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PubMed2000

Changes in keratin 6 and keratin 10 (co-)expression in lesional and symptomless skin of spreading psoriasis.

BACKGROUND: Keratin 6 (K6) and keratin 10 (K10) are markers for epidermal hyperproliferation and differentiation, respectively, and are both expressed in the suprabasal layers of the epidermis. They may be co-expressed in different stages of the spreading psoriatic lesion, but single expression can also occur. OBJECTIVE: To investigate to what extent keratinocytes express K6 and K10, and to what extent they co-express K6 and K10 in different stages of the psoriatic lesion. We studied this in spreading psoriatic plaques. METHODS: Three 3-mm punch biopsies were obtained from the inner involved margin of a spreading lesion, from the uninvolved skin immediately adjacent to the spreading plaque, and from the distant uninvolved skin of 8 patients with incipient psoriasis. From 9 healthy volunteers, 3-mm punch biopsies were obtained as controls. After preparation of single cell suspensions of these biopsies, a triple staining protocol was performed with markers for K6 (monoclonal antibody LHK6B), K10 (monoclonal antibody RKSE60) and DNA content (TO-PRO-3 iodide). Subsequently, cells were measured with a flow cytometer and the proportion of the markers was calculated using specific software. RESULTS: We observed a population of K6/K10-co-expressing cells, but also populations expressing only K6. These subpopulations varied with the involvement of the lesion. There was a statistically significant difference between the inner margin and the outer margin with respect to the proportion of K6- and K10-expressing cells, whereas more K6-positive and K10-negative cells were detected in the inner margin of the lesions. The proportion of K6/K10-co-expressing cells in the inner margin was significantly different from the distant uninvolved skin. CONCLUSION: We confirmed that individual keratinocytes in psoriasis can express K6 or K10 depending on their localization in involved or uninvolved skin. There is a unique subpopulation of cells in the psoriatic plaques which co-express K6 and K10. More studies are required to fully understand the pathogenic relevance of co-expression and single expression of K6 and K10.

Adult↗
PubMed2002

Symptom spread to contiguous body parts as a presentation of cerebral ischemia.

BACKGROUND: Ischemic stroke commonly presents with sudden onset of focal deficit that is maximal at onset. Symptom onset marked by the spread of symptoms to contiguous body parts may suggest migraine, seizure or cerebral amyloid angiopathy (CAA) that is mimicking ischemic symptoms. OBJECTIVE: To assess (1) if the spread of symptoms to contiguous body parts is an uncommon presentation of ischemic stroke and transient ischemic attack (TIA) and (2) if patients presenting with this symptom complex frequently have migraine, seizure or CAA mimicking stroke or TIA. METHODS: 110 consecutive patients presenting with stroke-like symptoms were prospectively evaluated for symptoms at onset, abnormalities on cerebral imaging, risk factors for stroke, discharge diagnosis, and development of subsequent TIA/stroke, migraine, seizure, or cerebral hemorrhage during follow-up. RESULTS: Of patients able to give a history of symptoms at onset, 23% described symptoms spreading to contiguous body parts. None had a history of migraine or seizure. None had clinical course or imaging features typical of CAA. During follow-up, 1 was diagnosed with migrainous stroke and none had suffered seizure or intracranial hemorrhage. CONCLUSIONS: The spread of symptoms to contiguous body parts is not uncommon at the onset of ischemic TIA/stroke. In our series, migrainous stroke was much less common and none had evidence of seizure or CAA.

Adult↗
PubMed2002

Correlations between extent and spread of adenomyosis and clinical symptoms.

OBJECTIVE: To correlate the histopathology of adenomyosis particularly the depth and spread of adenomyosis and symptomatology. STUDY DESIGN: Medical records of 94 patients who had undergone a hysterectomy and who were found to have adenomyosis on histopathologic examination were reviewed and histopathologic slides were reexamined. The symptoms were correlated with the presence of adenomyosis, the depth of penetration, and the spread of adenomyosis foci. RESULTS: Specimens were stratified according to the degree of adenomyosis penetration into 4 groups: group A consisted of specimens with adenomyosis penetration into the myometrium of up to 25%; group B, 26-50%; group C, 51-75%, and group D, >75%. There was a significant correlation between the depth of penetration and the number of adenomyosis foci (r = 0.3446; p = 0.0001). Hemosiderin deposition was found mainly in the specimens with penetration of >75%. The symptoms did not correlate with the degree of penetration (r = 0.088; p NS). However, the spread of adenomyosis correlated significantly with pelvic pain (r = 0.80, p = 0.02), and with dysmenorrhea (r = 0.81, p = 0.01), but not with menorrhagia or dyspareunia. CONCLUSIONS: Hemosiderin deposition and adenomyosis foci are found predominantly in specimens with deep adenomyosis penetration. It suggests that the deeper the penetration, the more extensive the adenomyosis. Symptoms of adenomyosis do not correlate with the depth of penetration, but there is a correlation between the spread of adenomyosis and pelvic pain, and dysmenorrhea.

Adult↗
PubMed2005

CD63 modulates spreading and tyrosine phosphorylation of platelets on immobilized fibrinogen.

CD63 is a member of the tetraspanin superfamily of integral membrane proteins. Present on a variety of cells, tetraspanins can form lateral associations with integrins and may act as 'organizers' of multimolecular networks that modulate integrinmediated signaling, cell morphology, motility and migration. In resting platelets, CD63 is present on the membranes of dense granules and lysosomes but relocates to the plasma membrane following platelet activation and exocytosis where it associates with the platelet integrin alphaIIBbeta3-CD9 complex and with the actin cytoskeleton in an alphaIIBbeta 3-dependent manner. D545, a monoclonal antibody directed at the second extracellular loop of CD63,was used to investigate the role of CD63 in platelet adhesion, spreading and tyrosine phosphorylation. Using immunofluorescence microscopy and confocal imaging, we have demonstrated that D545 does not alter adhesion of platelets to immobilized fibrinogen, but instead platelet spreading. In the presence of buffer or non-specific mouse IgG, activated platelets showed fully spread morphology, F-actin reorganization, redistribution of vinculin and extensive tyrosine phosphorylation, all of which were inhibited by D545. D545 also inhibited the phosphorylation of focal adhesion kinase in thrombin-activated adherent platelets. These results suggest that CD63 may modulate alphaIIBbeta3-dependent cytoskeletal reorganization. To identify signaling enzymes associated with CD63 that could affect this pathway, lipid kinase assays were performed on D545 immunoprecipitates. CD63 co-immunoprecipitated with a lipid kinase which, on the basis of enzymatic properties(stimulated by nonionic detergents, inhibited by adenosine), is consistent with PI 4-kinase type II. The CD63-PI 4-kinase complex was not activation-dependent as the constituents were co-purified from both resting and activated platelets. The linkage of CD63 with PI 4-kinase may result in the recruitment of this signaling enzyme to specific membrane locations in the platelet where it influences phosphoinositide-dependent signaling and platelet spreading.

1-Phosphatidylinositol 4-Kinase↗
PubMed2000

Angiotensin II and PDGF-BB stimulate beta(1)-integrin-mediated adhesion and spreading in human VSMCs.

beta(1)-Integrins play an important role for adhesion and spreading of human smooth muscle cells. In the present study we examined the influence of angiotensin II and platelet-derived growth factor (PDGF)-BB on beta(1)-integrin-dependent functions of human smooth muscle cells obtained from iliac arteries. Treatment of these cells with PDGF-BB (20 ng/mL) and Angiotensin II (1 micromol/L) did not change beta(1)-integrin expression up to 48 hours as analyzed by flow cytometry and reverse transcription polymerase chain reaction. beta(1)-integrins predominantly mediated adhesion of human smooth muscle cells to collagen I (79.7+/-4.4%, P<0.01) and fibronectin (66. 6+/-2.4%, P<0.01). Treatment of smooth muscle cells with Angiotensin II (1 micromol/L) and PDGF-BB (20 ng/mL) significantly increased the adhesion to collagen I by 56.5% and 44.3%, respectively, and to fibronectin by 49.6% and 36.4%, respectively (all P<0.05). Angiotensin II-induced effects were mediated by the AT(1) receptor. The PDGF-BB mediated increase of adhesion was inhibited in the presence of genestein, a tyrosine-kinase inhibitor and by protein kinase C downregulation with phorbol 12-myristate 13-acetate. Spreading of smooth muscle cells also was beta(1)-integrin dependent on collagen I and alpha(5)beta(1)-integrin dependent on fibronectin. Angiotensin II and PDGF-BB increased cell spreading on fibronectin up to 276% and 318%, respectively, and on collagen I up to 133% and 138% (all P<0.05). These increases were significantly inhibited by blocking antibodies against beta(1)-integrin, alpha(5)-integrin on fibronectin, the AT(1) receptor blocker irbesartan, and genestein. The present data demonstrate that angiotensin II and as well PDGF-BB enhance beta(1)-integrin-dependent adhesion and spreading of human vascular smooth muscle cells. Furthermore, the experiments with PDGF suggest an involvement of protein kinase C activation leading to these enhanced effects.

Angiotensin II↗
PubMed1991

The effects of substrate-adsorbed albumin on platelet spreading.

Adsorbed albumin appears to passivate nearly all materials, minimizing platelet adhesion and thrombus formation. Since in vitro platelet spreading can be an indicator of in vivo reactivity leading to thrombosis, and as in vitro platelet adhesion investigations are routinely done in the presence of bovine or human serum albumin (BSA or HSA), we examined the influence of albumin on platelet reactivity to material substrates. Platelet spreading was examined subsequent to adherence onto several related polyurethanes, and to Formvar, in the presence of bulk albumin concentrations sufficient to form an adsorbed monolayer or a multilayer. No other exogenous proteins were present. The spreading behavior of adherent platelets was analyzed using generalized linear interactive modeling (GLIM). The models showed that the polymer type always influenced platelet responses, irrespective of the albumin concentration. In many experiments, platelet behavior could be adequately modeled without including the effects of albumin. Thus, the polymer type appeared to be the primary determinant of platelet shape-change with adsorbed albumin producing a secondary effect. Additionally, somewhat different effects on spreading were observed with HSA and BSA, suggesting qualitatively different interactions between human platelets and HSA, than with BSA, which is commonly used in platelet preparations.

Adsorption↗
PubMed1987

Point spread functions and detail detection.

Point spread functions, intended to characterize local spatial transfer of the visual system, can be obtained psychophysically using a perturbation technique. Data of such point spread functions are shown for three experimental conditions: foveally at adaptation levels of 1200 and 10 Td, and in the parafovea at an eccentricity of 2 deg using a 1200 Td adaptation level. The results are consistent with earlier findings (Blommaert, F. J.J. and Roufs, J.A.J. 1981, Vision Res. 21, 1223-1233). On the basis of such point spread functions a simplified multiple unit model was constructed, the parameters of which were fitted to thresholds of discs with varying diameter. Threshold predictions from this model for annuli, thin lines and broad lines were found to be in fair quantitative agreement with experimental results. It is argued that for a certain class of slender stimuli, including alphanumeric characters, thresholds can be described with a single channel model containing only the experimentally determined point spread function as a basic component.

Humans↗
PubMed2003

Delayed spread and reduction in virus titer after anterior chamber inoculation of a recombinant of HSV-1 expressing IL-16.

PURPOSE: The timing of T-cell infiltration of the hypothalamus is crucial in the prevention of bilateral retinitis in mice inoculated with HSV-1 through the anterior chamber (AC). In H129-infected mice, T-cells are recruited to the suprachiasmatic nuclei of the hypothalamus too late to protect infected mice from development of bilateral retinitis. The purpose of these studies was to determine whether alteration of T-cell recruitment to the hypothalamus would affect the timing and pattern of virus spread after AC inoculation. METHODS: A recombinant of the H129 strain of HSV-1 expressing IL-16, a cytokine with lymphocytic and monocytic chemoattractant properties, was constructed, and mice were inoculated in the AC with H129wt, H129wt and H129/IL-16, or H129wt and H129/pGal10 (a recombinant virus containing vector only). RESULTS: AC inoculation of BALB/c mice with H129wt and H129/IL-16 resulted in a delay of virus spread to the hypothalamus and the contralateral retina, and this delay correlated with decreased virus titers in infected tissues, compared with mice infected with H129wt or mice infected with H129wt and H129/pGal10. Although the number of infiltrating T-cells in the brains of mice infected with H129wt, H129wt and H129/IL-16, or H129wt and H129/pGal10 was similar, more Mac-1-positive cells were detected early (postinoculation day 2) in the injected eyes of mice infected with H129wt and H129/IL-16 than in mice infected with H129wt and/or H129wt and H129/pGal10. CONCLUSIONS: These results suggest that early recruitment of Mac-1-positive cells to the injected eye may play a role in delaying virus spread in mice infected with H129wt and the IL-16-expressing recombinant virus. IL-16 delivery vectors could be exploited to prevent or delay HSV-1 infection of the hypothalamus, allowing development of the antiviral immune response and subsequent inhibition of virus spread into the optic nerve and retina.

Animals↗
PubMed2006

Inter- and intramolecular epitope spreading in equine recurrent uveitis.

PURPOSE: To test the hypothesis that inter- and intramolecular spreading to S-antigen (S-Ag) and interphotoreceptor retinoid binding protein (IRBP)-derived epitopes occurs in a spontaneous model of recurrent uveitis in the horse. METHODS: The immune response of eight horses with equine recurrent uveitis (ERU) was compared with that of five control horses with healthy eyes. Lymphocytes derived from peripheral blood (PBLs) were tested every 8 weeks for their reactivity against S-Ag and various S-Ag and IRBP-derived peptides for 12 to 39 months (median, 22 months). During uveitic episodes, additional blood samples were analyzed. RESULTS: Intermolecular epitope spreading was detectable in all ERU cases during the study. Intramolecular spreading occurred in seven (of eight) horses with ERU. Fourteen relapses were analyzed during the observation period. Ten uveitic episodes were accompanied by neoreactivity to S-Ag or IRBP-derived peptides during the relapse. Shifts in the immune response profile were also detectable without any clinical signs of inflammation. Eye-healthy control horses were negative at all time points in the in vitro proliferation assays. CONCLUSIONS: Inter- and intramolecular spreading was detectable in a spontaneous model of recurrent uveitis. The shifts in immunoreactivity could account for the remitting-relapsing character of the disease.

Animals↗
PubMedDate not supplied

Metastatic spread and common symptoms. Part six: Advanced cancer of the pancreas, prostate, stomach, and uterus.

This is the last article in a six-part series on metastatic spread and natural history of the 18 most lethal tumors. The articles summarize symptom/problem anticipation, cancer metastasis, and the 18 tumors that each cause more than 6000 deaths/year in the United States. Bladder and brain cancer were discussed, with information given on tumor types, metastatic spread and invasion, and common symptoms. Parts II, III, IV, and V charted the natural histories, problems, and assessment parameters of advanced cancers of the breast, colon and rectum, esophagus, kidney, liver, and lung; and leukemia, melanoma, multiple myeloma, non-Hodgkin's lymphoma, and cancers of the oral cavity (and pharynx) and ovary. Part VI finishes the series with discussions of cancers of the pancreas, prostate, stomach, and uterus. Each of these cancers is presented separately, with information given on mortality rates, the most common tumor types, sites of metastases, common problems, and common oncology emergencies. Sites of spread, resulting problems (including site-specific symptoms), and assessment parameters are presented as tables. Material is presented so that clinicians are able to anticipate the spread of these cancers and can thus identify problems early in their development so that the problems are more easily managed.

Female↗
PubMed2003

Calcium-and integrin-binding protein regulates focal adhesion kinase activity during platelet spreading on immobilized fibrinogen.

Platelet spreading on the subendothelium in response to vascular injury is fundamental to the regulation of physiologic hemostasis. Previously, we have shown that, when bound to glycoprotein IIb (GPIIb), calcium- and integrin-binding protein (CIB) regulates platelet spreading on immobilized fibrinogen (Fg). In this study, we investigated the signaling events that occur downstream of CIB in the absence of signaling that occurs as a result of granular secretion. Using Chinese hamster ovary (CHO) cells as a model, we demonstrate that CIB induces cell migration. Immunofluorescence analysis of CIB localization indicates that endogenous CIB accumulates in areas of focal adhesions, and its overexpression up-regulates the formation of focal adhesion complexes compared with control cells. Immunoprecipitation analysis indicates that CIB associates with focal adhesion kinase (FAK), a key regulator in focal complex formation, and up-regulates its activity. Overexpression of dominant-negative FAK, FRNK, along with CIB in CHO cells completely inhibits CIB-induced cell migration. Further, confirmation of these data in the platelet system indicates that CIB and FAK associate throughout all stages of platelet spreading but only on Fg binding to GPIIb/IIIa. Taken together, our results suggest that CIB regulates platelet spreading through the regulation of FAK activation.

Amino Acid Sequence↗
PubMed2005

The effect of posture and baricity on the spread of intrathecal bupivacaine for elective cesarean delivery.

Posture and baricity during induction of spinal anesthesia with intrathecal drugs are believed to be important in determining spread within the cerebrospinal fluid. In this double-blind prospective study, 150 patients undergoing elective cesarean delivery were randomized to receive a hyperbaric, isobaric, or hypobaric intrathecal solution of 10 mg bupivacaine during spinal anesthesia induced in either the sitting or right lateral position. After an intrathecal injection using a combined-spinal technique patients were placed in the supine wedged position. We determined the densities of the three intrathecal solutions from a previously validated formula and measured using a DMA-450 density meter. Data collection included sensory level, motor block, episodes of hypotension, and ephedrine use. Statistical analysis included analysis of variance and Cuzick's trend. In the lateral position, baricity had no effect on the spread of sensory levels for bupivacaine compared to the sitting position, where there was a statistically significant difference in spread with the hypobaric solution producing higher levels of analgesia than the hyperbaric solution (P = 0.002). However, the overall differences in maximal spread only differed by one dermatome, with the hyperbaric solution achieving a median maximum sensory level to T3 compared with T2 for the isobaric and hypobaric solutions. Motor block was significantly (P = 0.029) reduced with increasing baricity and this trend was significant (P = 0.033) for the lateral position only. Hypotension incidence and ephedrine use increased with decreasing baricity (P = 0.003 and 0.004 respectively), with the hypobaric sitting group having the most frequent incidence of hypotension (76%) as well as cervical blocks (24%; P = 0.032).

Adult↗
PubMed2002

Osteoclast spreading kinetics are correlated with an oscillatory activation of a calcium-dependent potassium current.

Cell movement and spreading involve calcium-dependent processes and ionic channel activation. During bone resorption, osteoclasts alternate between spread, motile and resorptive phases. We investigated whether the electrical membrane properties of osteoclasts were linked to their membrane morphological changes. Rabbit osteoclasts were recorded by time-lapse videomicroscopy performed simultaneously with patch-clamp whole cell and single channel recordings. Original image analysis methods were developed and used to demonstrate for the first time an oscillatory activation of a spontaneous membrane current in osteoclasts, which is directly correlated to the membrane movement rate. This current was identified as a calcium-dependent potassium current (IK(Ca)) that is sensitive to both charybdotoxin and apamin and was generated by a channel with unitary conductance of approximately 25+/-2 pS. Blockade of this current also decreased osteoclast spreading and inhibited bone resorption in vitro, demonstrating a physiological role for this current in osteoclast activity. These results establish for the first time a temporal correlation between lamellipodia formation kinetics and spontaneous peaks of IK(Ca), which are both involved in the control of osteoclast spreading and bone resorption.

Animals↗
PubMed2003

Mechanics of cell spreading: role of myosin II.

As it migrates over a substratum, a cell must exert different kinds of forces that act at various cellular locations and at specific times. These forces must therefore be coordinately regulated. The Rho-family GTPases Rac1 and Cdc42 promote actin polymerization that drives extension of the leading cell edge. Subsequently, RhoA regulates myosin-dependent contractile force, which is required for formation of adhesive contacts and stress fibers. During cell spreading, however, the activity of RhoA is reduced by a mechanism involving the tyrosine kinases c-Src and focal adhesion kinase (FAK), and the p190RhoGAP. It has been proposed that this reduction of RhoA activity facilitates edge extension by reducing myosin-dependent contractile forces that could resist this process. We have directly tested this hypothesis by correlating myosin activity with the rate of cell spreading on a substratum. The rate of spreading is inversely related to the myosin activity. Furthermore, spreading is inhibited by low concentrations of cytochalasin D, as expected for a process that depends on the growth of uncapped actin filaments. Cell indentation measurements show that a myosin-dependent viscoelastic force resists cell deformation.

Animals↗
PubMed1992

Mechanisms of epibolic tissue spreading analyzed in a model morphogenetic system. Roles for cell migration and tissue contractility.

The processes responsible for epithelial spreading during wound healing and embryonic morphogenesis were investigated in an organ culture model in which an epithelial tissue (chick embryo pigmented retinal epithelium) spread over the surface of an aggregate of mesenchyme cells (chick embryo cardiac mesenchyme). The heart mesenchyme aggregate is differentiated into a core of stellate cells associated with a fibronectin-poor matrix surrounded by a cortical zone, 2-5 cells in thickness, of flattened cells embedded in a fibronectin-rich extracellular matrix. Envelopment of the mesenchyme aggregate is accompanied by a movement of the cells and the fibronectin-rich extracellular matrix of the cortex over the core tissue in advance of the spreading pigmented retina tissue. Three distinct processes were identified as contributing to epithelial spreading in this system: (1) active migration of the pigmented retinal epithelium; (2) active contraction of the cortical cells of the mesenchyme aggregate to tow the attached epithelial tissue over the mesenchyme aggregate; and (3) ingression of surface-located cells of the mesenchyme aggregate to decrease the exposed surface area by decreasing the number of cells at the surface.

Animals↗
PubMed1993

Expression of integrin receptors and their role in adhesion, spreading and migration of normal human melanocytes.

Integrin receptors of human melanocytes in vivo and of melanocytes isolated and cultured from in vitro reconstituted normal human epidermis were investigated. Melanocytes were studied by high-resolution immunocytochemistry of in situ epidermis and were found to expose only the integrin subunits alpha 3, alpha 6, alpha v and beta 1 on their plasma membrane surface. Instead, cultured normal melanocytes expressed alpha 3 beta 1, alpha 5 beta 1, alpha 6 beta 1 and alpha v beta 3, which were immunoprecipitated from both metabolically and surface-labeled cells. Beta 1 integrins were diffused on the adhesion surface, while alpha v beta 3 was clustered in focal contacts both in control cells and upon dendrite induction with phorbol 12-myristate 13-acetate (PMA). The functional roles of integrins were studied in vitro by cell adhesion, spreading and migration assays. The sum of the data indicated that, in normal human melanocytes: (i) adhesion to defined substrata is mainly mediated by specific beta 1 integrins; (ii) spreading is mainly modulated by alpha v beta 3; (iii) the beta 1 and beta 3 heterodimers cooperate in regulating migration. The in vitro expression of two integrins (alpha v beta 3 and alpha 5 beta 1) that are not exposed in situ, and their role in the spreading and migratory properties of melanocytes, strongly suggest that they are involved in regenerating a normally pigmented epidermis during wound healing by controlling melanocyte spreading and migration over a provisional matrix. Tumor promoters, such as PMA, selectively increased the expression of alpha 3 beta 1. We suggest that this integrin might be involved in melanocyte migration on the newly formed basement membrane during wound healing as well as in intercellular recognition of adjacent keratinocytes.

Cell Adhesion↗
PubMed1996

Hydra regeneration from recombined ectodermal and endodermal tissue. I. Epibolic ectodermal spreading is driven by cell intercalation.

Cell-cell interaction and cell rearrangement were examined in the process of epithelial sheet formation during regeneration from hydra cell aggregates. The ectodermal and endodermal epithelial cell layers of Hydra magnipapillata were separated by procaine treatment. Each of the separated layers was then dissociated into single cells and reaggregated to produce ectodermal or endodermal cell aggregates. When the two aggregate types were recombined, a firm adhesion was quickly established between them. This was followed by a vigorous spreading of the ectodermal epithelial cells as a thin layer over the endoderm in a manner similar to the 'epiboly' in some developing embryos. Cell movement in this spreading process was examined using fluorescent dyestaining. It revealed that cells initially located in the inside of the aggregate migrated to intercalate themselves among the cells originally present in the contact surface. This radial cell intercalation took place continuously in the contact surface of both the ectodermal and endodermal aggregates, and produced a rapid growth of the contact surface, eventually leading to complete envelopment of the entire endoderm by the ectoderm. The resulting structure was a small sphere having a two-layered epithelial organization as in normal hydra. This sphere regenerated into a complete hydra a few days later. A tryptic extract of hydra membrane fraction specifically inhibited the ectodermal spreading over the endoderm, but not the initial adhesion or the later regeneration processes. These observations suggest that radial cell intercalation at the contact surface plays a crucial role in producing ectodermal spreading and establishing epithelial sheet organization in the recombined aggregates. The intercalation is presumably activated by a signal exchange through the contact surface. The inhibitory effect of the membrane extract suggests that it contains a factor that is involved in some way in this signaling mechanism.

Animals↗
PubMed1997

The alternatively spliced domains EIIIB and EIIIA of human fibronectin affect cell adhesion and spreading.

Fibronectin has a complex pattern of alternative splicing at the pre-mRNA level leading to the expression of different isoforms. The alternatively spliced domains EIIIB and EIIIA are known to be prominently expressed during development and wound healing. While the other spliced domain (CS-segment) is known to promote cell adhesion in a cell type specific manner, the biological functions of the spliced domains EIIIB and EIIIA are not well understood. In the present study, we have prepared expression proteins of specific domains of human fibronectin using a prokaryotic expression system and used the purified fragments to test their ability to support adhesion and spreading of cultured cells. Fragments from type-III domains #7 to #12 were prepared in various combinations to include or exclude the spliced domains EIIIB and EIIIA. The results indicate that cultured NIL fibroblasts adhere to many of the fragments tested. However, the cell adhesion and spreading are enhanced, especially at lower concentrations, to fragments including the domain EIIIB. The inclusion of domain EIIIA led to a decrease in the adhesion of cells and those that adhered did not spread well. When tested in a centrifugal cell adhesion assay, fragments including domain EIIIB resisted the detaching forces and stayed adhered. Fragments that included domain EIIIA were unable to resist the detaching centrifugal forces to the same extent as the fragments that included domain EIIIB alone. These results suggest that the spliced domain EIIIB may be serving important biological functions in enhancing cell adhesion and spreading. This is likely to be mediated by conformational effects because domain EIIIB alone neither exhibited any adhesive activity nor competed in inhibiting adhesion to fragments #7-10.

Actins↗