Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “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 1,135 records · Page 63Linked to original sources

Physician migration: views from professionals in Colombia, Nigeria, India, Pakistan and the Philippines.

There has been much debate recently about several issues related to the migration of physicians from developing to developed countries. However, few studies have been conducted to address these issues in a systematic fashion. In an attempt to begin the process of generating systematic data, we designed and distributed a questionnaire addressing several core issues surrounding physician migration to respondents selected on the basis of their special expertise or experience in India, Nigeria, Pakistan, Colombia, and the Philippines. The issues addressed relate to the reasons physicians migrate to developed countries, how migration is related to the structure of medical education, the effect that migration has on the health care infrastructure of developing countries, and various policy options for dealing with physician migration. Though responses varied somewhat by country, a desire for increased income, greater access to enhanced technology, an atmosphere of general security and stability, and improved prospects for one's children were the primary motivating factors for physician migration. A majority of respondents believed that physicians in developing counties are provided with highly specialized skills that they can better utilize in developed countries, but respondents were ambivalent with respect to the utility of educational reform. Responses varied significantly by country with regard to whether physician migration results in physician shortages, but there was widespread agreement that it exacerbates shortages in rural and public settings. With respect to policy options, increasing physician income, improving working conditions, requiring physicians to work in their home countries for a period following graduation from medical school, and creating increased collaboration between health ministries in developed and developing countries found the most favor with respondents.

Attitude of Health Personnel↗

Migration and maternal health services utilization in rural Guatemala.

This article examines the relationship between migration and the use of formal maternal health-care services among rural women in Guatemala. We identify assimilation, diffusion, and remittances as three potential pathways through which migration can affect health-care service utilization in rural areas. Using data from the 1995 Guatemalan Survey of Family Health and multi-level regression models, we estimate the impact of migration experience at the individual, household, and community level on the use of formal prenatal care and delivery assistance. We find that urban migration experience and having relatives abroad are associated with a greater likelihood of formal prenatal care utilization, after taking account of background characteristics and enabling resources. Migration experience at all levels is also strongly associated with formal delivery assistance; however, this association operates primarily through the positive association between migration and enabling resources. The differential effects of out-migration on maternal health-care service utilization reflect the different barriers to service use that exist for formal prenatal care and delivery assistance. Financial cost and geographic access are the most important barriers to formal delivery assistance, whereas awareness and acceptance remain as important barriers to the use of formal prenatal care in rural Guatemala. Urban migration experience and social ties to urban and international migrants lower the barriers to formal maternal health-care utilization through the acquisition and diffusion of new ideas and practices, and the return flow of financial resources.

Adolescent↗

Signalling pathways regulating human neutrophil migration induced by secretory phospholipases A2.

This study was designed to elucidate the signalling pathways by which secretory phospholipases A2 (sPLA2s) induce in vitro neutrophil migration. The cell migration assays were performed with Naja mocambique venom PLA2 (sPLA2 with high catalytic activity), bothropstoxin-I (sPLA2 devoid of catalytic activity) and platelet-activating factor (PAF), using a 48-well microchemotaxis chamber. Both the non-selective protein kinase inhibitor staurosporine (30-300 nM) and the selective protein kinase C (PKC) inhibitor 1-(5-isoquinolinesulfonyl)-2-methylpyperazine (H7; 50-200 microM) as well as the Gi inactivator pertussis toxin (30-300 nM) caused a concentration-dependent inhibition of the neutrophil migration induced by either N. mocambique venom PLA2 (100 microg/ml) or bothropstoxin-I (100 microg/ml). Pertussis toxin nearly abolished PAF-induced migration, while staurosporine and H7 partly (but significantly) inhibited the chemotactic responses to PAF. The dual inhibitor of cytosolic PLA2 and Ca2+ -independent PLA2 (iPLA2), arachidonil-trifluoromethyl-ketone (ATK; 0.2-20 microM), or the specific iPLA2 inhibitor bromoenol lactone (1-30 microM) caused a concentration-dependent inhibition of the migration induced by either sPLA2s. At the maximal concentration used for each compound, the migration was almost suppressed. In contrast, both of these compounds caused only slight inhibitions of PAF-induced migration. No rise in intracellular Ca2+ was observed in neutrophil-stimulated sPLA2, as determined in cells preloaded with fura 2-AM. In the experimental condition used, pertussis toxin, staurosporine, H7, ATK or bromoenol lactone did not induce cytotoxic effects, according to MTT assay. Our results suggest that activation of an endogenous PLA2 through activation of GTP-binding protein and PKC is the main mechanism by which exogenous sPLA2s cause neutrophil migration.

Calcium↗

The Drosophila transmembrane protein Fear-of-intimacy controls glial cell migration.

Development of complex organs depends on intensive cell-cell interactions, which help coordinate movements of many cell types. In a genetic screen aimed to identify genes controlling midline glia migration in the Drosophila nervous system, we have identified mutations in the gene kastchen. Here we show that during embryogenesis kastchen is also required for the normal migration of longitudinal and peripheral glial cells. During larval development, kastchen non-cell autonomously affects the migration of the subretinal glia into the eye disc. During embryonic development, kastchen not only affects glial cell migration but also controls the migration of muscle cells toward their attachment sites. In all cases, kastchen apparently functions in terminating or restricting cell migration. We identified the molecular nature of the gene by performing transgenic rescue experiments and by sequence analysis of mutant alleles. Kastchen corresponds to the recently described gene fear-of-intimacy (foi) that was identified in screen for genes affecting germ cell migration, suggesting that Foi-Kastchen is more generally involved in regulating cell migration. It encodes a member of an eight-transmembrane domain protein family of putative Zinc transporters or proteases. We determined the topology of the Foi protein by using antisera against luminal and intracellular domains of the protein and provide evidence that it does not act as a Zinc transporter. Genetic evidence suggests that one of the functions of foi may be associated with hedgehog signaling.

Animals↗

Tumor cell locomotion: differential dynamics of spontaneous and induced migration in a 3D collagen matrix.

Although great strides have recently been made in elucidating the factors initiating tumor cell migration and the relevant cellular pathways involved, the constituent components of migratory dynamics for individual tumor cell motion have still not been resolved. Utilizing a three-dimensional (3D) collagen assay and computer-assisted, continuous single cell tracking, we investigated the basic parameters for both the spontaneous and norepinephrine-induced migration of highly metastatic MBA-MB-468 breast, PC-3 prostate, and SW 480 colon carcinoma cells. We show that tumor cells do not migrate with uniform migrational structure and speed as previously thought, but rather, the induction of locomotion elicits significant increases in speed, break frequency, and total cell displacement, but decreases in break length and no change in the recruitment of nonlocomotory cells. We furthermore illustrate the corresponding morphological changes of induced tumor cell migration with emphasis on motion in a collagen matrix. These results demonstrate the complexity of tumor cell migration, and the compulsion for incorporating not only knowledge of intracellular pathways, but also fundamental parameters of migratory behavior into any expansive theory of tumor cell migration and metastasis formation. We furthermore establish the analytical methodology of investigating both the stimulation and potential pharmaceutical inhibition of tumor cell migration.

Biological Assay↗

Role of TGF alpha stimulation of the ERK, PI3 kinase and PLC gamma pathways in ovarian cancer growth and migration.

The Epidermal Growth Factor Receptor (EGFR) and its structural relative erbB2 are frequently over-expressed in ovarian cancers and both are strongly associated with poor patient survival. To investigate the relative roles of these receptors in the regulation of cell growth and migration, a panel of ovarian carcinoma cell lines were stimulated with TGF alpha and NRG1beta. TGF alpha had a much greater influence on cell migration than NRG1beta where growth effects were equivalent. The extent of TGF alpha-stimulated migration on collagen in these assays could be associated with erbB2 expression levels. In addition, TGF alpha was found to stimulate activation of the ERK, PI3 kinase and PLC gamma pathways. Direct blockade of the TGF alpha-interacting receptor EGFR inhibited both cell growth and migration, as well as downstream signaling induced by the growth factor. Specific blockade of the downstream proteins MEK and PI3 kinase significantly affected TGF alpha-induced mitogenesis in the cell lines tested but had less impact upon migration. Conversely, inhibition of the PLC gamma pathway had little effect on cell growth but significantly decreased TGF alpha-driven migration. These results corroborate the likely importance of migration as well as growth in erbB receptor over-expressing ovarian cancers and directly implicate the roles of ERK and PI3 kinase in growth control, and PLC gamma in the regulation of migration in this disease.

Cell Line, Tumor↗

Inhibition of SNARE-mediated membrane traffic impairs cell migration.

Cell migration occurs as a highly-regulated cycle of cell polarization, membrane extension at the leading edge, adhesion, contraction of the cell body, and release from the extracellular matrix at the trailing edge. In this study, we investigated the involvement of SNARE-mediated membrane trafficking in cell migration. Using a dominant-negative form of the enzyme N-ethylmaleimide-sensitive factor as a general inhibitor of SNARE-mediated membrane traffic and tetanus toxin as a specific inhibitor of VAMP3/cellubrevin, we conducted transwell migration assays and determined that serum-induced migration of CHO-K1 cells is dependant upon SNARE function. Both VAMP3-mediated and VAMP3-independent traffic were involved in regulating this cell migration. Inhibition of SNARE-mediated membrane traffic led to a decrease in the protrusion of lamellipodia at the leading edge of migrating cells. Additionally, the reduction in cell migration resulting from the inhibition of SNARE function was accompanied by perturbation of a Rab11-containing alpha(5)beta(1) integrin compartment and a decrease in cell surface alpha(5)beta(1) without alteration to total cellular integrin levels. Together, these observations suggest that inhibition of SNARE-mediated traffic interferes with the intracellular distribution of integrins and with the membrane remodeling that contributes to lamellipodial extension during cell migration.

Amino Acid Substitution↗

c-jun amino-terminal kinase and mitogen activated protein kinase 1/2 mediate hepatocyte growth factor-induced migration of brain endothelial cells.

Hepatocyte growth factor (HGF) influences several components of the angiogenic response, including endothelial cell migration. While recent studies indicate a crucial role of HGF in brain angiogenesis, the signaling pathways that regulate brain endothelial cell migration by HGF remain uncharacterized. Herein, we report that HGF stimulated human brain microvascular endothelial cell (HBMEC) migration in a dose- and time-dependent manner. Challenge of HBMECs with HGF activated the c-jun amino-terminal kinase (JNK), increased phosphorylation of the proline-rich tyrosine kinase 2 (Pyk-2) at Tyr(402) and activated c-Src. Inhibition of JNK by SP600125 or expression of a dominant negative JNK1 construct abrogated the migratory response of HBMECs to HGF. Treatment of HBMECs with the Src inhibitor PP2 markedly decreased HGF-stimulated JNK activation and migration to HGF. Moreover, expression of a mutant Pyk-2 construct prevented HGF-induced Pyk-2 phosphorylation at Tyr(402) and stimulation of HBMEC migration. Next, we examined activation of the extracellular signal regulated kinase (ERK) pathway. Stimulation of HBMECs by HGF led to rapid activation of ERK1/2, phosphorylation of Raf-1 at Ser(338) and Tyr(340/341) and MEK1/2 at Ser(222). Moreover, inhibition of ERK activation by UO126 and PD98059 markedly decreased HGF-stimulated HBMEC migration. HGF also activated AKT, while inhibition of AKT by LY294002 induced a modest decrease of HGF-induced HBMEC migration. These results highlight a model whereby JNK and ERK play a critical role in regulation of brain endothelial cell migration by HGF.

Brain↗

Lis1 is necessary for normal non-radial migration of inhibitory interneurons.

Type I lissencephaly is a central nervous system (CNS) malformation characterized by mental retardation and epilepsy. These clinical features suggest a deficit in inhibitory neurons may, in part, underlie the pathogenesis of this disorder. Mutations in, or deletions of, LIS1 are the most commonly recognized genetic anomaly associated with type I lissencephaly. The pathogenesis of type I lissencephaly is believed to be a defect in radial neuronal migration, a process requiring LIS1. In contrast the inhibitory neurons migrate non-radially from the basal forebrain to the neocortex and hippocampus. Given that Lis1 is expressed in all neurons, we hypothesized that Lis1 also functions in non-radial migrating inhibitory neurons. To test this hypothesis we used a combination of in vivo and in vitro studies with Lis1 mutant mice and found non-radial cell migration is also affected. Our data indicate Lis1 is required for normal non-radial neural migration and that the Lis1 requirement is primarily cell autonomous, although a small cell non-autonomous effect could not be excluded. These data indicate inhibitory neuron migration is slowed but not absent, similar to that found for radial cell migration. We propose that the defect in non-radial cell migration is likely to contribute to the clinical phenotype observed in individuals with a LIS1 mutation.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗

Rho mediates the shear-enhancement of endothelial cell migration and traction force generation.

The migration of vascular endothelial cells in vivo occurs in a fluid dynamic environment due to blood flow, but the role of hemodynamic forces in cell migration is not yet completely understood. Here we investigated the effect of shear stress, the frictional drag of blood flowing over the cell surface, on the migration speed of individual endothelial cells on fibronectin-coated surfaces, as well as the biochemical and biophysical bases underlying this shear effect. Under static conditions, cell migration speed had a bell-shaped relationship with fibronectin concentration. Shear stress significantly increased the migration speed at all fibronectin concentrations tested and shifted the bell-shaped curve upwards. Shear stress also induced the activation of Rho GTPase and increased the traction force exerted by endothelial cells on the underlying substrate, both at the leading edge and the rear, suggesting that shear stress enhances both the frontal forward-pulling force and tail retraction. The inhibition of a Rho-associated kinase, p160ROCK, decreased the traction force and migration speed under both static and shear conditions and eliminated the shear-enhancement of migration speed. Our results indicate that shear stress enhances the migration speed of endothelial cells by modulating the biophysical force of tractions through the biochemical pathway of Rho-p160ROCK.

Animals↗

Effects of 17 beta-estradiol and progesterone on migration of human monocytic THP-1 cells stimulated by minimally oxidized low-density lipoprotein in vitro.

OBJECTIVE: Many epidemiological studies have shown that postmenopausal hormone replacement therapy (HRT) has a beneficial effect on atherosclerotic cardiovascular disease. The aim of this study was to investigate the effects of estrogen and progestin on the migration of monocytes induced by minimally oxidized low-density lipoprotein (m-ox-LDL) in vitro. METHODS: Human monocytic THP-1 cells were used for the study. Migration assay was performed using a modified Boyden chamber. RESULTS: The presence of estrogen receptors was determined in THP-1 cells by Western and Northern blot analysis. Although native LDL had no significant effects on the migration of THP-1 cells, m-ox-LDL increased the migration of THP-1 cells in a dose-dependent manner. Although 17 beta-estradiol (E2, 10(-9)-10(-6) M) inhibited the 10 micrograms/ml-induced migration of THP-1 cells in a dose-dependent manner, estrone (E1), estriol (E3) and progesterone (P) had no significant effects. The combination of P (10(-9)-10(-6) M) did not show any effect on the inhibitory effect of 10(-7) M E2. Preincubation of THP-1 cells with the anti-estrogenic agent, tamoxifen (10(-6) M), significantly antagonized the inhibitory effect of 10(-7) M E2. m-ox-LDL stimulated MCP-1 secretion from THP-1 cells, which was reduced by E2. Anti-human MCP-1 neutralizing antibody inhibited the migration of THP-1 cells stimulated by m-ox-LDL. E2 also inhibited the 10 ng/ml MCP-1-induced migration of THP-1 cells in a dose-dependent manner. CONCLUSIONS: These findings suggest that the inhibitory effect of E2 on the migration of monocytes might be one of the factors involved in the decreased incidence of atherosclerotic cardiovascular disease in premenopausal women and postmenopausal HRT.

Adult↗

Activation of IP and EP(3) receptors alters cAMP-dependent cell migration.

Migration of vascular smooth cells from the media to the intima essentially contributes to neointima formation after percutaneous transluminal angioplasty and stent implantation. The stable prostacyclin mimetic iloprost has been shown to inhibit neointima formation in experimental restenosis, but it is currently unknown whether this may be caused by an antimigratory effect. Hence, the present study analyses (i) the influence of G(s)-coupled prostacyclin (IP) receptors on cell migration and (ii) verifies whether EP(3) receptors with opposite (i.e., G(i)) coupling may conversely stimulate cell migration. In a modified Boyden chamber model, it was shown that iloprost dose-dependently inhibits the migration of primary human arterial smooth muscle cells, which constitutively express the IP receptor. On the other hand, human arterial smooth muscle cell migration was stimulated by the EP(3) receptor agonist M&B 28.767. To independently study the effects of these receptors, IP or EP(3) receptors were stably overexpressed in chinese hamster ovary cells (CHO-IP and CHO-EP(3)). Chemotaxis of CHO cells transfected with G(s)-coupled IP receptors was concentration-dependently inhibited by iloprost (2-100 nM), while there was no effect of iloprost on mock-transfected CHO. By contrast, CHO-cells that overexpressed EP(3) receptors showed a significant, concentration dependent (1-100 nM) increase of cell migration in presence of the selective EP(3) agonist M&B 28.767. It is concluded that the prostacyclin mimetic iloprost inhibits vascular cell migration, which probably depends on a G(s)-mediated increase of intracellular cAMP. EP(3) receptors conversely stimulate CHO migration.

Animals↗

Actin organization in migrating corneal epithelium of rabbits in situ.

We have found previously that fibronectin enhances the migration of rabbit corneal epithelium both in vitro and in vivo. In this paper we report a change of actin localization in migrating corneal epithelium as determined by immunofluorescent microscopy. Rabbit cornea was cut into small blocks and cultured in TC-199 medium. In the normal cornea, actin was detected as diffuse fluorescence at each epithelial layer. After 8 hr of cultivation epithelial cells had not started to migrate significantly, but actin had accumulated at the cell membrane. After 24 hr, epithelial migration had begun, and actin-specific fluorescence was detected mainly in the basal cell layer at the leading edge. When fibronectin or epidermal growth factor was added to the culture medium, epithelial migration began 8 hr after initiation of culture, and at 24 hr actin-specific fluorescence at the basal side of the migrating epithelial cells appeared stronger than that of a control group cultured in TC-199 unsupplemented medium. At the same time, fibronectin-specific fluorescence was more intense beneath the migrating epithelial cells. It is known that fibronectin has an affinity to collagen, and thus it might coat the cut surface of the stroma. Epithelial cells may attach then to the stroma via coated fibronectin. When a large quantity of exogenous fibronectin is added or when fibronectin is synthesized by the addition of epidermal growth factor, it may further stimulate the organization of intracellular actin from globular form (G-actin) to fibrilar form (F-actin). As a result, the change of intracellular localization and appearance of organized actin molecule might lead to cellular migration.

Actins↗

A real time in vitro assay for studying leukocyte transendothelial migration under physiological flow conditions.

The mechanisms underlying leukocyte migration across endothelial barriers are largely elusive. Most of the current knowledge on transendothelial migration (TEM) of leukocytes has been derived from in vitro modified Boyden chamber transfilter migration assays. In these assays, leukocyte migration towards chemokine gradients constructed across the endothelial barrier is measured under shear-free conditions. These assays do not incorporate the contribution of shear flow to leukocyte adherence and migration across the endothelial barrier. Furthermore, transfilter assays do not reconstitute the physiological distribution of endothelial chemokines shown to be displayed in vivo at high levels on vessel walls. To overcome these two drawbacks, we have recently developed a novel in vitro assay to follow real time leukocyte migration across endothelial barriers under physiological flow conditions. Using this assay, we have found that apically displayed endothelial chemokines could trigger robust lymphocyte TEM through signaling to lymphocyte-expressed G-protein coupled receptors. This migration required continuous exposure of lymphocytes, adherent to the endothelial barrier, to fluid shear, but did not require a chemotactic gradient across the barrier. In the present review, we describe this new flow-based migration assay and discuss future applications for investigating TEM processes of different types of leukocytes across distinct endothelial barriers.

Cell Adhesion↗

An automated multi well cell track system to study leukocyte migration.

Design of automated image processing systems to determine migration characteristics of individual cells is not trivial. Every test sample requires separate recording and the analysis of individual cell tracks in two- or three-dimensional migration systems by time-lapse microscopy is extremely laborious. Here, we describe a new Automated Cell Track System (ACTS). In addition to contrast differences, which are used by existing analysis systems, the ACTS algorithms recognize cells on the basis of morphological similarities in successive images and adapt to the continuous shape changes of individual cells during migration. The system facilitates simultaneous analysis of multiple cells and the measurement of multiple wells in one single experiment. We validated the system studying HSB-2 T cell migration in standard 96-well microtiter plates coated with ICAM-1-Fc protein or control CD14-Fc protein. Migration of HSB-2 T cells on ICAM-1-Fc is Leukocyte Function-associated Antigen-1 (LFA-1)-mediated and both the number and the speed of migrating cells depend on the ICAM-1-Fc concentration. We show that automated analysis of the migration data yields similar results as manual analysis, but in a fraction of the time. We conclude that this system is extremely well suited to precisely monitor the migratory behavior of individual cells. The analysis of multiple wells in parallel makes this set-up appropriate in high throughput screening in which multiple components are simultaneously tested for their effect on cell migration.

Algorithms↗

Heparin inhibits human coronary artery smooth muscle cell migration.

Heparin, an anticoagulant, has been shown to reduce neointimal proliferation and restenosis following vascular injury in experimental studies, but the clinical trials of heparin in coronary balloon angioplasty have been negative. The current study, therefore, examined the effect of heparin on basal or stimulated migration by serum and platelet-derived growth factor (PDGF)-BB in cultured human coronary artery smooth muscle cells (SMCs) by Boyden's chamber method. In addition, the reversibility of the heparin effect on human coronary artery SMC migration was examined. Fetal calf serum (FCS) and PDGF-BB stimulated SMC migration in a concentration-dependent manner. Heparin in moderate to high concentration (10 to 100 U/mL) exhibited concentration-related inhibition of FCS- and PDGF-BB-stimulated SMC migration; however, a low concentration (1 U/mL) of heparin had no inhibitory effects. Heparin also had weak inhibitory effects on nonstimulated SMC migration. The SMCs that were exposed to a high concentration (100 U/mL) of heparin for 6 hours were capable of migrating after a short lag period of removal of heparin from the culture medium. These SMCs also showed recovery of responses to FCS and PDGF-BB by migrating significantly greater than the nonstimulated level. Furthermore, heparin-containing medium did not contain detached cells. These results indicate that heparin inhibits human coronary artery SMC migration, especially when stimulated by FCS or PDGF-BB, and that this inhibitory effect of heparin is reversible and not simply a function of killing cells.

Anticoagulants↗

Human keratocyte migration into collagen gels declines with in vitro ageing.

Although senescence in various cell types has been shown to have detrimental effects on wound repair, the effect of this phenomenon on corneal function with increasing age has yet to be elucidated. This study investigated the effect of in vitro ageing on keratocyte migration into a collagen gel matrix. The keratocyte cell strain EK1. BR was cultured to late passage and a comparison of early passage migration with that of late passage migration was carried out. Early or late passage keratocytes were seeded onto 6 collagen gels (1.75 mg ml(-1)) for each experiment. Gels were incubated at 37 degrees C for 72 h, stained with calcein AM (0.5 mg ml(-1)) and assayed for cell migration using fluorescent microscopy. Changes in the effect of EGF on keratocyte migration with age were assessed by the addition of EGF (20 ng ml(-1)) to 3 of the 6 gels in each experiment. Proliferative lifespan was measured by immunocytochemical detection of Ki67 activity. This study shows for the first time that keratocyte migration, and migration in response to EGF stimulation, significantly declines with increasing age of keratocytes in culture (P<0.001). As keratocyte migration in response to cytokine stimulation is vital for corneal repair, the accumulation of senescent keratocytes with age may impair corneal wound healing.

Cell Line↗

Osteoblast population migration characteristics on substrates modified with immobilized adhesive peptides.

The process of cell migration is inextricably linked with the process of cell adhesion and, therefore, with cell/substrate adhesiveness. The present study adapted an under-agarose cell migration assay to quantitatively examine population migration characteristics of osteoblasts, on substrates modified with adhesive peptides, in the absence and presence of growth factors. Short-term, that is, 48 h osteoblast migration distances on substrates modified with adhesive Arg-Gly-Asp-Ser peptides were significantly (P < 0.05) less than migration distances on substrates modified with non-adhesive Arg-Asp-Gly-Ser peptides, demonstrating that osteoblast population haptokinesis was significantly decreased on substrates modified with adhesive peptides. Random motility coefficients calculated in the present study for osteoblast populations were an order of magnitude lower than a published random motility coefficient for leukocytes, proving quantitatively that, compared to leukocytes, osteoblasts migrate via haptokinesis more slowly. The 48 and 72 h osteoblast population migration differentials in the presence of an initial mass of 60 ng of basic Fibroblast Growth Factor, on substrates modified with Arg-Gly-Asp-Ser or with Arg-Asp-Gly-Ser, were larger than all other chemotactic differentials on these substrates. Quantitative investigations (such as the present study) of cell population migration characteristics on model biomaterial surfaces will become increasingly necessary as the discipline of cell/tissue engineering matures.

Adhesiveness↗