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PubMed2001

VEGF-D promotes the metastatic spread of tumor cells via the lymphatics.

Metastasis to local lymph nodes via the lymphatic vessels is a common step in the spread of solid tumors. To investigate the molecular mechanisms underlying the spread of cancer by the lymphatics, we examined the ability of vascular endothelial growth factor (VEGF)-D, a ligand for the lymphatic growth factor receptor VEGFR-3/Flt-4, to induce formation of lymphatics in a mouse tumor model. Staining with markers specific for lymphatic endothelium demonstrated that VEGF-D induced the formation of lymphatics within tumors. Moreover, expression of VEGF-D in tumor cells led to spread of the tumor to lymph nodes, whereas expression of VEGF, an angiogenic growth factor which activates VEGFR-2 but not VEGFR-3, did not. VEGF-D also promoted tumor angiogenesis and growth. Lymphatic spread induced by VEGF-D could be blocked with an antibody specific for VEGF-D. This study demonstrates that lymphatics can be established in solid tumors and implicates VEGF family members in determining the route of metastatic spread.

Animals↗
PubMed1990

Metabolic and hemodynamic activation of postischemic rat brain by cortical spreading depression.

Following transient ischemia of the brain, the coupling between somatosensory activation and the hemodynamic-metabolic response is abolished for a certain period despite the partial recovery of somatosensory evoked responses. To determine whether this disturbance is due to alterations of the stimulus-induced neuronal excitation or to a breakdown of the coupling mechanisms, cortical spreading depression was used as a metabolic stimulus in rats before and after ischemia. Adult rats were subjected to 30 min of global forebrain ischemia and 3-6 h of recirculation. EEG, cortical direct current (DC) potential, and laser-Doppler flow were continuously recorded. Local CBF (LCBF), local CMRglc (LCMRglc), regional tissue contents of ATP, glucose, and lactate, and regional pH were determined by quantitative autoradiography, substrate-induced bioluminescence, and fluorometry. Amplitude and frequency of the DC shifts did not differ between groups. In control animals, spreading depression induced a 77% rise in cortical glucose consumption, a 66% rise in lactate content, and a drop in tissue pH of 0.3 unit. ATP and glucose contents were not depleted. During the passage of DC shifts, transient increases (less than 2 min) in laser-Doppler flow were observed, followed by a post-spreading depression hypoperfusion. A comparable although less expressed pattern of hemodynamic and metabolic changes was observed in the postischemic rats. Although baseline LCMRglc was depressed after ischemia, it was activated 47% during spreading depression. Lactate increased by 26%, pH decreased by 0.3 unit, and ATP and glucose remained unchanged. The extent of the transient increase in laser-Doppler flow did not differ from that of the control group, and a post-spreading depression hypoperfusion was also found.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Colonic spread of three rectally administered mesalazine (Pentasa) dosage forms in healthy volunteers as assessed by gamma scintigraphy.

BACKGROUND: Rectal administration of enemas, foams and suppositories is the most efficient method of delivering locally-acting drugs to the distal colon, sigmoid colon and rectum. Healthy volunteers provide an effective population to compare different formulations for rectal drug delivery. However, there is still only limited comparative information available on the dispersion of such dosage forms in human subjects. Therefore, the objective of this scintigraphic study was to compare colonic spread of an enema, a rectal foam and a suppository formulation in healthy volunteers. METHODS: This was a randomized, crossover study in eight healthy male volunteers. Each received Pentasa rectal formulations as either a 100 mL suspension enema (1 g mesalazine), one actuation of a non-CFC propellant rectal foam (1 g mesalazine in 5 mL concentrate, expanding to 40 mL on actuation), or one suppository (1 g mesalazine) on three separate occasions. The spread of the radiolabelled formulations was assessed over a 4-h period by gamma scintigraphy. RESULTS: The formulations were retained by all subjects for the whole of the 4-h imaging period. The enema spread to the splenic flexure in 7 out of 8 subjects, but was retained in the rectum and sigmoid colon in one individual. The foam spread as far as the descending colon in four subjects. In the remaining individuals the foam was retained in the rectum and sigmoid colon. The spread of the suppository was limited and confined to the rectum. CONCLUSIONS: The findings of this study are consistent with previous research and support the intended clinical uses of the enema, foam and suppository formulations to treat distal ulcerative colitis, proctosigmoiditis and proctitis, respectively. The results highlight the potential of gamma scintigraphy in providing in vivo 'proof of concept' data to help verify the targeting of pharmaceutical products to their intended site of delivery.

Administration, Rectal↗
PubMed1997

CD44-stimulated dendrite formation ('spreading') in activated B cells.

A rat monoclonal antibody (mAb) (NIM-R8), insolubilized by binding to plastic plates, induced a rapid and extensive formation of dendrite processes ('spreading') in B lymphocytes activated by anti-IgM and interleukin-4 (IL-4) or anti-CD38 and IL-4. In contrast, resting B cells were unable to spread similarly on the NIM-R8-coated plates. The NIM-R8 antibody recognized a 90,000 MW surface glycoprotein (gp90) present on both B and T lymphocytes. The expression of this molecule was greatly increased after polyclonal (lipopolysaccharide, anti-IgM plus IL-4 or concanavalin A) activation. The NIM-R8 mAb with or without IL-2 or IL-4 was unable to induce proliferation of splenic lymphocytes. Following the demonstration that the NIM-R8 mAb recognizes the murine equivalent of human CD44, the induction of spreading of activated B lymphocytes was studied using a panel of mAb recognizing different epitopes of murine CD44. All of these different mAb induced similar spreading of activated B cells. The ligand-inducible spreading of activated B lymphocytes may be an important mechanism for providing an increased cell-surface area for cell-cell or cell-matrix interactions, and thus may be an important factor controlling the response of activated lymphocytes.

Animals↗
PubMed1997

Intercontinental spread of promiscuous mercury-resistance transposons in environmental bacteria.

We demonstrate that horizontal spread of mer operons similar to worldwide spread of antibiotic-resistance genes in medically important bacteria occurred in bacteria found in ores, soils and waters. The spread was mediated by different transposons and plasmids. Some of the spreading transposons were damaged in different ways but this did not prevent their further spread. Certain transposons are mosaics composed of segments belonging to distinct sequence types. These mosaics arose as a result of homologous and site-specific recombination. Our data suggest that the mercury-resistance operons of Gram-negative environmental bacteria can be considered as a worldwide population composed of a relatively small number of distinct recombining clones shared, at least partially, by environmental and clinical bacteria.

Bacterial Proteins↗
PubMed2000

The development of a FACS-based strategy for the isolation of Shigella flexneri mutants that are deficient in intercellular spread.

In the disease course of bacillary dysentery, pathogenic Shigella flexneri invade colonic epithelial cells and spread both within and between host cells. The ability to spread intercellularly allows the organism to infect an entire epithelial layer without significant contact with the extracellular milieu. Using fluorescence activated cell sorter (FACS)-based technology, we developed a rapid and powerful selection strategy for the isolation of S. flexneri mutants that are unable to spread from cell to cell. The majority of mutants identified using this strategy harbour mutations that affect the structure of their lipopolysaccharide or the ability of the bacteria to move intracellularly via actin-based motility; both factors have previously been shown to be essential for cell-to-cell spread. However, using a modified strategy that eliminated both of these types of mutants, we identified several mutants that provide us with evidence that bacterial proteins of the type III secretion system, which are essential for bacterial entry into host cells, also play a role in cell-to-cell spread.

Caco-2 Cells↗
PubMed1999

Limitation of cholangiography in assessing longitudinal spread of extrahepatic bile duct carcinoma to the hepatic side.

BACKGROUND: Preoperative assessment of longitudinal spread of bile duct carcinoma (BDC) to the hepatic side remains a difficult problem for diagnostic imaging. METHODS: We studied the accuracy of cholangiography in assessing BDC. In 54 patients with extrahepatic bile duct cancer, cholangiographic findings were compared retrospectively with the histological findings of the resected specimens. RESULTS: Histological examination of specimens indicated longitudinal spread of the tumour to the hepatic side in 22 of 54 patients. The accuracy of cholangiography in assessing the extent of the longitudinal spread was only 34/54 (63%). When the cholangiographic images showed a main tumour with a collapsed edge, there was a significantly higher frequency of longitudinal spread compared with tumours with sharp edges (P< 0.05). In contrast, the accuracy of mapping biopsy under percutaneous transhepatic cholangioscopy (n=24) was 83%. CONCLUSIONS: Cholangiography cannot accurately assess the extent of the longitudinal spread of bile duct cancer. When cholangiographic images show a tumour with a collapsed edge, preoperative or intraoperative histological examination is essential to determine a suitable surgical line.

Adenocarcinoma↗
PubMed1999

Mammary Paget's disease: evidence of diverse origin of the disease with a subgroup of Paget's disease developing from the superficial portion of lactiferous duct and a discontinuous pattern of tumor spread.

The pattern of spread of intraductal carcinoma associated with mammary Paget's disease has not been well studied. The purpose of this study was to examine the site of origin and the pattern of tumor spread with a three-dimensional view by serial sectioning of the tissue blocks from 19 cases of Paget's disease. Intraductal carcinoma in the superficial portion of the lactiferous ducts was seen in continuity with the overlying epidermis with Paget's disease in all 19 cases. In seven cases that had adequate tissue sampling, five showed a continuous pattern of the intraductal carcinoma within the superficial as well as the deep breast tissue. In the remaining two cases, a portion of benign duct was identified between the intraductal carcinoma in the superficial lactiferous duct and the deep breast tissue. This discontinuous pattern of spread of the intraductal carcinoma was also identified in the foci of carcinoma in deep tissue. In the five cases in which the tumor involved the skin and only the superficial portions of the lactiferous duct, the leading edge of the intraductal carcinoma was seen orientated in the direction of the nipple towards the deep breast tissue. Our study of Paget's disease demonstrated that in addition to tumor spread along the lactiferous ducts from intraductal carcinoma in the deep tissue towards the nipple, there was a group of Paget's disease arising from the nipple. These lesions included: (i) lesions limited to the areolar tissue; and (ii) lesions with intraductal carcinoma involving the duct system in both superficial and deep breast tissue with and, possibly, without skip areas pattern of spread. Although certain cases of Paget's disease may appear superficial, an independent associated carcinoma in deep breast tissue has to be ruled out.

Breast Neoplasms↗
PubMed1998

Epitope spreading: lessons from autoimmune skin diseases.

Autoimmune diseases are initiated when patients develop aberrant T and/or B cell responses against self proteins. These responses presumably are directed to single immunogenic epitopes on these proteins. Recent data in animal models of autoimmune diseases suggest that the targets of immune responses in autoimmunity do not remain fixed, but can be extended to include other epitopes on the same protein or other proteins in the same tissue, a phenomenon termed "epitope spreading." The "epitope spreading" phenomenon also applies to situations in which tissue damage from a primary inflammatory process causes the release and exposure of a previously "sequestered" antigen, leading to a secondary autoimmune response against the newly released antigen. In experimental autoimmune animal diseases, "epitope spreading" seems to have significant physiologic importance in determining the course and duration of disease. In this paper, we review the current concepts in animal models of autoimmune diseases in order to define the "epitope spreading" phenomenon, and we then propose how this phenomenon might play a significant role in the development and the course of autoimmune skin diseases. Hopefully, an understanding of "epitope spreading" will help the dermatology community to better understand the pathogenesis of autoimmune skin diseases and to rationally fashion disease-specific immune therapy in the future.

Animals↗
PubMed2000

Unrecognizable intramucosal spread of diffuse-type mucosal gastric carcinomas of less than 20 mm in size.

BACKGROUND: Diffuse-type intramucosal gastric carcinomas sometimes spread within the mucosa beyond their macroscopic margins, often causing positive resection margins upon local resections such as endoscopic mucosal resection. PATIENTS AND METHODS: A consecutive series of 34 patients with solitary, small (less than 20 mm in diameter macroscopically), and macroscopically well demarcated diffuse-type mucosal carcinomas, who were treated with gastrectomy followed by detailed pathological examination, were included in the present study. Unrecognizable intramucosal spread is defined as an area of cancer which is indistinguishable macroscopically from its peripheral noncancerous area, and covered by normal epithelium with neither morphologic nor color changes. We examined the extent of unrecognizable intramucosal spread, measuring the maximum distances between macroscopic and microscopic margins on the sections, and investigated its relationship with four factors: location of the lesion, macroscopic size, histologic ulcer formation, and degree of atrophy of the background mucosa. RESULTS: The maximum distance between macroscopic and microscopic margins was significantly larger (maximum 10 mm) in the background mucosas with marked atrophy than in those with little or no atrophy. No other factors, including location, macroscopic size and ulcer formation, correlated with it. CONCLUSION: We should pay particular attention to unrecognizable intramucosal spread, especially in markedly atrophied mucosa, when treating small diffuse-type mucosal gastric cancer by local resections such as endoscopic mucosal resection. In addition, because of unrecognizable intramucosal spread, a surgical incision margin of at least 10 mm from the macroscopic margin is indicated.

Adult↗
PubMed2004

Spreading of block copolymer films and domain alignment at moving terrace steps.

We investigate spreading of phase separated copolymer films, where domain walls and thickness steps influence polymer flow. We show that at early stages of spreading its rate is determined by slow activated flow at terrace steps (i.e., thickness steps). At late stages of spreading, on the other hand, the rate is determined by the flow along terraces, with diffusionlike time dependence t(-1/2). This dependence is similar to de Gennes and Cazabat's prediction for generic layered liquids [P. G. de Gennes and A. M. Cazabat, C.R. Acad. Sci. Paris II 310, 1601 (1990)], as opposed to the classical Tanner's law of drop spreading. We also argue that chain hopping at the spreading terrace steps should lead to the formation of aligned, defect-free domain patterns on the growing terraces.

Journal Article↗
PubMed2001

Patterns of spread in recurrent head and neck squamous cell carcinoma.

OBJECTIVE: To examine the pattern of spread regarding recurrent disease in primary head and neck squamous cell carcinoma. STUDY DESIGN AND SETTING: A retrospective study reviewed 128 patients who underwent primary tumor resection and postoperative radiation and/or chemoradiation for squamous cell carcinoma at Loyola University Medical Center from July 1993 to August 1998. Patterns of spread of recurrent disease were grouped according to site of recurrence and compared with the histopathology. RESULTS: Of 128 patients, 40 (32%) had recurrent disease, 22 (17%) died without disease, and 66 (51%) are disease free. Although the recurrences in patients who were N0 were primarily local-regional (8/11), the majority of recurrences in patients that were N+ with extracapsular nodal spread involved distant sites (18/24); 17/18 involved metastasis to the lung. SIGNIFICANCE: This study gives the first report at our institution of patterns of spread in recurrent head and neck squamous cell cancer and compares these patterns within subgroups of patients based on the extent of neck disease at the time of primary surgical resection. CONCLUSION: Not only was there a higher rate of recurrent disease in patients with extracapsular nodal spread, there was a much higher involvement of distant metastatic sites as opposed to local-regional recurrence more often seen with the N0 neck. The most common site of distant metastasis was the lung.

Carcinoma, Squamous Cell↗
PubMed1985

Blockade of beta 1- but not of beta 2-adrenergic receptors replicates propranolol's suppression of the cerebral spread of an engram in mice.

Bitemporal injections of puromycin that primarily affect the hippocampal-entorhinal area induce amnesia of aversive maze-learning in mice for 3 days after training but are ineffective 6 or more days after training. At these later times, additional puromycin sites covering widespread forebrain areas are necessary to induce amnesia, a result that we attribute to the cerebral spread of the engram during the 6-day period. We have reported that blockade of about 60% of cerebral beta-adrenergic receptors by a single, subcutaneous injection of (-)-propranolol, a nonselective beta-receptor antagonist, inhibited engram spread for 60-90 days, at which time engram spread spontaneously occurred. In the present experiments using single doses of antagonists that appeared to block 60% of beta 2- or beta 1-adrenergic receptors, it was found that the selective beta 2 antagonist ICI 118,551 was without effect on engram spread, whereas the selective beta 1 antagonist betaxolol inhibited the spread for at least 3 months. Propranolol's effect consequently appears to be accounted for by its blockade of beta 1 receptors.

Adrenergic beta-Antagonists↗
PubMed1997

Isolation and identification of a plasmatocyte-spreading peptide from the hemolymph of the lepidopteran insect Pseudoplusia includens.

Insect blood cells (hemocytes) play an essential role in defense against parasites and other pathogenic organisms that infect insects. A key class of hemocytes involved in insect cellular immunity is plasmatocytes. Here we describe the isolation and identification of a peptide from the moth Pseudoplusia includens that mediates the spreading of plasmatocytes to foreign surfaces. This peptide, designated plasmatocyte-spreading peptide (PSP1), contains 23 amino acid residues in the following sequence: H-ENFNGGCLAGYMRTADGRCKPTF-OH. In vitro assays using the synthetic peptide at concentrations >/=2 nM induced plasmatocytes from P. includens to spread on the surface of culture dishes. Injection of this peptide into P. includens larvae caused a transient depletion of plasmatocytes from circulation. Labeling studies indicated that this peptide induced 75% of plasmatocytes that were double-labeled by the monoclonal antibodies 49G3A3 and 43E9A8 to spread, whereas plasma induced significantly more plasmatocytes to spread. This suggests that only a certain subpopulation of plasmatocytes responds to the peptide and that other peptidyl factors mediate plasmatocyte adhesion responses.

Amino Acid Sequence↗
PubMed1999

Enhancement of cell adhesion and spreading by a cartilage-specific noncollagenous protein, cartilage matrix protein (CMP/Matrilin-1), via integrin alpha1beta1.

Cartilage matrix protein (CMP; also known as matrilin-1), one of the major noncollagenous proteins in most cartilages, binds to aggrecan and type II collagen. We examined the effect of CMP on the adhesion of chondrocytes and fibroblasts using CMP-coated dishes. The CMP coating at 10-20 micrograms/ml enhanced the adhesion and spreading of rabbit growth plate, resting and articular chondrocytes, and fibroblasts and human epiphyseal chondrocytes and MRC5 fibroblasts. The effect of CMP on the spreading of chondrocytes was synergistically increased by native, but not heated, type II collagen (gelatin). The monoclonal antibody to integrin alpha1 or beta1 abolished CMP-induced cell adhesion and spreading, whereas the antibody to integrin alpha2, alpha3, alpha5, beta2, alpha5beta1, or alphaVbeta5 had little effect on cell adhesion or spreading. The antibody to integrin alpha1, but not to other subunits, coprecipitated 125I-CMP that was added to MRC5 cell lysates, indicating the association of CMP with the integrin alpha1 subunit. Unlabeled CMP competed for the binding to integrin alpha1 with 125I-CMP. These findings suggest that CMP is a potent adhesion factor for chondrocytes, particularly in the presence of type II collagen, and that integrin alpha1beta1 is involved in CMP-mediated cell adhesion and spreading. Since CMP is expressed almost exclusively in cartilage, this adhesion factor, unlike fibronectin or laminin, may play a special role in the development and remodeling of cartilage.

Animals↗
PubMed2000

Protein kinase C-regulated dynamitin-macrophage-enriched myristoylated alanine-rice C kinase substrate interaction is involved in macrophage cell spreading.

Macrophage spreading requires the microtubule cytoskeleton and protein kinase C (PKC). The mechanism of involvement of the microtubules and PKC in this event is not fully understood. Dynamitin is a subunit of dynactin, which is important for linking the microtubule-dependent motor protein dynein to vesicle membranes. We report that dynamitin is a Ca(2+)/calmodulin-binding protein and that dynamitin binds directly to macrophage-enriched myristoylated alanine-rice C kinase substrate (MacMARCKS), a membrane-associated PKC substrate involved in macrophage spreading and integrin activation. Dynamitin was found to copurify with MacMARCKS both during MacMARCKS purification with conventional chromatography and during the immunoabsorption of MacMARCKS using anti-MacMARCKS antibody. Vice versa, MacMARCKS was also found to cosediment with the 20 S dynactin complex. We determined that the effector domain of MacMARCKS is required to interact with the N-terminal domain of dynamitin. MacMARCKS and dynamitin also partially colocalized at peripheral regions of macrophages and in the cell-cell border of 293 epithelial cells. Treatment with phorbol esters abolished this colocalization. Disrupting the interaction with a short peptide derived from the MacMARCKS-binding domain of dynamitin caused macrophages to spread and flatten. These data suggest that the dynamitin-MacMARCKS interaction is involved in cell spreading. Furthermore, the regulation of this interaction by PKC and Ca(2+)/calmodulin provides a possible regulatory mechanism for cell adhesion and spreading.

Adenosine Triphosphatases↗
PubMed2001

Alanine-scanning mutagenesis of plasmatocyte spreading peptide identifies critical residues for biological activity.

Plasmatocyte spreading peptide (PSP) is a 23-amino acid cytokine that induces a class of insect immune cells called plasmatocytes to spread on foreign surfaces. The structure of PSP consists of a disordered N terminus (residues 1-6) and a well-defined core (residues 7-23) stabilized by a disulfide bridge between Cys(7) and Cys(19), hydrophobic interactions, and a short beta-hairpin. Structural comparisons also indicate that the core region of PSP adopts an epidermal growth factor (EGF)-like fold very similar to the C-terminal subdomain of EGF-like module 5 of thrombomodulin. To identify residues important for plasmatocyte spreading activity, we bioassayed PSP mutants in which amino acids were either replaced with alanine or deleted. Within the well-defined core of PSP, alanine replacement of Cys(7) and Cys(19) (C7.19A) eliminated all activity. Alanine replacement of Arg(13) reduced activity approximately 1000-fold in comparison to wild-type PSP, whereas replacement of the other charged residues (Asp(16), Arg(18), Lys(20)) surrounding Cys(19) diminished activity to a lesser degree. The point mutants Y11A, T14A, T22A, and F23A had activity identical or only slightly reduced to that of wild-type PSP. The mutant PSP-(7-23) lacked the entire unstructured domain of PSP and was found to have no plasmatocyte spreading activity. Surprisingly, E1A and N2A had higher activity than wild-type PSP, but F3A had almost no activity. We thus concluded that the lack of activity for PSP-(7-23) was largely due to the critical importance of Phe(3). To determine whether reductions in activity correlated with alterations in tertiary structure, we compared the C7.19A, R13A, R18A, and F3A mutants to wild-type PSP by NMR spectroscopy. As expected, the simultaneous replacement of Cys(7) and Cys(19) profoundly affected tertiary structure, but the R13A, R18A, and F3A mutants did not differ from wild-type PSP. Collectively, these results indicate that residues in both the unstructured and structured domains of PSP are required for plasmatocyte-spreading activity.

Alanine↗
PubMed2001

The cell adhesion domain of type XVII collagen promotes integrin-mediated cell spreading by a novel mechanism.

Type XVII collagen (BP180) is a keratinocyte transmembrane protein that exists as the full-length protein in hemidesmosomes and as a 120-kDa shed ectodomain in the extracellular matrix. The largest collagenous domain of type XVII collagen, COL15, has been described previously as a cell adhesion domain (Tasanen, K., Eble, J. A., Aumailley, M., Schumann, H., Baetge, J, Tu, H., Bruckner, P., and Bruckner-Tuderman, L. (2000) J. Biol. Chem. 275, 3093-3099). In the present work, the integrin binding of triple helical, human recombinant COL15 was tested. Solid phase binding assays using recombinant integrin alpha(1)I, alpha(2)I, and alpha(10)I domains and cell spreading assays with alpha(1)beta(1)- and alpha(2)beta(1)-expressing Chinese hamster ovary cells showed that, unlike other collagens, COL15 was not recognized by the collagen receptors. Denaturation of the COL15 domain increased the spreading of human HaCaT keratinocytes, which could migrate on the denatured COL15 domain as effectively as on fibronectin. Spreading of HaCaT cells on the COL15 domain was mediated by alpha(5)beta(1) and alpha(V)beta(1) integrins, and it could be blocked by RGD peptides. The collagen alpha-chains in the COL15 domain do not contain RGD motifs but, instead, contain 12 closely related KGD motifs, four in each of the three alpha-chains. Twenty-two overlapping, synthetic peptides corresponding to the entire COL15 domain were tested; three peptides, all containing the KGD motif, inhibited the spreading of HaCaT cells on denatured COL15 domain. Furthermore, this effect was lost by mutation from D to E (KGE instead of KGD). We suggest that the COL15 domain of type XVII collagen represents a specific collagenous structure, unable to interact with the cellular receptors for other collagens. After being shed from the cell surface, it may support keratinocyte spreading and migration.

Amino Acid Motifs↗