scholarly journals Juxtaposition between two cell types is necessary for dorsal appendage tube formation

2005 ◽  
Vol 122 (2) ◽  
pp. 241-255 ◽  
Author(s):  
Ellen J. Ward ◽  
Celeste A. Berg
Keyword(s):  
Cell Types ◽  
Tube Formation ◽  
Dorsal Appendage

scholarly journals Developmental decisions in Aspergillus nidulans are modulated by Ras activity.

1994 ◽  
Vol 14 (8) ◽  
pp. 5333-5348 ◽  
Author(s):  
T Som ◽  
V S Kolaparthi
Keyword(s):  
Aspergillus Nidulans ◽  
Essential Gene ◽  
Cell Types ◽  
Tube Formation ◽  
Stage Of Development ◽  
Initial Stage ◽  
Concentration Threshold ◽  
High Level ◽  
Multicellular Organisms ◽  
Further Development

To better understand how Ras controls development of multicellular organisms, we have chosen Aspergillus nidulans as a model system. When grown on solid medium, this fungus follows a well-defined program of development, sequentially giving rise to several cell types which produce three distinct structures: vegetative hyphae, aerial hyphae, and the conidiophore structure. Here we describe a ras homolog found in this fungus (Aras) and demonstrate that it is an essential gene that regulates the ordered program of development. We created dominant alleles of this gene and expressed them to different levels in order to vary the ratio of GTP-bound (active) to GDP-bound (inactive) A-Ras protein. When the amount of active Ras is large, nuclear division proceeds, but further development is inhibited at the early step of germ tube formation. At an intermediate level of active Ras, aerial hypha formation is inhibited, while at a low level, conidiophore formation is inhibited. Maintenance of an even lower level of the active Ras is essential for initiation and progression of conidiophore formation, the final stage of development. When the level of active Ras is artificially lowered, each stage of development is initiated prematurely except germination, the initial stage of development. Therefore, the progression of the ordered developmental pathway of A. nidulans is dependent upon an initial high level of active Ras followed by its gradual decrease. We propose that several concentration threshold exist, each of which allows development to proceed to a certain point, producing the proper cell type while inhibiting further development.

scholarly journals TTF1, in the Form of Nanoparticles, Inhibits Angiogenesis, Cell Migration and Cell Invasion in VitroandIn Vivoin Human Hepatoma through STAT3 Regulation

2016 ◽  
Author(s):  
Bin Xiao ◽  
Dongjing Lin ◽  
Xuan Zhang ◽  
Meilan Zhang ◽  
Xuewu Zhang
Keyword(s):  
Cell Migration ◽  
Cancer Cell ◽  
Hepg2 Cells ◽  
Binding Capacity ◽  
Hepatocellular Cancer ◽  
Cell Types ◽  
Tube Formation ◽  
Migration And Invasion ◽  
Nude Mouse Model ◽  
Anti Cancer

TTF1-NP(5,2′,4′-trihydroxy-6,7,5′-trimethoxyflavone nanoparticles), derived from the traditional Changbai Mountain medicinal plant Sorbaria sorbifolia (SS), has been showedits anti-cancer effect in various liver cancer cell types and tissues. The present study was designed to evaluate the antitumor mechanism of the TTF1-NP against HepG2 hepatoma cells and HepG2 cells-induced hepatocarcinoma (HCC) in nude mouse model. Here we demonstrated that TTF1-NP inhibits tube formation of HUVECs and HepG2 cell migration and invasion, and inhibits tumor growth in nude mice implanted with HepG2 cells through the downregulation of STAT3 protein and activation, along with VEGF, KDR, bFGF, MMP2 and MMP9 levels. We further revealed that TTF1-NP decreased the DNA-binding capacity of STAT3. Together our results provide a mechanism by which TTF1-NP suppresses cancer cell migration, invasion and angiogenesis through the action of STAT3 and suggests TTF1-NP as a potential therapy for hepatocellular cancer treatment.

scholarly journals Endothelial tubulogenesis within fibrin gels specifically requires the activity of membrane-type-matrix metalloproteinases (MT-MMPs)

2002 ◽  
Vol 115 (17) ◽  
pp. 3427-3438 ◽  
Author(s):  
Marc A. Lafleur ◽  
Madeleine M. Handsley ◽  
Vera Knäuper ◽  
Gillian Murphy ◽  
Dylan R. Edwards
Keyword(s):  
Growth Factor ◽  
Cell Types ◽  
Tube Formation ◽  
Matrix Metalloproteinase 2 ◽  
Mrna Levels ◽  
Fibrin Gels ◽  
Fibrin Matrix ◽  
Inhibition Of Angiogenesis ◽  
Membrane Type ◽  
Endothelial Growth Factor

Macro- and microvascular endothelial cells (EC) formed tubular structures when cultured within a 3D fibrin matrix, a process that was enhanced by vascular endothelial growth factor (VEGF), fibroblast growth factor-2 (FGF-2),hepatocyte growth factor/scatter factor (HGF/SF) and an angiogenic cocktail composed of nine angiogenic factors. Endothelial tubulogenesis was also increased in co-culture with tumour cells such as U87 glioma cells, but not with non-tumorigenic cell types such as Madin-Darby canine kidney (MDCK)epithelial cells. VEGF/FGF-2-stimulated tube formation was dependent on metalloproteinase function [it is inhibited by the addition of tissue inhibitor of metalloproteinases-2 (TIMP-2)], whereas aprotinin, E64[trans-epoxysuccinyl-L-leucylamido (4-guanidino)-butane] and pepstatin had no effect. In addition, TIMP-4 also inhibited tubulogenesis, but TIMP-1 or the C-terminal haemopexin domain of matrix metalloproteinase-2 (MMP-2) (PEX) and an anti-MMP-2 function-blocking antibody were unable to block tube formation. This suggests that MMP-2 and other soluble MMPs are not essential for tubulogenesis in fibrin gels, instead TIMP-1-insensitive MMPs, such as members of the membrane type-MMPs (MT-MMP) sub-group (MT1-, MT2-, MT3- or MT5-MMP),are required for this process. Further support for a role for MT1-MMP in endothelial tubulogenesis is that recombinant Y36G N-terminal TIMP-2 mutant protein, which retains an essentially unaltered apparent inhibition constant(Kiapp) for several MMPs compared to wild-type N-TIMP-2 but is a 40-fold poorer inhibitor of MT1-MMP, was unable to block tubulogenesis. Furthermore, when EC were cultured within fibrin gels, the mRNA levels of several MMPs (including MT1-MMP, MT2-MMP, MT3-MMP and MMP-2)increased during tubulogenesis. Therefore MT-MMPs and specifically MT1-MMP are likely candidates for involvement during endothelial tubulogenesis within a fibrin matrix, and thus their blockade may be a viable strategy for inhibition of angiogenesis.

scholarly journals Detecting New Allies: Modifier Screen Identifies a Genetic Interaction Between Imaginal disc growth factor 3 and combover, a Rho-kinase Substrate, During Dorsal Appendage Tube Formation in Drosophila

2020 ◽  
Vol 10 (10) ◽  
pp. 3585-3599
Author(s):  
Claudia Y. Espinoza ◽  
Celeste A. Berg
Keyword(s):  
Growth Factor ◽  
Imaginal Disc ◽  
Genetic Interaction ◽  
Genetic Modifier ◽  
Rho Kinase ◽  
Tube Formation ◽  
Apical Surface ◽  
Link Type ◽  
Dorsal Appendage ◽  
Cell Intercalation

Biological tube formation underlies organ development and, when disrupted, can cause severe birth defects. To investigate the genetic basis of tubulogenesis, we study the formation of Drosophila melanogaster eggshell structures, called dorsal appendages, which are produced by epithelial tubes. Previously we found that precise levels of Drosophila Chitinase-Like Proteins (CLPs), encoded by the Imaginal disc growth factor (Idgf) gene family, are needed to regulate dorsal-appendage tube closure and tube migration. To identify factors that act in the Idgf pathway, we developed a genetic modifier screen based on the finding that overexpressing Idgf3 causes dorsal appendage defects with ∼50% frequency. Using a library of partially overlapping heterozygous deficiencies, we scanned chromosome 3L and found regions that enhanced or suppressed the Idgf3-overexpression phenotype. Using smaller deletions, RNAi, and mutant alleles, we further mapped five regions and refined the interactions to 58 candidate genes. Importantly, mutant alleles identified combover (cmb), a substrate of Rho-kinase (Rok) and a component of the Planar Cell Polarity (PCP) pathway, as an Idgf3-interacting gene: loss of function enhanced while gain of function suppressed the dorsal appendage defects. Since PCP drives cell intercalation in other systems, we asked if cmb/+ affected cell intercalation in our model, but we found no evidence of its involvement in this step. Instead, we found that loss of cmb dominantly enhanced tube defects associated with Idgf3 overexpression by expanding the apical area of dorsal appendage cells. Apical surface area determines tube volume and shape; in this way, Idgf3 and cmb regulate tube morphology.

Developmental decisions in Aspergillus nidulans are modulated by Ras activity

1994 ◽  
Vol 14 (8) ◽  
pp. 5333-5348
Author(s):  
T Som ◽  
V S Kolaparthi
Keyword(s):  
Aspergillus Nidulans ◽  
Essential Gene ◽  
Cell Types ◽  
Tube Formation ◽  
Stage Of Development ◽  
Initial Stage ◽  
Concentration Threshold ◽  
High Level ◽  
Multicellular Organisms ◽  
Further Development

To better understand how Ras controls development of multicellular organisms, we have chosen Aspergillus nidulans as a model system. When grown on solid medium, this fungus follows a well-defined program of development, sequentially giving rise to several cell types which produce three distinct structures: vegetative hyphae, aerial hyphae, and the conidiophore structure. Here we describe a ras homolog found in this fungus (Aras) and demonstrate that it is an essential gene that regulates the ordered program of development. We created dominant alleles of this gene and expressed them to different levels in order to vary the ratio of GTP-bound (active) to GDP-bound (inactive) A-Ras protein. When the amount of active Ras is large, nuclear division proceeds, but further development is inhibited at the early step of germ tube formation. At an intermediate level of active Ras, aerial hypha formation is inhibited, while at a low level, conidiophore formation is inhibited. Maintenance of an even lower level of the active Ras is essential for initiation and progression of conidiophore formation, the final stage of development. When the level of active Ras is artificially lowered, each stage of development is initiated prematurely except germination, the initial stage of development. Therefore, the progression of the ordered developmental pathway of A. nidulans is dependent upon an initial high level of active Ras followed by its gradual decrease. We propose that several concentration threshold exist, each of which allows development to proceed to a certain point, producing the proper cell type while inhibiting further development.

scholarly journals Characterization of Heparin Affin Regulatory Peptide Signaling in Human Endothelial Cells

2005 ◽  
Vol 280 (23) ◽  
pp. 22454-22461 ◽  
Author(s):  
Apostolos Polykratis ◽  
Panagiotis Katsoris ◽  
José Courty ◽  
Evangelia Papadimitriou
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Tyrosine Phosphatase ◽  
Neuronal Cell ◽  
Cell Types ◽  
Tube Formation ◽  
Regulatory Peptide ◽  
Intracellular Signals ◽  
Umbilical Vein Endothelial Cells ◽  
Interfering Rna

Heparin affin regulatory peptide (HARP) is an 18-kDa secreted growth factor that has a high affinity for heparin and a potent role on tumor growth and angiogenesis. We have previously reported that HARP is mitogenic for different types of endothelial cells and also affects cell migration and differentiation (12). In this study we examined the signaling pathways involved in the migration and tube formation on matrigel of human umbilical vein endothelial cells (HUVEC) induced by HARP. We report for the first time that receptor-type protein-tyrosine phosphatase β/ζ (RPTPβ/ζ), which is a receptor for HARP in neuronal cell types, is also expressed in HUVEC. We also document that HARP signaling through RPTPβ/ζ leads to activation of Src kinase, focal adhesion kinase, phosphatidylinositol 3-kinase, and Erk1/2. Sodium orthovanadate, chondroitin sulfate-C, PP1, wortmannin, LY294002, and U0126 inhibit HARP-mediated signaling and HUVEC migration and tube formation. In addition, RPTPβ/ζ suppression using small interfering RNA technology interrupts intracellular signals and HUVEC migration and tube formation induced by HARP. These results establish the role of RPTPβ/ζ as a receptor of HARP in HUVEC and elucidate the HARP signaling pathway in endothelial cells.

scholarly journals Mesenchymal Stromal Cells Support Endometriotic Stromal CellsIn Vitro

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Fawaz Abomaray ◽  
Sebastian Gidlöf ◽  
Bartosz Bezubik ◽  
Mikael Engman ◽  
Cecilia Götherström
Keyword(s):  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Inflammatory Diseases ◽  
Umbilical Vein ◽  
Cell Types ◽  
Tube Formation ◽  
Migration And Invasion ◽  
Endometrial Cells ◽  
Umbilical Vein Endothelial Cells

Endometriosis is an inflammatory disease marked by ectopic growth of endometrial cells. Mesenchymal stromal cells (MSC) have immunosuppressive properties that have been suggested as a treatment for inflammatory diseases. Therefore, the aim herein was to examine effects of allogeneic MSC on endometriosis-derived cellsin vitroas a potential therapy for endometriosis. MSC from allogeneic adipose tissue (Ad-MSC) and stromal cells from endometrium (ESCendo) and endometriotic ovarian cysts (ESCcyst) from women with endometriosis were isolated. The effects of Ad-MSC on ESCendoand ESCcystwere investigated usingin vitroproliferation, apoptosis, adhesion, tube formation, migration, and invasion assays. Ad-MSC significantly increased proliferation of ESC compared to untreated controls. Moreover, Ad-MSC significantly decreased apoptosis and increased survival of ESC. Ad-MSC significantly increased adhesion of ESCendoand not ESCcyston fibronectin. Conditioned medium from cocultures of Ad-MSC and ESC significantly increased tube formation of human umbilical vein endothelial cells on matrigel. Ad-MSC may significantly increase migration of ESCcystand did not increase invasion of both cell types. The data suggest that allogeneic Ad-MSC should not be considered as a potential therapy for endometriosis, because they may support the pathology by maintaining and increasing growth of ectopic endometrial tissue.

scholarly journals Evidence of Amniotic Epithelial Cell Differentiation toward Hepatic Sinusoidal Endothelial Cells

2018 ◽  
Vol 27 (1) ◽  
pp. 23-30 ◽  
Author(s):  
Monica Serra ◽  
Michela Marongiu ◽  
Antonella Contini ◽  
Toshio Miki ◽  
Erika Cadoni ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Regenerative Medicine ◽  
Cell Cycle Progression ◽  
Cell Types ◽  
Tube Formation ◽  
Sinusoidal Endothelial Cells ◽  
Liver Repopulation ◽  
Hepatic Sinusoidal Endothelial Cells

Amniotic epithelial cells (AECs) represent a useful and noncontroversial source for liver-based regenerative medicine, as they can differentiate into hepatocytes upon transplantation into the liver. However, the possibility that AECs can differentiate into other liver cell types, such as hepatic sinusoidal endothelial cells (HSECs), has never been assessed. In order to test this hypothesis, rat- and human-derived AECs (rAECs and hAECs, respectively) were subjected to endothelial cell tube formation assay in vitro. Moreover, to evaluate differentiation in vivo, the retrorsine (RS) model of liver repopulation was used. Pyrrolizidine alkaloids (including RS) are known to target both hepatocytes and endothelial cells, inducing cell enlargement and inhibition of cell cycle progression. rAECs and hAECs were able to form capillary-like structures when cultured under proangiogenic conditions. For in vivo experiments, rAECs were obtained from dipeptidyl peptidase type IV (DPP-IV, CD26) donors and were transplanted into the liver of recipient CD26 negative animals pretreated with RS. rAEC-derived cells were engrafted in between hepatocytes and resembled HSECs as assessed by morphological analysis and the pattern of expression of CD26. Donor-derived CD26+ cells coexpressed HSEC markers RECA-1 and SE-1, while they lacked expression of typical hepatocyte markers (i.e., cytochrome P450, hepatocyte nuclear factor 4α). As such, these results provide the first evidence that AECs can respond to proangiogenic signals in vitro and differentiate into HSECs in vivo. Furthermore, they support the conclusion that AECs possesses great plasticity and represents a promising tool in the field of regenerative medicine both in the liver and in other organs.

Pericardin, aDrosophilatype IV collagen-like protein is involved in the morphogenesis and maintenance of the heart epithelium during dorsal ectoderm closure

Development ◽  
2002 ◽  
Vol 129 (13) ◽  
pp. 3241-3253 ◽  
Author(s):  
Aymeric Chartier ◽  
Stéphane Zaffran ◽  
Martine Astier ◽  
Michel Sémériva ◽  
Danielle Gratecos
Keyword(s):  
Extracellular Matrix ◽  
Matrix Protein ◽  
Cell Types ◽  
Tube Formation ◽  
Extracellular Matrix Protein ◽  
Heart Cells ◽  
Dorsal Closure ◽  
Heart Tube ◽  
Pericardial Cells ◽  
Dorsal Ectoderm

The steps that lead to the formation of a single primitive heart tube are highly conserved in vertebrate and invertebrate embryos. Concerted migration of the two lateral cardiogenic regions of the mesoderm and endoderm (or ectoderm in invertebrates) is required for their fusion at the midline of the embryo. Morphogenetic signals are involved in this process and the extracellular matrix has been proposed to serve as a link between the two layers of cells.Pericardin (Prc), a novel Drosophila extracellular matrix protein is a good candidate to participate in heart tube formation. The protein has the hallmarks of a type IV collagen α-chain and is mainly expressed in the pericardial cells at the onset of dorsal closure. As dorsal closure progresses, Pericardin expression becomes concentrated at the basal surface of the cardioblasts and around the pericardial cells, in close proximity to the dorsal ectoderm. Pericardin is absent from the lumen of the dorsal vessel.Genetic evidence suggests that Prc promotes the proper migration and alignment of heart cells. Df(3)vin6 embryos, as well as embryos in which prc has been silenced via RNAi, exhibit similar and significant defects in the formation of the heart epithelium. In these embryos, the heart epithelium appears disorganized during its migration to the dorsal midline. By the end of embryonic development, cardial and pericardial cells are misaligned such that small clusters of both cell types appear in the heart; these clusters of cells are associated with holes in the walls of the heart. A prc transgene can partially rescue each of these phenotypes, suggesting that prc regulates these events. Our results support, for the first time, the function of a collagen-like protein in the coordinated migration of dorsal ectoderm and heart cells.

The fine structure of Entomophthora apiculata and its penetration of Trichoplusia ni

1977 ◽  
Vol 23 (4) ◽  
pp. 452-464 ◽  
Author(s):  
James T. Lambiase ◽  
William G. Yendol
Keyword(s):  
Fine Structure ◽  
Trichoplusia Ni ◽  
Germ Tube ◽  
Cell Types ◽  
Body Cavity ◽  
Tube Formation ◽  
Cabbage Looper ◽  
Wall Structure ◽  
Entomogenous Fungus ◽  
Resting Spores

The fine structure of conidia and immature resting spores of the entomogenous fungus Entomophthora apiculata is described. The two cell types contain comparable organelles and quantities of lipid, and possess a similar cell wall structure. The large quantity of stored lipid and numerous mitochondria in each cell type indicate a capacity for great metabolic activity. Numerous dense, microbody-like organelles were observed in conidia and resting spores, and their possible functions are discussed.Third instar larvae of the cabbage looper Trichoplusia ni were exposed to conidia of E. apiculata. Fungal germ tube formation and penetration of the host integument were observed. The germ tubes did not form appressoria and appeared to penetrate the epicuticle by enzymatic and physical means. After penetration of the epicuticle the germ tube often bifurcates, and expands as two or more digit-like projections parallel to the lamellae of the exocuticle. The hyphae gradually extend inward, cleaving the lamellae of cuticle, and eventually enter the host's body cavity.

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