Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “elevational migration”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources

Differentiation associated changes in thymidylate synthetase and thymidine kinase activities in intestinal cells.

Proliferative and mature intestinal cells of the jejunum and colon of rat, colon of man, and the surface cells of neoplastic colon lesions of man were assayed for thymidylate synthetase and thymidine kinase activities. Cells from the proliferative region of rat jejunal mucosa were found to have higher enzyme activities than cells from the non-proliferative region. Thymidylate synthetase activity was observed to decrease as cells migrated from base to upper crypt, whereas thymidine kinase activity increased during crypt migration and then declined as cells migrated onto villi. Thymidine kinase activity also remained elevated longer than thymidylate synthetase during cell migration in colonic mucosa of rat and man. High thymidine kinase: thymidylate synthetase ratios similar to those observed in flat mucosa before cells become fully mature were found in cells removed from expanding neoplastic lesions of man.

Adenoma↗

Cyclic AMP-mobilizing agents and glucocorticoids modulate human smooth muscle cell migration.

Hyperplasia and cell migration of smooth muscle are features of both airway and pulmonary vascular diseases. The precise cellular and molecular mechanisms that regulate smooth muscle migration in the lungs remain unknown. In this study, we examined the effect of cAMP-mobilizing agents and steroids on smooth muscle cell migration. Platelet-derived growth factor (PDGF), transforming growth factor-alpha, vascular endothelial growth factor, and basic fibroblast growth factor significantly stimulated cell migration in pulmonary vascular smooth muscle (PVSM) cells. Airway smooth muscle (ASM) migration was also stimulated by PDGF, transforming growth factor-alpha, and basic fibroblast growth factor, but vascular endothelial growth factor was without effect. Interestingly, the smooth muscle mitogen thrombin did not stimulate migration of either cell type. Agents capable of elevating intracellular cAMP inhibited basal (unstimulated) cell migration in both cell types, whereas their effects on PDGF-stimulated migration were more variable. Prostaglandin E2, salmeterol, and the phosphodiesterase type 4 inhibitor cilomolast inhibited basal ASM and PVSM migration by 30-60%. Prostaglandin E2 and cilomolast also inhibited PDGF-stimulated migration of ASM and PVSM cells, but salmeterol was without effect. Preincubation of ASM cells with dexamethasone or fluticasone inhibited basal and PDGF-stimulated migration, and enabled an inhibitory effect of salmeterol on PDGF-induced cell migration. Steroids alone did not stimulate cAMP production or cAMP/PKA-dependent gene transcription (CRE-Luc activity), but slightly augmented salmeterol-stimulated CRE-Luc activity. Collectively, these findings demonstrate that cAMP-mobilizing agents and steroids modulate human smooth muscle cell migration, likely by distinct mechanisms.

Albuterol↗

Cell specific effects of glycosaminoglycans on the attachment and proliferation of vascular wall components.

Capillary formation has been correlated with changes in basement membrane-associated glycosaminoglycans (GAGs). During capillary growth when endothelial cells (EC) undergo extensive proliferation and migration and pericytes are scarce, hyaluronic acid (HA) levels are elevated. Upon capillary maturation when EC migration and proliferation cease and pericytes appear, the dominant GAG is heparan sulfate (HS). To investigate the potential role of GAGs in the angiogenic process, we studied the effect of HA, heparin, chondroitin sulfate, and dermatan sulfate on the attachment and proliferation of vascular wall cells in vitro. Cell attachment was studied by determining the number of cells attached to GAG-treated substrates. Whereas HA inhibited the attachment of both pericytes and smooth muscle cells (SMC) by nearly 80% after 8 hr, it enhanced capillary EC attachment by more than 30%. Retinal pigment epithelial cells and dermal fibroblasts were employed as controls and none of the GAGs examined significantly altered the attachment of these cells. The effect of GAGs on cell proliferation was determined by the addition of soluble GAGs to cells cultured for the time required for three population doublings. Heparin addition resulted in a dose-dependent inhibition of both pericyte and SMC proliferation with maximal inhibition of 50% at 100 micrograms/ml, whereas this concentration of heparin moderately enhanced capillary EC proliferation. These effects were not observed for any other cell type or with any other GAG and indicate that GAGs have cell-specific effects on the attachment and proliferation of cells of the vascular wall.

Animals↗

Metastasis is driven by sequential elevation of H-ras and Smad2 levels.

Metastasis is a multistep process that involves local tumour invasion followed by dissemination to, and re-establishment at, distant sites. Here we show that during multistage tumorigenesis, discrete expression thresholds of activated Smad2 and H-ras are sequentially surpassed, driving tumour progression through distinct phases from a differentiated squamous carcinoma to a motile invasive stage, followed by an overt change from epithelial to mesenchymal cell type, finally culminating in metastatic tumour spread. Smad2 activation alone induces migration of tumour cells. Elevated H-ras levels, however, are required for nuclear accumulation of Smad2, both of which are essential for the epithelial mesenchymal transition (EMT). Having undergone EMT, fibroblastoid carcinoma cells with elevated levels of activated Smad2, gain the capability to spread to a wide variety of tissues by a further increase in Smad2 expression. These findings have far-reaching implications for the prevention of tumour growth, invasion and metastasis.

Animals↗

Stimulatory effect of insulin on aortic smooth muscle cell migration induced by 12-L-hydroxy-5,8,10,14-eicosatetraenoic acid and its modulation by elevated extracellular glucose levels.

In investigations on the role of insulin on migration of rat aortic smooth muscle cells, migration of the cells was measured by a modified Boyden chamber technique with 12-L-hydroxy-5,8,10,14-eicosatetraenoic acid (12-HETE) as a chemoattractant. Insulin itself was not a chemoattractant for these cells, and insulin added just before the migration assay did not affect cell migration in the presence or absence of 12-HETE. Cells pretreated with insulin in culture dishes for a long period, however, showed a significant increase in migration induced by 12-HET, and the increase depended on the insulin concentration: concentrations of insulin of greater than 50 microIU/ml caused about twofold increase in cell migration. On the other hand, long-term incubation with various concentrations of insulin (0.15-1000 microIU/ml) did not affect nonspecific cell migration in the absence of 12-HETE. The stimulatory effect of insulin on cell migration gradually increased with the duration of insulin treatment, reaching a plateau after 4 days. Thus, insulin stimulated 12-HETE-induced smooth muscle cell migration in a time- and dose-dependent manner. When the extracellular D-glucose concentration in the Boyden chamber was increased from 100 to 300 mg/dl, the stimulatory effect of insulin on 12-HETE-induced cell migration was augmented. This modulation by D-glucose was not due to an increase in the osmotic pressure of the medium, since addition of mannitol to increase the osmotic pressure did not enhance the effect of insulin on cell migration.(ABSTRACT TRUNCATED AT 250 WORDS)

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

Migration of solid silicone encircling element through four rectus muscles.

Anterior migration of an encircling element through a rectus muscle is an unusual complication of scleral buckling surgery. We describe two patients with migration of a solid silicone encircling element through the insertions of all four rectus muscles after retinal detachment surgery. Buckle migration was associated with elevated intraocular pressure and glaucomatous optic atrophy. Rectus muscle function was preserved in both patients. Despite transsection of the anterior ciliary blood supply, anterior segment ischemia did not develop.

Adult↗

[Macrophage migration inhibition by T-cells in rats after overcoming natural tolerance to alpha fetoprotein].

Cellular immunity to alpha-fetoprein (AFP) was studied in rats by the macrophage migration inhibition (MMI) test after breakage of tolerance to homologous AFP of rat (RAFP). A single injection of cross-reacting AFP of mouse (MAFP) has induced the capacity of peritoneal exudate cells of rats to react in the MMI test to both MAFP and RAFP. The second injection of MAFP results in reduction of the MMI reaction to both antigens and the appearance of stimulation in the macrophage migration together with further elevation of antibody titer to MAFP and RAFP. The fractionation of rat peritoneal cells has shown the T-cell nature of MMI reaction to both MAFP and RAFP.

Animals↗

Targeted inhibition of wound-induced PAI-1 expression alters migration and differentiation in human epidermal keratinocytes.

In the adult epidermis, keratinocytes do not normally express the type-1 inhibitor of plasminogen activator (PAI-1). Basal epithelial cell-specific PAI-1 synthesis, however, accompanies epidermal wound repair in vivo in which PAI-1 transcripts and immunoreactive protein are confined to epithelial cells in the migrating tongue and the hyperproliferative zone. A model system using human keratinocytes (HaCaT cells) was developed to assess functional relationships between epithelial growth state transitions and PAI-1 expression. PAI-1 synthesis was maximal in low population density, exponentially growing HaCaT cultures; relative PAI-1 mRNA and protein levels progressively declined as cells attained, and were maintained in, a postconfluent condition. While the fraction of PAI-1(+) keratinocytes remained stable (at approximately 85-90% of the population) throughout the culture period, both PAI-1 mRNA abundance and mean cell-associated PAI-1 protein declined by >90% during prolonged (i.e., 8-day) growth arrest. Similar to epidermal trauma in vivo, scrape wounding of HaCaT monolayers resulted in the rapid and location-specific induction of PAI-1 protein (an increase of 11- to 16-fold relative to unwounded cultures) in cells immediately bordering the injury site. PAI-1 expression was evident in keratinocytes that comprised the opposed migrating fronts and remained elevated until wound closure. Down-regulation of PAI-1 synthesis in HaCaT cells transfected with an inducible LacSwitch-based antisense vector system markedly impaired both the rate and the extent of wound closure. All injuries created in antisense PAI-1 monolayers remained unhealed at day 8 postinjury compared to the 3-day complete repair typical of control cultures. Vector-driven modulation of PAI-1 synthesis was also associated with an increase in the percentage of suprabasal-type keratinocytes within the wound field. PAI-1 expression by migrating HaCaT cells appears necessary to maintain the basal epidermal phenotype and/or appropriate cell-to-substrate adhesion during injury repair.

Cell Differentiation↗

Quantitation of macrophage migration inhibitory factor (MIF) using the one-step sandwich enzyme immunosorbent assay: elevated serum MIF concentrations in patients with autoimmune diseases and identification of MIF in erythrocytes.

We raised monoclonal antibodies against human macrophage migration inhibitory factor (MIF), and developed a one-step sandwich enzyme-linked immunosorbent assay (ELISA) method highly specific for human MIF. The ELISA system utilizes a solid phase monoclonal antibody as a capture antibody and a horseradish peroxidase-conjugated monoclonal antibody as a detector antibody. We used this ELISA method to evaluate the serum level of MIF in 240 healthy volunteers (140 males and 100 females). We found no significant difference in MIF concentration with respect to age. A significant difference was found with respect to sex, with the mean value (+/- SD) for male subjects of 5.3+/-2.3, and that for female subjects of 4.6+/-2.3 ng/ml (p<0.05). We next measured the serum MIF contents of patients with autoimmune diseases, and found that MIF levels were significantly elevated in patients with systemic lupus erythematosus and rheumatoid arthritis, 20.0+/-11.0 ng/ml and 21. 7+/-11.2 ng/ml, respectively. Using anti-MIF antibody-immobilized sepharose column chromatography, we discovered for the first time that MIF was present in erythrocytes. Taken together these results suggest that MIF plays a major role in autoimmune diseases and, moreover, potentially induces various patho-logical outcomes in cases of hemolytic disorders.

Adult↗

Glucose-induced transmigration of monocytes is linked to phosphorylation of PECAM-1 in cultured endothelial cells.

The adherence of circulating monocytes to the endothelium, their migration into the subendothelium, and the subsequent formation of foam cells are initial events in the pathogenesis of atherosclerosis. However, the effect of hyperglycemia on the transendothelial migration of monocytes is not known. Exposure of human umbilical vein endothelial cells (HUVEC) cultured in a Transwell chamber to 25 mM D-glucose (a concentration representing a hyperglycemic state) for 2 h resulted in a twofold increase in the migration of vitamin D3-differentiated monocyte-like HL-60 cells. The migration was inhibited by addition of either an antibody to platelet-endothelial cell adhesion molecule-1 (PECAM-1) or a protein kinase C inhibitor, GF-109203X. In HUVEC, high concentrations of D-glucose (25 mM), but not of other sugars such as L-glucose, 2-deoxyglucose, D-galactose, or D-mannitol, caused a sevenfold increase in the phosphorylation of PECAM-1 as a result of activation of protein kinase C. The 25 mM D-glucose-induced PECAM-1 phosphorylation and transmigration of monocyte-like HL-60 cells were further increased by treatment of HUVEC with the phosphatase inhibitor calyculin A. These results suggest that direct phosphorylation of PECAM-1 in response to elevated glucose promotes transendothelial migration of monocytes, contributing to accelerated atherogenesis in diabetics.

Cell Movement↗

In vivo and in vitro granulocyte migration in patients with extrinsic and intrinsic bronchial asthma.

Sixty-five patients with atopic asthma, 54 with infectious asthma, and 30 healthy controls were evaluated by in vitro granulocyte migration and by the in vivo skin window method of Southam. Quantitative IgM, IgG, IgA, IgE serum concentrations were measured. In vivo migration of granulocytes was decreased in patients with atopic asthma and elevated levels of IgE as well as in patients with infectious asthma and elevated levels of IgG. In vivo migration of granulocytes showed significant decreases in both asthmatic groups only during asthmatic attacks.

Asthma↗

Epithelial regeneration after limbus-to-limbus debridement. Expression of alpha-enolase in stem and transient amplifying cells.

PURPOSE: To examine the expression of the glycolytic enzyme alpha-enolase after limbus-to-limbus epithelial debridement in the rabbit. METHODS: Corneas were debrided, leaving limbal epithelium intact, and were allowed to heal from 2 days to 8 weeks. Immunofluorescence microscopy was used to observe the expression of alpha-enolase. To quantitate changes in alpha-enolase levels 2 days to 4 weeks after wounding, epithelium was harvested, homogenized, and assayed using anti-alpha-enolase in immunoslot blots. RESULTS: Expression of alpha-enolase appeared to increase in the limbus and the central cornea during epithelial migration (2-day time point) with intense labeling of all basal cells. These levels were maintained until wound closure (1 week). By 2 weeks, expression in the limbal basal cells decreased to levels present in unwounded corneas. Expression in the corneal epithelium decreased after 2 weeks, progressing from central cornea to the periphery. At 4 weeks, antibody binding decreased concomitantly with a change in the shape of the basal cells from flattened or ovoid to columnar. At 8 weeks, expression of alpha-enolase was similar to that in control corneas. Immunoslot blot data indicated that alpha-enolase made up 0.28% of the total soluble protein in unwounded corneal epithelium and 0.73%, 1.22%, 0.96%, and 0.49% at 2 days, 1 week, 2 weeks, and 4 weeks after debridement, respectively. CONCLUSIONS: These data indicate that expression of alpha-enolase is elevated during corneal epithelial migration initiating from the stem (limbal basal) cell population and that expression is linked to active migration. Furthermore, it appears that limbal basal cells are metabolically active during the period of epithelial sheet movement, whereas peripheral corneal basal cells remain activated as long as 4 weeks after wounding.

Animals↗

ATP-induced CA2+-signaling enhances rat gastric microvascular endothelial cell migration.

The effects of exogenous ATP on Ca2+ signaling and wound healing were investigated in rat gastric microvascular endothelial cells (RGMEC). ATP (10 microM) triggered a significant rise in intracellular Ca2+ concentration ([Ca2+]i) from 46+/-2 nM at baseline to peak values averaging 283+/-31 nM (n = 5 experiments, 132 cells). Return to the basal [Ca2+]i was delayed by slowly declining plateau phase that persisted for 200+/-30 s. Removal of extracellular Ca2+ did not significantly affect the peak rise in [Ca2+]i, but reduced the plateau. ATP (10 microM) also significantly increased the migration of RGMEC in a wounded monolayer. Addition of the non-subtype selective purinergic receptor antagonist, suramin, abrogated the effects of ATP on [Ca2+]i and migration. We conclude that local elevation of ATP acting through purinergic receptors induce Ca2+ signals in RGMEC and may contribute to endothelial cell migration.

Adenosine Triphosphate↗

Relevance of the palatal protein kinase A pathway to the pathogenesis of cleft palate by secalonic acid D in mice.

Secalonic acid-D (SAD) is a teratogenic mycotoxin inducing cleft palate (CP) in the offspring of the exposed mice by reducing palatal shelf size secondary to reduced proliferation of the palatal mesenchymal (PM) cells. Co-administration of dimethylsulfoxide (DMSO) reversed the CP-inducing effect of SAD. Although SAD has been shown to affect both protein kinases A (PKA) and C (PKC) pathways, the relevance of each of these pathways to its CP induction is unknown. The present studies were designed to test the hypothesis that the protective effect of DMSO is mediated by its specific reversal of the effect(s) of SAD on one of these two pathways using ELISA-based activity assays, Western blot analysis, electrophoretic mobility shift assays (EMSA), and murine embryonic PM (MEPM) cell growth in culture. Within the PKA pathway, SAD inhibited the activity of the catalytic subunit of PKA and its migration into the nucleus, elevated phosphorylated cyclic AMP (cAMP) response element (CRE)-binding protein (pCREB) level, and reduced the binding of CREB to CRE. In the PKC pathway, SAD reduced the activity of PKC and the binding of transcription factors (TF) to 12-O-tetradecanoate-13 phorbol acetate-response element (TRE). SAD also inhibited MEPM cell growth and the expression of the CRE- and TRE-containing gene, proliferating cell nuclear antigen (PCNA). Reversal, by DMSO, of the effects of SAD on MEPM cell growth, on PCNA expression and on all components of the PKA, but not of PKC, pathway suggests that the perturbation of the PKA pathway by SAD is relevant to its induction of CP in mice.

Animals↗

Presenilin/gamma-secretase-mediated cleavage of the voltage-gated sodium channel beta2-subunit regulates cell adhesion and migration.

The voltage-gated sodium channel beta2-subunit (beta2) is a member of the IgCAM superfamily and serves as both an adhesion molecule and an auxiliary subunit of the voltage-gated sodium channel. Here we found that beta2 undergoes ectodomain shedding followed by presenilin (PS)-dependent gamma-secretase-mediated cleavage. 12-O-Tetradecanoylphorbol-13-acetate treatment or expression of an alpha-secretase enzyme, ADAM10, resulted in ectodomain cleavage of beta2 in Chinese hamster ovary cells. Subsequent cleavage of the remaining 15-kDa C-terminal fragment (beta2-CTF) was independently inhibited by three specific gamma-secretase inhibitors, expression of the dominant negative form of PS1, and in PS1/PS2 knock-out cells. gamma-Secretase inhibitor treatment also increased endogenous beta2-CTF levels in neuroblastoma cells and mouse primary neuronal cultures. In a cell-free gamma-secretase assay, we detected gamma-secretase activity-dependent generation of a 12 kDa beta2 intracellular domain (ICD), which was loosely associated with the membrane fraction. To assess the functional role of beta2 processing by gamma-secretase, we tested whether N-[N-(3,5-difluorophenylacetyl-l-alanyl)]-S-phenylglycine t-butylester (DAPT), a specific gamma-secretase inhibitor, would alter beta2-mediated cell adhesion and migration. We found that DAPT inhibited cell-cell aggregation and migration in a wound healing assay carried out with Chinese hamster ovary cells expressing beta2. DAPT also reduced migration of neuroblastoma cells in a modified Boyden chamber assay. Since DAPT treatment resulted in increased beta2-CTF levels, we also tested whether beta2-CTFs or beta2-ICDs would directly affect cell migration by overexpressing recombinant proteins. Interestingly, elevated levels of beta2-CTFs, but not ICDs, also blocked cell migration by 81 to 93%. Together, our findings show for the first time that beta2 is a PS/gamma-secretase substrate and gamma-secretase mediated cleavage of beta2-CTF is required for cell-cell adhesion and migration of beta2-expressing cells.

Amino Acid Sequence↗

Food-contact epoxy resin: co-variation between migration and degree of cross-linking.

In order to predict the behaviour towards foodstuffs of an epoxy resin composed of bisphenol A diglycidyl ether (BADGE), 4,4'-methylenedianiline (MDA) and additives (plasticizers: dibutylphthalate (DBP), dioctylphthalate (DOP); accelerator: salicylic acid; inorganic fillers), a co-variation was established between the parameters evaluating the degree of cross-linking of the three-dimensional network and the migration of constituent molecules into various food simulants (distilled water, distilled water/ethanol/acetic acid, distilled water/ethanol). Varied degrees of cross-linking were obtained by subjecting the resin to different curing temperatures: respectively, 5 degrees C, 20 degrees C, 50 degrees C and 90 degrees C for 7 days. Irrespective of the food stimulant tested, specific migrations (DBP, DOP, salicylic acid, primary aromatic amines) diminished greatly as the curing temperature increased. At the same time, the degree of cross-linking increased with curing temperature, as indicated by the increase in glass transition temperature, the decrease in residual reaction exotherms and increased stability of the rubber storage modulus E'rub (increase in cross-link nodes), the fall in relaxation enthalpies (reduction in physical ageing) and the decreased amplitude of the loss-factor, tan delta (reduction in chain mobility). Maximum cross-linking was obtained in the resin cured at 90 degrees C (temperature above Tg infinity). In contrast to the degree of cross-linking, evaporation contributed little to the reduction of migration due to the elevation of curing temperature.

Chemical Phenomena↗

Migration patterns and breast cancer risk in Asian-American women.

BACKGROUND: Breast cancer incidence rates have historically been 4-7 times higher in the United States than in China or Japan, although the reasons remain elusive. When Chinese, Japanese, or Filipino women migrate to the United States, breast cancer risk rises over several generations and approaches that among U.S. Whites. PURPOSE: Our objective was to quantify breast cancer risks associated with the various migration patterns of Asian-American women. METHODS: A population-based, case-control study of breast cancer among women of Chinese, Japanese, and Filipino ethnicities, aged 20-55 years, was conducted during 1983-1987 in San Francisco-Oakland, California, Los Angeles, California, and Oahu, Hawaii. We successfully interviewed 597 case subjects (70% of those eligible) and 966 control subjects (75%). RESULTS: A sixfold gradient in breast cancer risk by migration patterns was observed. Asian-American women born in the West had a breast cancer risk 60% higher than Asian-American women born in the East. Among those born in the West, risk was determined by whether their grandparents, especially grandmothers, were born in the East or the West. Asian-American women with three or four grandparents born in the West had a risk 50% higher than those with all grandparents born in the East. Among the Asian-American women born in the East, breast cancer risk was determined by whether their communities prior to migration were rural or urban and by the number of years subsequently lived in the West. Migrants from urban areas had a risk 30% higher than migrants from rural areas. Migrants who had lived in the West for a decade or longer had a risk 80% higher than more recent migrants. Risk was unrelated to age at migration for women migrating at ages less than 36 years. Ethnic-specific incidence rates of breast cancer in the migrating generation were clearly elevated above those in the countries of origin, while rates in Asian-Americans born in the West approximated the U.S. White rate. CONCLUSIONS: Exposure to Western lifestyles had a substantial impact on breast cancer risk in Asian migrants to the United States during their lifetime. There was no direct evidence of an especially susceptible period, during either menarche or early reproductive life. IMPLICATIONS: Because heterogeneity in breast cancer risk in these ethnic populations is similar to that in international comparisons and because analytic epidemiologic studies offer the opportunity to disentangle correlated exposures, this study should provide new insights into the etiology of breast cancer.

Adult↗

Fer kinase is required for sustained p38 kinase activation and maximal chemotaxis of activated mast cells.

Mast cells play important roles in inflammation and immunity and express the high-affinity immunoglobulin E receptor (Fc epsilon RI) and the receptor protein-tyrosine kinase Kit. Aggregation of Fc epsilon RI via antigen binding elicits signals leading to the release of preformed inflammatory mediators as well as de novo-synthesized lipid mediators and cytokines and to elevated cell adhesion and migration. Here, we report that in mouse bone marrow-derived mast cells, Fer kinase is activated downstream of activated Fc epsilon RI and activated Kit receptor, and this activation is abolished in cells homozygous for a kinase-inactivating mutation in Fer (fer(DR/DR)). Interestingly, the highly related Fps/Fes kinase is also activated upon Fc epsilon RI aggregation. This report represents the first description of a common signaling pathway activating Fer and Fps/Fes. While Fer-deficient cells showed similar activation of the Erk mitogen-activated protein (MAP) kinases, p38 MAP kinase activation was less sustained than that in wild-type cells. Although no major defects were observed in degranulation, leukotriene biosynthesis, and cytokine secretion, Fer-deficient cells displayed increased adhesion and decreased motility upon activation of Fc epsilon RI and the Kit receptor. The restoration of Fer kinase activity in fer(DR/DR) mast cells resulted in prolonged p38 kinase activation and increased antigen-mediated cell migration of sensitized mast cells. Thus, Fer is required for maximal p38 kinase activation to promote the chemotaxis of activated mast cells. Further studies with mast cells derived from fps/fes-deficient mice will be required to provide insight into the role of Fps/Fes in mast cell activation.

Animals↗