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At least 145 records · Page 8Linked to original sources
PubMed2003

Distal intramural spread is an independent prognostic factor for distant metastasis and poor outcome in patients with rectal cancer: a multivariate analysis.

BACKGROUND: The aim of this study was to clarify the prognostic value of distal intramural spread of tumor for survival and recurrence in patients with rectal cancer. METHODS: Microscopic distal intramural spread was examined in 134 consecutive specimens of resected rectal cancer. Correlations among distal intramural spread, established clinicopathologic factors, and patients' prognoses were examined by univariate and multivariate analyses. American Joint Committee on Cancer classification and stage groupings were used for tumor assessment. RESULTS: Thirty-three patients (24.6%) had distal intramural spread. Multivariate logistical regression analysis revealed that T3/T4 and M1 were independent predictive variables for the presence of distal intramural spread. Patients with distal intramural spread had a shorter disease-specific or disease-free survival time after curative surgery than those without distal intramural spread (P =.0003 and P =.0006, respectively). Most patients with distal intramural spread developed distant recurrence. Cox's regression with multiple covariates showed that distal intramural spread is an independent factor in predicting distant recurrence and worse outcomes after curative surgery in patients with rectal cancer. CONCLUSIONS: Distal intramural spread is an independent risk factor for distant metastasis and poor prognosis in patients with rectal cancer.

Adenocarcinoma↗
PubMed1989

Modulation of survival and proliferation of BSC-1 cells through changes in spreading behavior caused by the tumor-promoting phorbol ester TPA.

The effect of a tumor-promoting phorbol ester on spreading behavior was investigated to clarify the involvement of the interactions between cells and substratum in the maintenance of cell viability and the control of cell proliferation. BSC-1 cells did not spread and lost cell viability after a 24-h incubation in the absence of calf serum. Addition of calf serum initially induced radial spreading and then polarized spreading, with the formation on stress fibers and focal contact-like structure, and enhanced survival. Vitronectin also induced both radial spreading and polarized spreading, and enhanced cell survival. 12-O-Tetradecanoylphorbol-13-acetate (TPA) induced radial spreading with actin ribbons in the absence of serum. It improved the survival of cells attached to the substratum, but not in suspension. TPA suppressed polarized spreading, formation of stress fibers and of focal contact-like structure, and cell proliferation, in the presence of serum. Phorbol did not have any effect. These results suggest that enhancement of radial spreading and inhibition of polarized spreading of BSC-1 cells by TPA are closely related to the enhancement of cell survival and inhibition of cell growth.

Animals↗
PubMed2006

Influence of temperature on the spreading velocity of simplified-step adhesive systems.

BACKGROUND: Flowability and viscosity vary for different adhesive systems owing to differences in their composition. These characteristics can be modified by environmental temperature. PURPOSE: The purpose of this study was to determine the influence of temperature on the spreading (flow capacity) of simplified-step adhesive systems. MATERIALS AND METHODS: Spreading velocities of adhesive systems (Adper Single Bond and Single Bond Plus [3M ESPE, St. Paul, MN, USA]; Prime & Bond 2.1 and Prime & Bond NT [Dentsply Indústria e Comércio Ltda, Petrópolis, RJ, Brazil]; Adper Prompt [3M ESPE]; and One Up Bond F [Tokuyama Corp, Tokyo, Japan]) were analyzed at intervals of 10, 15, 20, and 30 seconds at both 25 degrees C and 37 degrees C by placing 10 microL drops on a glass slide surface with an inclination of 45 degrees. The spreading of each adhesive system was measured in millimeters per second. RESULTS: Data were analyzed by two-way analysis of variance and Student-Newman-Keuls tests. Regression analysis was used to determine a correlation between spreading velocity and time. Statistical significance was considered at a confidence level of 95%. Temperature influenced the spreading velocity, increasing it for Single Bond and Prime & Bond 2.1 and decreasing it for Adper Prompt (p < .05). No differences on spreading were observed for the other adhesives studied (p >.05). Regression analysis of each adhesive system demonstrated an inverse correlation between mean spreading velocity and time (R2 = .999) on both temperatures. CONCLUSIONS: Temperature increases yielded an increase of spreading for Single Bond and Prime & Bond 2.1. The influence of temperature on the spreading velocity was material dependent. CLINICAL SIGNIFICANCE: Environmental temperature can influence the rate of spreading of the adhesive system in clinically relevant times and may influence adhesive thickness on cavity walls.

Acetone↗
PubMed2005

Pathological study of distal mesorectal cancer spread to determine a proper distal resection margin.

AIM: Local recurrence after curative surgical resection for rectal cancer remains a major problem. Several studies have shown that incomplete removal of cancer deposits in the distal mesorectum contributes a great share to this dismal result. Clinicopathologic examination of distal mesorectum in lower rectal cancer was performed in the present study to assess the incidence and extent of distal mesorectal spread and to determine an optimal distal resection margin in sphincter-saving procedure. METHODS: We prospectively examined sepecimens from 45 patients with lower rectal cancer who underwent curative surgery. Large-mount sections were performed to microscopically observe the distal mesorectal spread and to measure the extent of distal spread. Tissue shrinkage ratio was also considered. Patients with involvement in the distal mesorectum were compared with those without involvement with regard to clinicopathologic features. RESULTS: Mesorectal cancer spread was observed in 21 patients (46.7%), 8 of them (17.8%) had distal mesorectal spread. Overall, distal intramural and/or mesorectal spreads were observed in 10 patients (22.2%) and the maximum extent of distal spread in situ was 12 mm and 36 mm respectively. Eight patients with distal mesorectal spread showed a significantly higher rate of lymph node metastasis compared with the other 37 patients without distal mesorectal spread (P = 0.043). CONCLUSION: Distal mesorectal spread invariably occurs in advanced rectal cancer and has a significant relationship with lymph node metastasis. Distal resection margin of 1.5 cm for the rectal wall and 4 cm for the distal mesorectum is proper to those patients who are arranged to receive operation with a curative sphincter-saving procedure for lower rectal cancer.

Adult↗
PubMed1999

Intraductal spread of invasive breast carcinoma has a positive correlation with c-erb B-2 overexpression and vascular invasion.

BACKGROUND: Studies of the histologic characteristics and biologic behavior of the intraductal spread of breast carcinoma are critically important in that they may lead to the identification of a unique spread pattern rather than a noninvasive lesion. METHODS: Paraffin embedded specimens of 187 primary invasive breast carcinomas and 4 noninvasive ductal carcinomas, obtained by wide excision, quadrantectomy, total glandectomy, or mastectomy, were studied immunohistochemically. The overexpression of c-erb B-2, p53, bcl-2, and MIB-1, as well as the histologic characteristics of intraductal spread (such as histologic features and histologic grade), were assessed. Chi-square and Fisher exact tests were conducted to evaluate significant differences; the Macintosh for Expert StatView 4.0 system was used to conduct these tests. RESULTS: The histologic characteristics of intraductal spread were similar to those of noninvasive ductal carcinoma. However, the expressions of c-erb B-2, p53, and other biologic markers of intraductal spread were similar to those of the main invasive tumor. The overexpression of c-erb B-2 protein was found more often in the group that was positive for intraductal spread than in the group that was negative (P < 0.01). Intraductal spread was found more often in the group that was positive for lymphatic and venous invasion than in the group that was negative (P < 0.005). Subnipple margin positive status was related closely to intraductal spread (P < 0.0001). CONCLUSIONS: The positive correlation between intraductal spread and c-erb B-2 overexpression as well as lymphatic, venous invasion was recognized, and it was determined that intraductal spread of invasive breast carcinoma possesses an invasive and metastatic potential that is distinct from noninvasive ductal carcinoma.

Antigens, Nuclear↗
PubMed2001

[Distal intramural spread of rectal cancer studied on large slices].

OBJECTIVE: To study the length of distal intramural spread of rectal cancers, and provide evidence for anal-preserving operations. METHODS: Specimens of ninety-eight patients with rectal cancers who had been operated from August, 1996 to October, 1997, were collected and their large pathologic slices examined. The length of intramural spread distal to rectal cancers was measured under light microscope. The actual length of spread in live conditions was estimated according to equal proportional shrinkage. RESULTS: In 48 of the 98 patients, distal intramural spread of the tumor was observed. The length of spread varied from 0.1 cm to 2.5 cm. In 77% of the 48 patients, the length of tumor spread was < 0.5 cm. In only 5 patients was the distance of spread > or = 1.0 cm. Four different ways of tumor invasion were observed: contiguous, lymphatic, neural and venous invasion. Distal intramural spread could be via mucosa, submucosa, inner circular muscular layer, outer longitudinal muscular layer or serosa, either separately or concomitantly. CONCLUSION: Distal intramural spread of rectal cancers can be detected in about 1/2 of the specimens examined on large pathologic slice. In most of them the distance of spread is < 0.5 cm. Occasionally it may be > or = 1 cm. To set the edge of resection > or = 3 cm distal to the rectal cancers is relatively safe in anal-preserving operations.

Colorectal Neoplasms↗
PubMed1985

Stimulation of haptotaxis and migration of tumor cells by serum spreading factor.

A central feature of tumor metastasis is the migration of malignant cells through interstitial tissues and vascular structures as they spread throughout the body. Various components of the extracellular matrix and of basement membranes, consisting of genetically distinct collagens, proteoglycans, and noncollagenous glycoproteins, are known to modulate certain aspects of cell behavior, including cell movement. Serum spreading factor is a glycoprotein component of human serum that is also found in interstitial tissues. Two native forms are seen in human serum, a Mr 65,000 and a Mr 75,000 component. Spreading factor promotes substratum attachment and spreading of diverse cell types, including epithelial and fibroblastic cells, and will affect the growth rate and differentiation of cells in serum-free culture media. Serum spreading factor was shown to promote the directed migration of the following tumor cell lines in modified Boyden chamber assays: murine melanoma K-1735 (clones M2, M4, and 16); human breast carcinoma MCF-7; and human fibrosarcoma HT-1080. The stimulation of movement occurred over a concentration range of 0.5 to 50 micrograms of serum spreading factor per ml with a maximum response between 5 and 10 micrograms/ml. The maximal response varied with the cell line and ranged from 5- to 50-fold greater migration than control. A monoclonal antibody to spreading factor, previously shown to inhibit the attachment and spreading-promoting activity, abrogated this migration response. Experiments using filters that were precoated with spreading factor indicated that cells could migrate on an insolubilized layer of this protein by haptotaxis. Tumor cell migration to spreading factor in vitro suggests a possible role for this protein in the phenotypic behavior of metastatic cells.

Animals↗
PubMed1988

Surface movements during the spreading of blood platelets.

When human blood platelets spread on a substratum they increase their surface area as much as 4-fold. We investigated the mechanism of spreading by light microscopy and by scanning and transmission electron microscopy. Contact of a platelet with a glass surface induces formation of thin extensions which spread out over the substratum. These extensions resemble the actin-containing microspikes and lammelipodia of tissue cells in culture and appear to be drawn from the peripheral cortical layer associated with the plasma membrane. If platelets are initially labeled on their external surface with cationic ferritin or lentil-conjugated gold particles and then allowed to spread, the labels are retained in the central region, or granulomere. Proteins released by the spreading platelet--fibronectin and fibrinogen--also remain in this central unspread region. Peripheral regions of spread platelet surface (hyalomere) were unlabeled following the above procedures but could be labeled with cationic ferritin or lentil-conjugated gold provided these were applied after spreading was completed. These markers are cleared with time from the periphery, moving centripetally to accumulate at the granulomere. We suggest, on the basis of these observations, that platelets spread onto a substratum by a closely similar mechanism to that used by cells such as fibroblasts. In both cases the spreading involves the peripheral actin cortex and is accompanied by a continual centripetal movement of surface components--a "membrane flow"--which continues even after spreading is completed.

Actins↗
PubMed1993

Laminin oligosaccharides play a pivotal role in cell spreading.

The basement membrane glycoprotein laminin promotes cell adhesion, spreading and neurite outgrowth. We can uncouple cell adhesion and spreading (or neurite outgrowth) when unglycosylated laminin is used as a substratum. Mouse melanoma cells, B16F1 line, readily attach to unglycosylated laminin but fail to spread once adherent. Spreading can be restored by titration with glycosylated laminin or with laminin glycopeptides. When the laminin substratum is absent in the test chambers, the cells do not adhere when either intact laminin or its glycopeptides are then added. Analyses show that these added substances are recoverable from the culture medium and do not bind to the chamber surfaces. Use of selective inhibitors which interfere with carbohydrate processing yields several glycoforms of laminin which we have isolated and examined for their ability to support cell adhesion and spreading. Laminin which is enriched in high mannose oligosaccharides is much more effective in promoting cell spreading than laminin which is enriched in hybrid oligosaccharides. These results are consistent with earlier studies which showed that ConA, which primarily recognizes mannose residues, could also uncouple cell adhesion and spreading. Although mono- and disaccharides failed to restore cell spreading, we have found that addition of various mannose oligosaccharides to adherent cells effectively reestablishes their spreading behavior. The extent of cell spreading which is achieved by the added saccharides is related to their amount, their duration of addition, and their molecular structures.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

Cyclooxygenase-2 mediates the development of cortical spreading depression-induced tolerance to transient focal cerebral ischemia in rats.

We examined the role of cyclooxygenase-2 in the development of ischemic tolerance induced by cortical spreading depression against transient, focal brain ischemia. Cortical spreading depression was continuously induced for 2 h with topical KCl (13+/-1 depolarizations/2 h) in male Wistar rats. At 1, 2, 3, 4, and 5 days following recovery, the middle cerebral artery was transiently occluded for 120 min. Four days later, the animals were killed and infarct volume was determined. Additionally, cyclooxygenase-2 levels in the cerebral cortex and 15 deoxy-Delta(12, 14) PGJ2 levels in cerebrospinal fluid were determined at these times with Western blotting and immunoassay, respectively. Infarct volume was reduced compared with non-cortical spreading depression control animals (274.3+/-15.3 mm3) when cortical spreading depression was performed 3 and 4 days before middle cerebral artery occlusion (163.9+/-14.2 mm3, 154.9+/-14.2 mm3) but not at 1, 2 and 5 days (280.4+/-17.3 mm3, 276.3+/-16.9 mm3 and 268.5+/-17.3 mm3). Cyclooxygenase-2 levels increased most dramatically starting at 2 days, peaked at 3 days, and started to return toward baseline at 4 days after cortical spreading depression. 15 Deoxy-Delta(12, 14) PGJ2 levels increased from 134.7+/-83 pg/ml at baseline to 718+/-98 pg/ml at 3 days. Administration of N-[2-cyclohexyloxy-4-nitrophenyl] methanesulphonamide (10 mg/kg, i.v.), a selective cyclooxygenase-2 inhibitor, at 1 h prior to middle cerebral artery occlusion in cortical spreading depression preconditioned animals did not affect infarct volume (162.6+/-62.1 mm3). However, administration of N-[2-cyclohexyloxy-4-nitrophenyl] methanesulphonamide given three times prior to middle cerebral artery occlusion prevented the reduced infarct volume induced by cortical spreading depression preconditioning (272.9+/-63.2 mm3). Administration of L-nitro-arginine methyl ester (4 mg/kg, i.v.) prior to cortical spreading depression blocked increases in cyclooxygenase-2 normally seen at 3 and 4 days. We conclude that NO-mediated cyclooxygenase-2 upregulation by cortical spreading depression protects the brain against ischemic damage.

Animals↗
PubMed1991

Cerebral blood flow and oxygen consumption in cortical spreading depression.

We determined the effects of spreading depression on local cerebral O2 supply, oxygenation, and O2 consumption in the anesthetized rat. Spreading depression was induced by application of 0.5 M KCl to the frontal cortex. Regional cerebral blood flow was determined with [14C]iodoantipyrine and regional O2 extraction was determined microspectrophotometrically. The passage of the spreading depression wave was determined with a multiprobe assembly that recorded NADH redox state (surface fluorometry), extracellular K+ activity, and DC steady potential (surface minielectrodes). As the wave of spreading depression passed, there was an increase in extracellular K+ and a decrease in NADH. Cerebral blood flow was significantly increased (120 +/- 51 ml/min/100 g, mean +/- SD) during the wave as compared with other regions. In the affected cortex, blood flow was not different from that in the contralateral cortex (69 +/- 28 ml/min/100 g) either before or after the wave of spreading depression passed. Arterial and venous O2 saturation were unaffected by the wave and the histogram of O2 saturations of examined veins followed a similar normal distribution in all regions. Oxygen extraction was not altered by the wave of spreading depression. Oxygen consumption was significantly increased during the wave to 7.4 +/- 3.7 ml O2/min/100 g compared with the contralateral cortex (5.1 +/- 2.6 ml/min/100 g) and other regions. It can be concluded that spreading depression caused an increase in cerebral O2 consumption that was adequately matched by an increase in local blood flow. Oxygen delivery was not limited during spreading depression and its effects were quickly over as evidenced by the lack of alteration in oxygenation after the wave of spreading depression passed.

Animals↗
PubMed1997

Premyofibrils in spreading adult cardiomyocytes in tissue culture: evidence for reexpression of the embryonic program for myofibrillogenesis in adult cells.

Do adult cardiomyocytes use the same pathways hypothesized for the formation of myofibrils in embryonic cardiomyocytes in tissue culture. [Rhee, et al., Cell Motil. Cytoskeleton 28:1-24, 1994]? Premyofibrils in embryonic cardiomyocytes are composed of short sarcomeric units of alpha-actinin (Z-bodies) and actin filaments held together by short nonmuscle myosin IIB filaments. Premyofibrils are believed to be transformed into nascent myofibrils by their capture of muscle-specific myosin II filaments aligned in aperiodic arrays. Nascent myofibrils are thought to transform into mature myofibrils by the loss of nonmuscle myosin IIB, the fusion of the Z-bodies into Z-bands, and the periodic alignment of muscle myosin II filaments into A-bands. Freshly isolated cat and rat adult cardiomyocytes placed in tissue culture lack premyofibrils and nascent myofibrils. Adult cardiomyocytes spreading in culture reinitiate the synthesis of nonmuscle myosin IIB. Moreover, patterns similar to the proposed embryonic myofibrillar program first detected in spreading chick embryonic hearts were also detected in these spreading adult mammalian cardiomyocytes. The isolated adult cardiomyocytes begin to spread after 1 day in culture by sending out lamellipodia. When these cells are injected with fluorescently labeled alpha-actinin, linear arrays of short spacings of beaded alpha-actinin bodies are detected in the spreading edges of the adult cardiomyocytes. These dense bodies (Z-bodies) stain positively for the same sarcomeric-specific isoform of alpha-actinin that is in the Z-bands of mature sarcomeres. These linear arrays of alpha-actinin-containing Z-bodies have other characteristics of premyofibrils and are detected only in the spreading regions of the cells. Thus, these premyofibrils at the edges of the spreading adult cardiomyocytes stain positively for nonmuscle myosin IIB but negatively for muscle-specific myosin II. Initially, no vinculin is associated with any parts of the premyofibrils in the spreading regions of the early spreading cardiomyocytes. However, later, vinculin is found to be associated with the ends of the premyofibrils. Fibers that stain solidly for muscle-specific myosin II (i.e., nascent myofibrils) are localized between the peripheral premyofibrils and the centrally positioned, mature myofibrils. It is suggested that the puzzling ability of cardiomyocytes in hypertrophic hearts to reinitiate the synthesis of fetal sarcomeric proteins may be related to the reinitiation of the embryonic premyofibril program for myofibrillogenesis.

Animals↗
PubMed1997

A phospholipase D and protein kinase C inhibitor blocks the spreading of murine mammary adenocarcinoma cells altering f-actin and beta1-integrin point contact distribution.

Spreading is a critical process involved in motility and growth of tumor cells during the metastatic cascade. Focal adhesion kinase, src-proteins and PKC have been reported to participate in the regulation of cytoskeleton organization in both normal and transformed cells during spreading. The role of other signaling enzymes such as PLD and PAP has not been studied during spreading in tumor cells. We now show that the spreading of murine mammary adenocarcinoma LM3 cells was significantly reduced by n-butanol, a PLD and PKC inhibitor, with a maximal inhibition of 54% (p < 0.001) in both the presence and absence of serum, as measured by phase-contrast microscopy. PMA only stimulated cell spreading over the control in the absence of serum and n-butanol inhibition was completely reversed by PMA treatment in both conditions. PA, the product of PLD activity, stimulated LM3 cell spreading and the same effect was observed with staurosporine. Spreading was enhanced when cells were seeded on collagen-IV- or fibronectin-coated surfaces and n-butanol could inhibit both integrin-derived signals. Cell spreading inhibition correlated with the absence of f-actin bundles and fewer beta1-integrin point contacts as determined by double immunofluorescence microscopy. In addition, n-butanol inhibited the proliferation of LM3 cells in the presence of serum (p < 0.01). These results suggest that beta1-integrin and f-actin/point contact assembly, involved in spreading and proliferation, require the participation of PLD-PKC regulatory pathways in LM3 cells.

1-Butanol↗
PubMed1994

Management of ductal carcinoma in situ with nipple discharge. Intraductal spreading of carcinoma is an unfavorable pathologic factor for breast-conserving surgery.

BACKGROUND: Surgical management of ductal carcinoma in situ (DCIS) has been a controversial issue in the selection of breast-conserving surgery as a method of treatment. The definition of intraductal spreading of carcinoma becomes an important factor in the decision making process, but little is known about how much intraductal extension influences the spreading of tumor in the whole breast. To define any unfavorable pathologic factors existing in limited surgery for patients with DCIS, the authors investigated histopathologic characteristics using a sequential slicing of tissues. METHODS: Duct-lobular segmentectomy, a limited surgery, was performed on 110 patients with a bloody nipple discharge. Six patients with invasive carcinoma and 17 patients with DCIS subsequently received a total mastectomy. The specimens obtained by segmentectomy and mastectomy were histopathologically examined. Using subserial sections, the authors examined the relationship between intraductal spreading of carcinoma in the segmentectomy specimens and carcinoma residue in the mastectomy specimens. RESULTS: Among 16 mastectomy specimens, the authors found residual DCIS in 6, and atypical ductal hyperplasia in 4. Intraductal spreading of carcinoma was detected in 8 of 16 segmentectomy specimens. Six of eight patients with intraductal spreading had residual DCIS. The other two patients had atypical hyperplasia in breasts. No residual DCIS was detected in the other eight patients without intraductal spreading. Among 12 patients under observation who did not have a mastectomy, invasive carcinoma subsequently developed in 3. Two of three patients had intraductal spreading in segmentectomy specimens. Only 1 of 10 patients without intraductal spreading, however, developed carcinoma. CONCLUSIONS: Intraductal spreading of carcinoma is an unfavorable pathologic factor in breast-conserving surgery for patients with ductal carcinoma in situ with nipple discharge.

Adolescent↗
PubMed1992

The lipoxygenase metabolite 12(S)-HETE promotes alpha IIb beta 3 integrin-mediated tumor-cell spreading on fibronectin.

Tumor-cell interaction with the vessel wall during metastasis involves adhesion, induction of endothelial-cell retraction and spreading on the exposed sub-endothelial matrix. The signals for initiation of tumor-cell spreading and the receptors involved are unknown. A protocol was developed to distinguish between initial tumor-cell (B16 amelanotic melanoma; B16a) adhesion to and spreading on fibronectin. The time for maximum spreading was 50 min. Treatment with a lipoxygenase metabolite of arachidonic acid [12(S)-HETE] resulted in maximum spreading in 15 min (max. effect approx. 0.1 microM). Other lipoxygenase metabolites were ineffective. 12(S)-HETE treatment induced a rearrangement of F-actin, vinculin, vimentin intermediate filaments and integrin alpha IIb beta 3, but not integrin alpha 5 beta 1. Antibodies to alpha IIb beta 3 but not alpha 5 beta 1 blocked the 12(S)-HETE effect on B16a spreading. B16a-cell attachment to fibronectin resulted in increased metabolism of arachidonic acid to 12(S)-HETE, which was inhibited by lipoxygenase but not by cyclo-oxygenase inhibitors. Accordingly, lipoxygenase inhibitors but not cyclo-oxygenase inhibitors blocked spontaneous B16a-cell spreading. The protein-kinase-C inhibitors calphostin C, H7 and staurosporine also inhibited spreading, while the protein-kinase-A inhibitor H8 was ineffective. These data suggest that B16a-cell spreading on fibronectin is initiated by a lipoxygenase metabolite [12(S)-HETE] of arachidonic acid and is mediated by protein kinase C.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMedDate not supplied

The influence of substratum surface free energy on growth and spreading of human fibroblasts in the presence and absence of serum proteins.

To determine whether the surface free energy of polymer materials influences the spreading of 13 polymers and glass were related to spreading and growth of human skin fibroblasts. Experiments were performed in both the presence and absence of serum proteins. We calculated the surface free energy from contact angles of phosphate-buffered saline (PBS), n-propanol/PBS mixtures, and alpha-bromonaphthalene on the polymers, using the concept of polar and dispersion components accounting for spreading pressures. Cell spreading and substratum surface free energy (gamma s) showed a characteristic sigmoid relationship both in the presence and in the absence of serum proteins; good spreading only occurred when gamma s was higher than approximately 57 erg . cm-2. In the presence of serum proteins, cell spreading is similar on most materials; only few materials show relatively high cell spreading. Cell growth in the presence of serum proteins did not differ significantly on the various polymers with reference to their gamma s values. In contrast, two groups of polymers could be distinguished in the absence of serum with respect to cell growth. The first group showed increasing cell growth with increasing gamma s, whereas the second group showed consistently low cell growth. The results demonstrate the complex relationship between cell spreading and substratum surface free energy as well as the role of serum proteins in modifying the surface characteristics of polymers in relation to cell spreading and growth.

Biocompatible Materials↗
PubMed1999

The beta1-integrin cytosolic domain optimizes phospholipase A2-mediated arachidonic acid release required for NIH-3T3 cell spreading.

Inhibition of PLA2 activity and rescue by addition of exogenous AA was used to demonstrate that AA production is essential for integrin-mediated NIH-3T3 murine cell spreading. Both AA release and cell spreading after attachment to a FN substrate were inhibited by the PLA2 inhibitor mepacrine. AA release was essential for signaling spreading since the inhibition of spreading induced by mepacrine was overcome by exogenous AA. Cells ectopically expressing full-length chicken beta1-integrins both released AA and spread fully on a substrate of anti-chicken beta1-integrin monoclonal antibody, and inhibition of PLA2 by mepacrine suppressed both spreading and AA release. Exogenous AA also reversed this mepacrine-induced inhibition of spreading. The role of the beta1-integrin cytosolic domain in AA release was examined by comparing responses of cells expressing full-length chicken beta1-integrins versus cells expressing a deletion mutant chicken beta1-integrin with a truncated cytosolic domain. Cells expressing a truncated chicken beta1-integrin released significantly less AA and failed to spread on the anti-chicken beta1-integrin antibody substrate. Furthermore, clustering full-length receptors with soluble antibody stimulated greater AA release than clustering of receptors having truncated cytosolic domains. These data suggest the beta1-integrin cytosolic domain is required for optimal PLA2 activation to produce AA necessary for cell spreading.

3T3 Cells↗
PubMed1984

Spreading of explants of embryonic chick mesenchymes and epithelia on fibronectin and laminin.

Tissues from 2.5-day chick embryos were explanted onto glass coated with adsorbed fibronectin or laminin, or extracellular matrices (ECM) of deoxycholate-extracted chick embryo cells. Spreading of somitic and trunk neural-crest mesenchyme cells was equally rapid and extensive on fibronectin, laminin and on the fibronectin-rich, laminin-poor ECM produced by mesenchymal cells. No preference for fibronectin over laminin was displayed by these two mesenchymes when a choice of mutually exclusive alternating tracks was provided. Epithelial cells did not spread from explants of the neural tube on any substrate tested up to 24 h in vitro, but adhesion of the explant and outgrowth of axons was greatest on laminin. Explants of endodermal epithelium spread rapidly on or near ECM formed by endoderm cells. This ECM was deficient in laminin but contained dense fibronectin fibers. Spreading was less rapid on fibronectin, and even more retarded on laminin. Ectodermal epithelium explants spread rapidly on and near fibronectin-rich, laminin-poor ECM produced by ectoderm cells, and almost as rapidly on laminin, but spreading was strongly delayed and reduced on fibronectin. The observations suggest that the mesenchymal nature of somite and neural crest cells does not correspond to a lowered responsiveness to laminin relative to fibronectin, while the relationship between laminin and superior epithelial cell spreading should not be generalized. The spreading of the epithelia on complex ECM also indicates the presence of a component(s) other than fibronectin or laminin, which strongly promote(s) spreading. In addition, the methods used indicate that plasma fibronectin and laminin do not specifically bind to each other, and that bovine serum albumen may be inadequate in preventing the attachment of proteins, especially laminin, to cell culture substrates.

Animals↗