Fig. 6. Apoptotic MSCs exert in vivo immunosuppression in a TH2-type inflammation model in the absence of cytotoxic cells. Apoptotic MSCs exert in vivo.

Fig. 4. Expression of HGF in liver ECs cooperates with NOX4 inhibition to enhance engraftment of regenerative hepatocytes. Expression of HGF in liver ECs.

Fig. 4. Actin polymerization rhythms are required for circadian regulation of adhesion and wound-healing efficacy by fibroblasts. Actin polymerization.

Fig. 2. Circulating VEGF in GCA patients up-regulates microvascular endothelial Jagged1. Circulating VEGF in GCA patients up-regulates microvascular endothelial.

Fig. 7 BRD0705 impairs colony formation in AML cell lines and patient cells and shows in vivo efficacy in multiple AML mouse models. BRD0705 impairs colony.

Fig. 2. Resistance to S63845-induced apoptosis through loss of BAK or elevated BCL-XL. Resistance to S63845-induced apoptosis through loss of BAK or elevated.

Fig. 1. Drug combination screen identifies BETi as acting synergistically with PARPi. Drug combination screen identifies BETi as acting synergistically.

Nec‐1 inhibits the phosphorylation and aggregation of tau

Fig. 2. Binding of recombinant full-length Lm-411 to muscle receptors, myotubes, and self-polymerization is enhanced by mag and αLNNd. Binding of recombinant.

Fig. 5 Local gel scaffold for T cell memory response.

Fig. 2 Fas controls IL-1RA–sEV secretion in murine MSCs.

Fig. 1 BX795 suppresses HSV-1 infection.

Fig. 8 SQLE inhibitor terbinafine suppresses NAFLD-HCC growth in vitro and in vivo. SQLE inhibitor terbinafine suppresses NAFLD-HCC growth in vitro and.

Fig. 5. Nutlin-3 treatment rescues the proliferation and differentiation of NPCs in vitro. Nutlin-3 treatment rescues the proliferation and differentiation.

Fig. 1. Bexarotene promotes PPARδ activation to ameliorate the neurotoxicity of mutant huntingtin. Bexarotene promotes PPARδ activation to ameliorate the.

Fig. 2 In vitro and preclinical study with 18F-MPG.

Bexarotene is neuroprotective in mouse and human HD neurons in vitro

Fig. 4. Acute lung injury in miR-223−/y mice.

Fig. 3 CSF1 is expressed in human melanoma.

Fig. 6 DMF inhibits NF-κB translocation upon infection.

JAK2 knockdown abrogates tumorsphere expansion after chemotherapy

Fig. 1 LB100 and LB102 specifically inhibit PP2A phosphatase activity and the growth of BCR-ABL+ cells. LB100 and LB102 specifically inhibit PP2A phosphatase.

Correlation of reovirus RNA/protein with proliferating tumor cells

Fig. 6 Combination therapy with LVSOD2 and LVshCTGF preserves flap volume and reduces fibrosis after RT. Combination therapy with LVSOD2 and LVshCTGF preserves.

Fig. 4 ALRN-6924 inhibits cellular proliferation and clonogenic capacity, and induces cell cycle arrest and apoptosis in AML cell lines. ALRN-6924 inhibits.

PERK signaling is constitutively activated upon EMT and promotes malignancy. PERK signaling is constitutively activated upon EMT and promotes malignancy.

Fig. 2. BET inhibition enhances PARPi-induced DNA damage.

Tsg protein stimulates endothelial cell migration, proliferation and collagen gel spheroid sprouting. Tsg protein stimulates endothelial cell migration,

LTB4 production is elevated in preclinical and clinical lymphedema

Volume 15, Issue 2, Pages (February 2007)

Fig. 6. Combinatorial VCPI and OV M1 treatment is efficacious in vivo and ex vivo. Combinatorial VCPI and OV M1 treatment is efficacious in vivo and ex.

Presentation transcript:

Fig. 3. LTB4 exhibits concentration-dependent effects on HLEC lymphangiogenesis and survival. LTB4 exhibits concentration-dependent effects on HLEC lymphangiogenesis and survival. (A) Representative images of HLEC network formation, fibrin gel sprouting, and 3D spheroid sprouting assays. HLECs were treated with various concentrations of LTB4: 5.0 to 10 nM LTB4 has prolymphangiogenic activity, and 200 to 400 nM is the antilymphangiogenic concentration. Scale bars, 100 or 25 μm, as indicated; n = 5. (B to E) Quantitative analysis of (A). (F to I) Quantitative analysis of HLECs subjected to VEGF-C (50 ng/ml) and 400 nM LTB4 with or without 10 μM U75302 (a BLT1 inhibitor) or lentiviral shLtb4r1 in network formation, migration, wound healing, and fibrin gel sprouting assays in fig. S6B. Lentiviral short hairpin RNA (shRNA) transduction particles targeting turbo green fluorescent protein (shGFP) were used as controls; n = 5. (J) Quantification of Matrigel plug assay in fig. S6F. Growth factor–reduced Matrigel containing HLECs pretreated with VEGF-C (50 ng/ml) and 400 nM LTB4 with or without 10 μM U75302 was injected subcutaneously into SCID mice. Lymphangiogenesis in vivo was determined as percentage of lymphatic vascular area; n = 5. (K) Analysis of HLEC viability, apoptosis, and cytotoxicity 24 hours after LTB4 culture; n = 6. (L) Western blotting of cleaved caspase 3 in HLECs; n = 3. In (B) to (J) and (L), data are presented as means and SEM; comparisons with the control groups were made using Kruskal-Wallis test followed by Dunn’s multiple comparisons test for post hoc analyses. In (K), mean fluorescence readings are shown. Wen Tian et al., Sci Transl Med 2017;9:eaal3920 Published by AAAS