Regions Of Cell Proliferation Research Articles

Angiolipoma in a Dog

Background: Angiolipoma is a benign tumor composed of endothelial cells and mature adipocytes. Tumors reported in domestic species include two variants; infiltrative or non-infiltrative. Bitches and intact males seem predisposed. This mesenchyme tumor is commonly mistaken with lipoma due to its soft texture and subcutaneous site and often requires histopathology to confirm its diagnosis. Microscopic examination also enables the evaluation of surgical margins and rule out possible infiltrative sites. Complete surgical excision is usually curative. This study reports a case of non-infiltrating angiolipoma in a dog.Case: A 14-year-old mixed-breed dog was presented to a veterinary clinic in the city of Rio de Janeiro, RJ, Brazil. On palpation, a painless mass was noted, with high mobility and covered by intact hirsute skin in the right subcutaneous ventrolateral region. Computed tomography of the chest showed an expansive mass of uptake only from the edges of the soft tissues of the right subcutaneous ventrolateral region. The mass was homogeneous and well delimited, suggesting a neoplastic process. Subsequently, the mass was surgically removed, fixed in 10% buffered formalin, and sent for histopathological analysis. On macroscopic examination, the mass was well delimited, without skin coverage, and measured 2.3 × 1.9 × 0.6 cm. The consistency was smooth and unctuous in appearance with a compact cream-colored surface with blackish multifocal spots. Under microscopy, the histological sections showed neoplasm of mature adipocytes and of endothelial cells of blood vessels benign were filled with a marked amount of red blood cells. Multifocal fibrin thrombi and a mild inflammatory infiltrate composed of lymphocytes and rare mast cells were evident. There was no infiltration in the regional skeletal musculature. Thus, a diagnosis of non-infiltrative angiolipoma was established.Discussion: The diagnosis of non-infiltrating angiolipoma in this case was established through the results of histopathological examination. The occurrence of this neoplasm in dogs is uncommon, and the data reported in the veterinary medicine literature are scarce. However, in this study, it was found that the neoplasm on screening presented a behavior like that of lipomas, with noninvasive growth and the absence of local recurrence. The canine species does not commonly convey pain on palpation during a clinical examination, as observed in the present case. In humans, multiple angiolipoma nodules are common; this clinical presentation differs from that in animals, in which solitary nodules are generally observed. In dogs, as in the present case, they seem to have a predilection for the trunk. In animals, the pathogenesis of angiolipomas is not established, but in humans, it is based on theories that include the reaction to harmful stimuli and congenital malformation of adipose tissue. In humans, the presence of fibrin thrombi on the periphery of the region of cell proliferation are microscopic findings that can assist in the diagnosis of angiolipomas, an approach that was implemented in the present case. The occurrence of this neoplasm in dogs is uncommon, and the data reported in the veterinary medicine literature are scarce. The importance of an adequate description of angiolipomas is based on the need to provide information about its epidemiology, biological behavior, and prognosis.

A gibberellin-stimulated transcript, OsGASR1, controls seedling growth and α-amylase expression in rice

From a T-DNA-tagging population in rice, we identified OsGASR1 (LOC_Os03g55290), a member of the GAST (gibberellin (GA)-Stimulated Transcript) family that is induced by salt stress and ABA treatment. This gene was highly expressed in the regions of cell proliferation and panicle development, as revealed by a GUS assay of the mutant line. In the osgasr1 mutants, the second leaf blades were much longer than those of the segregating wild type due to an increase in cell length. In addition, five α-amylase genes were up-regulated in the mutants, implying that OsGASR1 is a negative regulator of those genes. These results suggest that OsGASR1 plays important roles in seedling growth and α-amylase gene expression.

A multi-scale model of the interplay between cell signalling and hormone transport in specifying the root meristem of Arabidopsis thaliana

The growth of the root of Arabidopsis thaliana is sustained by the meristem, a region of cell proliferation and differentiation which is located in the root apex and generates cells which move shootwards, expanding rapidly to cause root growth. The balance between cell division and differentiation is maintained via a signalling network, primarily coordinated by the hormones auxin, cytokinin and gibberellin. Since these hormones interact at different levels of spatial organisation, we develop a multi-scale computational model which enables us to study the interplay between these signalling networks and cell–cell communication during the specification of the root meristem. We investigate the responses of our model to hormonal perturbations, validating the results of our simulations against experimental data. Our simulations suggest that one or more additional components are needed to explain the observed expression patterns of a regulator of cytokinin signalling, ARR1, in roots not producing gibberellin. By searching for novel network components, we identify two mutant lines that affect significantly both root length and meristem size, one of which also differentially expresses a central component of the interaction network (SHY2). More generally, our study demonstrates how a multi-scale investigation can provide valuable insight into the spatio-temporal dynamics of signalling networks in biological tissues.

The Recessive Epigenetic swellmap Mutation Affects the Expression of Two Step II Splicing Factors Required for the Transcription of the Cell Proliferation Gene STRUWWELPETER and for the Timing of Cell Cycle Arrest in the Arabidopsis Leaf

Generally, cell division can be uncoupled from multicellular development, but more recent evidence suggests that cell cycle progression and arrest is coupled to organogenesis and growth. We describe a recessive mutant, swellmap (smp), with reduced organ size and cell number. This defect is partially compensated for by an increase in final cell size. The mutation causes a precocious arrest of cell proliferation in the organ primordium and possibly reduces the rate of cell division there. The mutation proved to be an epigenetic mutation (renamed smp(epi)) that defined a single locus, SMP1, but affected the expression of both SMP1 and a second very similar gene, SMP2. Both genes encode CCHC zinc finger proteins with similarities to step II splicing factors involved in 3' splice site selection. Genetic knockouts demonstrate that the genes are functionally redundant and essential. SMP1 expression is associated with regions of cell proliferation. Overexpression of SMP1 produced an increase in organ cell number and a partial decrease in cell expansion. The smp(epi) mutation does not affect expression of eukaryotic cell cycle regulator genes CYCD3;1 and CDC2A but affects expression of the cell proliferation gene STRUWWELPETER (SWP) whose protein has similarities to Med150/Rgr1-like subunits of the Mediator complex required for transcriptional activation. Introduction of SWP cDNA into smp(epi) plants fully restored them to wild-type, but the expression of both SMP1 and SMP2 were also restored in these lines, suggesting a physical interaction among the three proteins and/or genes. We propose that step II splicing factors and a transcriptional Mediator-like complex are involved in the timing of cell cycle arrest during leaf development.

The Arabidopsis flowering-time gene LUMINIDEPENDENS is expressed primarily in regions of cell proliferation and encodes a nuclear protein that regulates LEAFY expression.

Mutations in the LUMINIDEPENDENS (LD) gene of Arabidopsis thaliana (L.) Heynh. (Arabidopsis) confer a late-flowering phenotype, indicating that LD normally functions to promote the floral transition. RNA and protein blot analyses, along with the analysis of transgenic plants containing a fusion between a genomic fragment of LD and the reporter gene uidA (GUS), indicate that LD is expressed primarily ipical proliferative regions of the shoot and root, including the shoot apical meristem and leaf primordia. Subcellular localization studies indicate that LD is a nuclear protein, consistent with its previously proposed transcriptional regulatory role. We have also found that in an apetala1 cauliflower (ap1 cal) background the ld mutation converts the reproductive shoot apex to a more vegetative state, a phenotype that is similar to that seen for the leafy (lfy) mutant. Furthermore, in situ hybridization analysis indicates that LFY levels are drastically reduced at the apex of ld ap1 cal plants after bolting. These data are consistent with the idea that at least one function of LD is to participate in the regulation of LFY.

Anatomy of shoots and tumors of in vitro habituated rhododendron ‘montego’ (Ericaceae) cultures with tissue proliferation

Tissue proliferation (TP) is characterized primarily by the formation of galls or tumors at the crown of container-grown rhododendrons that were initially propagated in vitro. In the cultivar 'Montego', TP-like symptoms are first observed in vitro as shoot clusters with small leaves and nodal tumors. In addition, unlike the normal in vitro non-TP (TP-) shoots, in vitro TP (TP+) shoots proliferate rapidly without the presence of the plant growth regulator cytokinin in the tissue culture medium. Comparisons of the anatomy of TP+ and TP- shoot tips showed that TP+ shoots had a less developed vascular system, longer cells in the pith and cortex, and altered internodal elongation at the shoot apex. In addition, TP+ axillary buds were abnormal in that they were displaced onto the stem above the leaf axil, and a small group of proliferating cells replaced the shell zone at the base of the bud. Initiation of tumor formation began with the expansion of this region of cell proliferation (RCP) and shoot growth from the abnormal axillary bud (tumor bud). Organization of the tumor bud and extension of the RCP characterized the further development of two types of tumors. In polar shoot tumors, shoot growth continued from the persistent tumor bud and the tumor at the base of the shoot remained small in size. The RCP extends downward to the vascular junction of the subtending leaf and the stem of the TP+ shoot. In nonpolar tumors, continuous de novo meristem formation led to the development of large tumors with or without shoots. The RCP is present throughout the tumor and is associated with de novo meristem formation. Comparisons to the anatomy of other tumor-like structures showed that TP tumors of Rhododendron 'Montego' are most similar to tobacco genetic tumors.

Promotion and control of selective adhesion and proliferation of endothelial cells on polymer surface by carbon deposition.

The adhesion and proliferation of endothelial cells can be drastically improved when cultivated on a carbon-deposited polymer surface. When the surface of segmented polyurethane, in which endothelial cells are not capable of proliferating, is modified by carbon deposition, cell adhesion and proliferation occurred selectively on the carbon-deposited region. Carbon deposition to a tissue culture-treated polystyrene surface on which cells are capable of proliferating further promoted cell spreading and proliferation. Cell patterning on carbon-deposited segmented polyurethane was also attempted by controlling the direction or region of cell proliferation. Carbon deposition onto the polymer surface brought about a decrease in the water contact angle of the surface. Precoating fibronectin or laminin on the carbon-deposited polymer surface brought about cell adhesion and proliferation in the carbon-deposited region, but not in the non-carbon-deposited region. Our data suggest that promotion of cell proliferation on a carbon-deposited surface is probably due to selective adhesion of adhesive proteins to the surface.

Promotion and control of selective adhesion and proliferation of endothelial cells on polymer surface by carbon deposition

The adhesion and proliferation of endothelial cells can be drastically improved when cultivated on a carbon-deposited polymer surface. When the surface of segmented polyurethane, in which endothelial cells are not capable of proliferating, is modified by carbon deposition, cell adhesion and proliferation occurred selectively on the carbon-deposited region. Carbon deposition to a tissue culture-treated polystyrene surface on which cells are capable of proliferating further promoted cell spreading and proliferation. Cell patterning on carbon-deposited segmented polyurethane was also attempted by controlling the direction or region of cell proliferation. Carbon deposition onto the polymer surface brought about a decrease in the water contact angle of the surface. Precoating fibronectin or laminin on the carbon-deposited polymer surface brought about cell adhesion and proliferation in the carbon-deposited region, but not in the noncarbon-deposited region. Our data suggest that promotion of cell proliferation on a carbon-deposited surface is probably due to selective adhesion of adhesive proteins to the surface. © 1996 John Wiley & Sons, Inc.

PRODUCTION OF SOLUTES IN GROWING EPIDERMAL CELLS

Growth by cell enlargement, which is characteristic of plant cells, may be defined as the irreversible increment in the volume without appreciable increment in the mass of the protoplasm. Investigation of this kind of growth was given considerable impetus by Ursprung and Blum (12) when they discovered that the turgor of young cells is minimum when the growth is maximum, and also by Went (14) and his school when they proved that the growth-promoting substance which induces this kind of growth originates in the region of cell proliferation. Although it appears evident that the growth-promoting substance must exercise its effect on the living protoplasm (cf. 10) there is still some question about the effect produced directly or indirectly on the cell wall and the production of solute in the protoplasm which is osmotically active in the cell sap cavity. Klebs (5) concluded from his experiments that the protoplasm is directly responsible for cell enlargement, which is, of course, hardly tenable in view of the facts known to us at present. Hegler, Sachs, deVries (3, 7, 13) and others assumed that cell enlargement is directly due to the stretching of the wall, which itself is caused by the turgor. This view was decidedly disputed by Schwendener and Krabe (8), who contended that the wall grows actively by a process of intussusception with the cooperation of the protoplasm. Pfeffer (6) explains how the growth of the wall may be the result of active and passive growth, with consequent changes in the elastic constants of the wall. The fact which Ursprung and Blum established beyond a doubt, that the turgor is minimum in the most actively growing cells (12) makes it certain that the turgor plays at most a secondary r?le in the process of cell enlargement. It also makes it questionable if the solutes which are necessary to maintain the turgor are elaborated by the protoplasm to a degree which is commensurate with the growth of the cell.