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Biomedical subjects

S Greenberg

Publications and source records attributed to S Greenberg.

At least 37 records · Page 2Linked to original sources
PubMed2000

Psychosocial intervention in stroke: Families in Recovery from Stroke Trial (FIRST).

A family-focused psychosocial intervention for stroke survivors is described and illustrated with case studies. It is designed to improve functional recovery through four specific pathways: increased knowledge, efficacy, and control through stroke education; optimized social support; increased network cohesion; and improved problem-solving abilities. Rationales for these pathways are presented and methods of implementing them discussed.

Aged↗
PubMed2000

Captopril and L-arginine have a synergistic cardioprotective effect in ischemic-reperfusion injury in the isolated rat heart.

OBJECTIVES: The present study was designed to evaluate the possible effect of the combined administration of both captopril (Cap) and L-arginine (L-a) in the isolated ischemic rat heart model. BACKGROUND: Recent studies suggest that L-arginine and angiotensin-converting enzyme (ACE) inhibitors possess independent cardioprotective effects in ischemic hearts. The pharmacological effect of the combination of both drugs has not yet been investigated in the ischemic myocardium. METHODS: Using the modified Langendorf model, rats were perfused with either Cap 360 micromol/L (n = 6) or (L-a) 3mmol/L (n = 6), both captopril and L-arginine (Cap+L-a) (n = 8), or saline control (Con) (n = 8). The study design included 30 minutes of perfusion, 30 minutes of global ischemia, and 30 minutes of reperfusion thereafter. RESULTS: Hearts treated with both Cap+L-a demonstrated an improved performance in all parameters. After 10 minutes of reperfusion, the P(max) in the Cap+L-a group was 98 +/- 8 mmHg (P <.001), 59 +/- 14 mmHg in the Cap group (P <.02), and 44.3 +/- 10 mmHg in the L-a group (P = NS), compared with only 42 +/- 8 mmHg in the control. After 10 minutes of reperfusion the dP/dt(min) was: in the Cap+L-a group: -1,650 +/- 223 mmHg/s (P <. 006); in the Cap group: -1,051 +/- 302 mmHg/s (P <.03); in the L-a group: -870 +/- 131 mmHg/s (P = NS), compared with only -487 +/- 131 mmHg/s in the control. Coronary flow was significantly increased in all 3 groups: Cap+L-a group: 22.3 +/- 1.5 mL/min (P <.001); Cap group: 18 +/- 1.6 mL/min (P <.01); L-a group: 19.8 +/- 0.9 mL/min (P <.02), compared with 12.6 +/- 0.9 mL/min in the Con group. Total NO level was significantly increased in the Cap+L-a group: 13.4 +/- 2 micromol (P <.03) vs. 6.1 +/- 1 micromol for the L-a group. NO levels of both the Cap group and the Con group were beneath detectable values. CONCLUSION: Combined administration of captopril and L-arginine has a synergistic, protective effect on heart function and coronary flow that may be mediated by enhanced NO production.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Design and methodology of the ESPRIT trial: evaluating a novel dosing regimen of eptifibatide in percutaneous coronary intervention.

BACKGROUND: Clinical trials of the glycoprotein (GP) IIb/IIIa inhibitors have shown that these potent antiplatelet agents are effective in reducing the ischemic complications of percutaneous coronary interventions. However, even though stents are now implanted in >75% of percutaneous interventional procedures, only one study, a trial of the monoclonal antibody abciximab, has formally evaluated adjunctive GP IIb/IIIa inhibition in this setting. METHODS AND RESULTS: Eptifibatide, a nonimmunogenic and rapidly reversible inhibitor of the platelet receptor integrin IIb/IIIa, has also undergone evaluation as an adjunct to coronary intervention. In clinical trials performed heretofore, however, it has appeared to have less relative clinical efficacy than the monoclonal antibody abciximab. Since the early seminal trials, it has been recognized that the doses of eptifibatide previously used achieved only 30% to 50% of maximal platelet GP IIb/IIIa integrin inhibition. This is considerably less than the 80% level of receptor inhibition that has been proposed to prevent coronary thrombus formation in animal models and that has been achieved in clinical trials with abciximab. CONCLUSIONS: The Enhanced Suppression of the Platelet IIb/IIIa Receptor with Integrilin Therapy (ESPRIT) trial was designed to test the safety and efficacy of a high-dose, "180/2.0/180" double-bolus regimen of eptifibatide (a 180-microg/kg bolus followed 10 minutes later by a second 180-microg/kg bolus of eptifibatide combined with a 2.0-microg/kg per minute infusion) as an adjunct to nonacute percutaneous coronary intervention with stent implantation. In this report, we review the rationale, design, and methods of this clinical investigation.

Angioplasty, Balloon, Coronary↗
PubMed2000

The role of nitric oxide in mediating adenosine-induced increases in uterine blood flow in the oophorectomized nonpregnant sheep.

OBJECTIVE: Adenosine administration to the uterine vasculature of the nonpregnant oophorectomized sheep results in dose-related increases in uterine blood flow. This study was designed to determine whether these adenosine-induced increases in uterine blood flow are mediated in part by nitric oxide release. STUDY DESIGN: Five nonpregnant oophorectomized ewes had catheters placed in the femoral artery and vein and in the lateral branches of the right and left main uterine arteries. Adenosine dissolved in isotonic sodium chloride solution was infused into the uterine artery at sequentially increasing doses (1, 3, 10, 30, 100, and 300 microg/min), and a dose-response curve was constructed. After determination of control responses to adenosine a 10-mg/kg dose of the nitric oxide synthase inhibitor N omega-nitro-L -arginine methyl ester was administered into the femoral vein; the dose-response curves to adenosine were then determined again. Responses after N omega-nitro-L -arginine methyl ester administration were compared with those obtained before nitric oxide blockade. RESULTS: Adenosine increased uterine blood flow in a dose-related fashion, from a baseline of 11 +/- 2 mL/min to 140 +/- 19 mL/min. No further increase was seen with adenosine doses >300 microg/min. There were no significant alterations in systemic arterial pressure or heart rate in response to uterine infusion of adenosine. N omega-nitro-L -arginine methyl ester administration increased baseline blood pressure 24% +/- 4% and decreased heart rate 13% +/- 4%. Responses to adenosine after N omega-nitro-L -arginine methyl ester administration were significantly reduced, from a maximum at the highest dose of 140 +/- 19 mL/min to 95 +/- 13 mL/min (P <.001). CONCLUSION: A significant portion of adenosine-induced vasodilation in the uterine vasculature appears to be mediated by the release of nitric oxide.

Adenosine↗
PubMed2000

A cardiac evoked response algorithm providing threshold tracking: a North American multicenter study. Clinical Investigators of the Microny-Regency Clinical Evaluation Study.

The purpose of this study was to evaluate a pacing system using the recognition of cardiac evoked response for the automatic adjustment of pacing output. Patients were prospectively followed after primary implantation of VVIR pacemakers using AutoCapture (St. Jude Medical CRMD). Sensing and pacing thresholds, polarization signal, evoked response, and AutoCapture performance were evaluated with serial visits and 24-hour Holter monitoring. Three hundred ninety-eight patients (mean age 71 +/- 15 years) were followed for an average duration of 1 year (3 days-1.75 years) with the algorithm functional in > 90% of patients. Backup pacing in the event of exit block was confirmed in all patients. Pacing thresholds remained stable at 0.89 +/- 0.34 V with a pulse width of 0.31 ms (with chronic output autoset at 0.3 V above the actual threshold). Evoked response exhibited a small but statistically significant increase with time (8.92 mV at implant, 9.60 mV at 12 months), however, this finding did not result in any change in AutoCapture function during our follow-up period. The polarization signal remained stable with minimal variation (1.12 mV at implant, 1.18 at 12 months). No clinical adverse events were observed using the AutoCapture algorithm. In this initial experience with the AutoCapture algorithm the evoked response and polarization measurements remained adequate, allowing the system to function in the majority of patients with safe, low output pacing. High energy backup pacing provided an added safety feature over fixed output devices in cases of unexpected threshold rises. Longer follow-up is required for continued long-term validation of the algorithm.

Aged↗
PubMed1999

A requirement for phosphatidylinositol 3-kinase in pseudopod extension.

Phagocytosis requires actin assembly and pseudopod extension, two cellular events that coincide spatially and temporally. The signal transduction events underlying both processes may be distinct. We tested whether phagocytic signaling resembles that of growth factor receptors, which induce actin polymerization via activation of phosphatidylinositol 3-kinase (PI 3-kinase). Fcgamma receptor-mediated phagocytosis was accompanied by a rapid increase in the accumulation of phosphatidylinositol 3,4,5-trisphosphate in vivo, and addition of wortmannin (WM) or LY294002, two inhibitors of PI 3-kinase(s), inhibited phagocytosis but not Fcgamma receptor-directed actin polymerization. However, both compounds prevented maximal pseudopod extension, suggesting that PI 3-kinase inhibition produced a limitation in membrane required for pseudopod extension. Availability of plasma membrane was not limiting for phagocytosis, because blockade of ingestion in the presence of WM was not overcome by reducing the number of particles adhering to macrophages. However, decreasing bead size, and hence the magnitude of pseudopod extension required for particle engulfment, relieved the inhibition of phagocytosis in the presence of WM or LY294002 by up to 80%. The block in phagocytosis of large particles occurred before phagosomal closure, because both compounds inhibited spreading of macrophages on substrate-bound IgG. Macrophage spreading on IgG was accompanied by exocytic insertion of membrane from an intracellular source, as measured by the dye FM1-43. These results indicate that one or more isoforms of PI 3 kinase are required for maximal pseudopod extension but not phagocytosis per se. We suggest that PI 3-kinase is required for coordinating exocytic membrane insertion and pseudopod extension.

Androstadienes↗
PubMed1999

Modular components of phagocytosis.

Phagocytosis is an evolutionarily ancient host cell endocytic response to particulate stimuli. Phagocytic leukocytes utilize highly conserved programs of signaling and motility to engulf foreign pathogens. Particle ingestion requires actin assembly and pseudopod extension, two cellular events that coincide spatially and temporally. This review presents evidence that phagocytosis proceeds in discrete but coordinated stages. In the case of receptors for the Fc portion of IgG (FcgammaRs), engagement of the IgG ligands results in receptor aggregation and recruitment of cytosolic tyrosine kinases, most notably Syk. Phosphorylation of tyrosine residues occurs within immunoreceptor tyrosine activation motif (ITAM) consensus sequences found in FcgammaR subunits, which leads to further recruitment and activation of Syk via its SH2 domains. Syk tyrosine kinase activity is required for FcgammaR-mediated actin assembly, which is controlled by several GTPases, including Rac1 and Cdc42. Phagocytosis and Rac-mediated cytoskeletal alterations also require the participation of another low molecular GTPase, ARF6. Simultaneously, phosphatidylinositol 3-kinase is recruited to the plasma membrane, which triggers exocytosis from an intracellular membrane source that is required for pseudopod extension. The source of this membrane is as yet unknown. This review focuses on individual components of phagocytosis and emphasizes that the signaling requirements for each of these is distinct.

ADP-Ribosylation Factor 6↗
PubMed1999

Seroprevalence of IgG antibodies to the chlamydia-like microorganism 'Simkania Z' by ELISA.

The newly described microorganism 'Simkania Z', related to the Chlamydiae, has been shown to be associated with bronchiolitis in infants and community acquired pneumonia in adults. The prevalence of infection in the general population is unknown. A simple ELISA assay for the detection of serum IgG antibodies to 'Simkania Z' was used to determine the prevalence of such antibodies in several population samples in southern Israel (the Negev). The groups tested included 94 medical and nursing students, 100 unselected blood donors, 106 adult members of a Negev kibbutz (communal agricultural settlement), and 45 adult Bedouin, residents of the Negev. IgG antibodies to 'Simkania Z' were found in 55-80% of these presumably healthy individuals, independently of antibodies to Chlamydia trachomatis and Chlamydia pneumoniae. The Bedouin had a seropositivity rate of 80%, while all other groups had rates of between 55 and 64%. These results indicate that 'Simkania Z' infection is probably common in southern Israel.

Adolescent↗
PubMed1999

YopJ of Yersinia spp. is sufficient to cause downregulation of multiple mitogen-activated protein kinases in eukaryotic cells.

Pathogenic Yersinia spp. utilize a plasmid-encoded type III secretion system to deliver a set of Yop effector proteins into eukaryotic cells. Previous studies have shown that the effector YopJ is required for Yersinia to cause downregulation of the mitogen-activated protein (MAP) kinases c-Jun N-terminal kinase (JNK), p38, and extracellular signal-regulated kinase (ERK) 1 and 2 in infected macrophages. Here we demonstrate that YopJ is sufficient to cause downregulation of multiple MAP kinases in eukaryotic cells. Cellular fractionation experiments confirmed that YopJ is delivered into the cytoplasmic fraction of macrophages by the type III system. Production of YopJ in COS-1 cells by transfection significantly reduced (5- to 10-fold) activation of JNK, p38, and ERK in response to several different stimuli, including serum and tumor necrosis factor alpha. JNK activation mediated by RacV12, an activated mutant of Rac1, was also blocked by YopJ in COS-1 cells, indicating that YopJ acts downstream of this small GTPase to downregulate MAP kinase signaling. Analysis of transfected COS-1 cells by immunofluorescence microscopy revealed that YopJ is recruited from the cytoplasmic compartment to the cell periphery in response to stimuli (e.g., serum) that induce membrane ruffling. These data indicate that YopJ functions as a "MAP kinase toxin" to selectively block nuclear responses that are triggered by Yersinia-host cell interaction.

Animals↗
PubMed1999

ARF6 is required for growth factor- and rac-mediated membrane ruffling in macrophages at a stage distal to rac membrane targeting.

Activation of Rac1, a member of the Rho family of GTPases, is associated with multiple cellular responses, including membrane ruffling and focal complex formation. The mechanisms by which Rac1 is coupled to these functional responses are not well understood. It was recently shown that ARF6, a GTPase implicated in cytoskeletal alterations and a membrane recycling pathway, is required for Rac1-dependent phagocytosis in macrophages (Q. Zhang et al., J. Biol. Chem. 273:19977-19981, 1998). To determine whether ARF6 is required for Rac1-dependent cytoskeletal responses in macrophages, we expressed wild-type (WT) or guanine nucleotide binding-deficient alleles (T27N) of ARF6 in macrophages coexpressing activated alleles of Rac1 (Q61L) or Cdc42 (Q61L) or stimulated with colony-stimulating factor 1 (CSF-1). Expression of ARF6 T27N but not ARF6 WT inhibited ruffles mediated by Rac1 Q61L or CSF-1. In contrast, expression of ARF6 T27N did not inhibit Rac1 Q61L-mediated focal complex formation and did not impair Cdc42 Q61L-mediated filopodial formation. Cryoimmunogold electron microscopy demonstrated the presence of ARF6 in membrane ruffles induced by either CSF-1 or Rac1 Q61L. Addition of CSF-1 to macrophages led to the redistribution of ARF6 from the interior of the cell to the plasma membrane, suggesting that this growth factor triggers ARF6 activation. Direct targeting of Rac1 to the plasma membrane did not bypass the blockade in ruffling induced by ARF6 T27N, indicating that ARF6 regulates a pathway leading to membrane ruffling that occurs after the activation and membrane association of Rac. These data demonstrate that intact ARF6 function is required for coupling activated Rac to one of several effector pathways and suggest that a principal function of ARF6 is to coordinate Rac activation with plasma membrane-based protrusive events.

ADP-Ribosylation Factor 6↗
PubMed1999

The Effect of Agmatine on Ischemic and Nonischemic Isolated Rat Heart.

OBJECTIVE: the natural polyamines play a protective role during ischemic injury. We studied the effects of agmatine on ischemic and nonischemic isolated rat hearts. METHODS: Thirty-one rats were randomly assigned to one of four experimental groups. Sixteen rats were injected with saline (group 1, n = 9; group 3, n = 7), and 15 rats were injected with 100 mg/kg of agmatine (group 2, n = 8; group 4, n = 7). Injections were given twice: 24 hours and 1 hour before the experiment. Using the modified Langendorf model, rat hearts were perfused with Krebs-Henseleit solution for 105 minutes during phase 1 of the experiment (groups 1 and 2). During phase 2, hearts were exposed to 45 minutes of global ischemia (groups 3 and 4). RESULTS: During phase 1, no statistically significant differences were observed between the agmatine and the control groups. During phase 2, agmatine caused a significant increase in left ventricular pressure (P <.003). At the end of reperfusion, P(max) was 111% +/- 10% from the baseline levels versus only 82% +/- 5% in the control group. After 20 minutes of reperfusion, dP/dt (first-time derivative of the ventricular pressure) in the agmatine group reached full recovery of 106% +/- 12% versus only 64% +/- 14% in the saline group (P =.059). Agmatine also caused a significant increase in coronary flow rate (P <.004) throughout the reperfusion period. Quantitative immunohistochemical staining disclosed reduced cell damage in the agmatine-treated hearts (P <.02) versus the control group. CONCLUSION: Agmatine injection given before induced ischemia improves hemodynamic recovery by mechanisms that may be attributed to its vasodilatory properties.

Journal Article↗
PubMed1999

Evolving trends in critical care nursing practice: results of a certification role delineation study.

BACKGROUND: In 1997, the AACN Certification Corporation, in conjunction with Professional Examination Service, undertook a role delineation study as 1 component of a large-scale, comprehensive, and systematic study of practice to update previous data. Focus groups made up of practicing critical care nurses were used to determine trends and changes in adult, pediatric, and neonatal critical care nursing practice. METHODS: Sixteen focus groups (6 adult, 5 pediatric, and 5 neonatal) used specially prepared protocols to guide discussions. Questions were designed to elicit descriptions of changes in critical care nursing practice in the preceding 5 years. Qualitative comments of the participants were analyzed across all the focus groups, rather than separately for the adult, pediatric, and neonatal focus groups. Then data for the focus groups for each patient-age range were aggregated and reviewed to abstract themes. RESULTS: Trends and changes in practice for adult, pediatric, and neonatal critical care nurses were determined. Common themes include ethical and legal issues, changes in the population of patients, psychosocial factors, and the impact of managed care. CONCLUSIONS: The results of these focus groups can be used to update the test blueprints that underlie the CCRN certification examination programs for adult, pediatric, and neonatal critical care nurses. Critical care nursing practice is changing. Specific knowledge of the changes is important for educators, managers, and clinicians. The results of this role delineation study can be used to teach, adapt systems, and validate practice.

Adult↗
PubMed1998

Involvement of guanosine triphosphatases and phospholipase C-gamma2 in extracellular signal-regulated kinase, c-Jun NH2-terminal kinase, and p38 mitogen-activated protein kinase activation by the B cell antigen receptor.

Mitogen-activated protein (MAP) kinase family members, including extracellular signal-regulated kinase (ERK), c-Jun NH2-terminal kinase ( JNK), and p38 MAP kinase, have been implicated in coupling the B cell antigen receptor (BCR) to transcriptional responses. However, the mechanisms that lead to the activation of these MAP kinase family members have been poorly elucidated. Here we demonstrate that the BCR-induced ERK activation is reduced by loss of Grb2 or expression of a dominant-negative form of Ras, RasN17, whereas this response is not affected by loss of Shc. The inhibition of the ERK response was also observed in phospholipase C (PLC)-gamma2-deficient DT40 B cells, and expression of RasN17 in the PLC-gamma2-deficient cells completely abrogated the ERK activation. The PLC-gamma2 dependency of ERK activation was most likely due to protein kinase C (PKC) activation rather than calcium mobilization, since loss of inositol 1,4,5-trisphosphate receptors did not affect ERK activation. Similar to cooperation of Ras with PKC activation in ERK response, both PLC-gamma2-dependent signal and GTPase are required for BCR-induced JNK and p38 responses. JNK response is dependent on Rac1 and calcium mobilization, whereas p38 response requires Rac1 and PKC activation.

Adaptor Proteins, Signal Transducing↗
PubMed1998

A requirement for ARF6 in Fcgamma receptor-mediated phagocytosis in macrophages.

Phagocytosis requires extension of F-actin-rich pseudopods and is accompanied by membrane fusion events. Members of the ARF family of GTPases are essential for many aspects of membrane trafficking. To test a role for this family of proteins in Fcgamma receptor-mediated phagocytosis, we utilized the fungal metabolite brefeldin A (BFA). The addition of 100 microM BFA to a subclone of RAW 264.7 macrophages disrupted the appearance and function of the Golgi apparatus as indicated by altered immunofluorescent distribution of beta-COP and reduced efflux of BODIPY C5-ceramide, a phospholipid that normally accumulates in the Golgi apparatus. In contrast, BFA had no effect on phagocytosis of IgG-coated erythrocytes. These results suggested that activation of BFA-sensitive ARFs is not required for phagocytosis. ARF6 is unique among members of the ARF family in that its membrane association is unaffected by BFA. Expression of ARF6 mutants defective in either GTP hydrolysis (Q67L) or binding (T27N) inhibited phagocytosis of IgG-coated erythrocytes and attenuated the focal accumulation of F-actin beneath the test particles. These results indicate a requirement for ARF6 in Fcgamma receptor-mediated phagocytosis and suggest that ARF6 is an important mediator of cytoskeletal alterations after Fcgamma receptor activation.

ADP-Ribosylation Factors↗
PubMed1998

Special perspective an immodest proposal: should treating mental health professionals be barred from testifying about their patients?

Notwithstanding ethical rules that address therapeutic and forensic role conflicts for psychologists and psychiatrists, overzealous patient advocacy by therapists, tightened reimbursement for therapy, and a growth market for forensic psychology and psychiatry, have led many therapists to appear willingly as forensic experts on behalf of their patients. Existing ethical rules, as well as other proposed approaches to address this problem, assume that it can be resolved by modest changes in existing practice that permit therapists to testify as long as their testimony avoids psycholegal opinions. This essay questions whether these modest changes can adequately address this problem and advances consideration of a more radical proposal to address this problem, prohibiting therapists from testifying about their patients.

Conflict of Interest↗
PubMed1998

Effect of natural beta-carotene supplementation in children exposed to radiation from the Chernobyl accident.

Attempts were made to evaluate 709 children (324 boys and 385 girls) who had been exposed long-term to different doses of radiation during and after the Chernobyl accident and had moved to Israel between 1990 and 1994. Upon arrival, all of them underwent a check-up for most common clinical disorders and were then divided into three groups according to their residences (distance from the reactor) and the level of irradiation exposure: no radiation, <5 Ci/m2, and >5 Ci/m2, respectively. Blood serum analyses for total carotenoids, retinol, alpha-tocopherol and oxidized conjugated dienes in 262 of the children showed increased HPLC levels of conjugated dienes, indicating increased levels of oxidation of in vivo blood lipids in children from the contaminated areas. The levels were higher in girls than in boys. Some 57 boys and 42 girls were given a basal diet with a diurnal supplementation of 40 mg natural 9-cis and all-trans equal isomer mixture beta-carotene in a capsulated powder form of the alga Dunaliella bardawil, for a period of 3 months. Blood serum analyses were regularly conducted before supplementation to determine the baseline effect of radiation exposure to the children, after 1 and 3 months of natural beta-carotene supplementation. After supplementation, the levels of the oxidized conjugated dienes decreased in the children's sera without any significant changes in the level of total carotenoids, retinol or alpha-tocopherol. Other common blood biochemicals were within the normal range for all tests and no statistical differences before or after supplementation of beta-carotene were noted. High pressure liquid chromatography (HPLC) analyses for carotenoids in the blood detected mainly oxycarotenoids, and to a lesser extent, all-trans beta-carotene, alpha-carotene, but not 9-cis beta-carotene. The results suggest that irradiation increases the susceptibility of lipids to oxidation in the Chernobyl children and that natural beta-carotene may act as an in vivo lipophilic antioxidant or radioprotector.

Adolescent↗
PubMed1997

Requirements for both Rac1 and Cdc42 in membrane ruffling and phagocytosis in leukocytes.

Specific pathways linking heterotrimeric G proteins and Fcgamma receptors to the actin-based cytoskeleton are poorly understood. To test a requirement for Rho family members in cytoskeletal events mediated by structurally diverse receptors in leukocytes, we transfected the full-length human chemotactic peptide receptor in RAW 264.7 cells and examined cytoskeletal alterations in response to the chemotactic peptide formyl-methionyl-leucyl-phenylalanine (FMLP), colony stimulating factor-1 (CSF-1), IgG-coated particles, and phorbol 12-myristate 13-acetate (PMA). Expression of Rac1 N17, Cdc42 N17, or the GAP domain of n-chimaerin inhibited cytoskeletal responses to FMLP and CSF-1, and blocked phagocytosis. Accumulation of F-actin- rich "phagocytic cups" was partially inhibited by expression of Rac1 N17 or Cdc42 N17. In contrast, PMA-induced ruffling was not inhibited by expression of Rac1 N17, but was blocked by expression of Cdc42 N17, indicating that cytoskeletal inhibition by these constructs was nonoverlapping. These results demonstrate differential requirements for Rho family GTPases in leukocyte motility, and indicate that both Rac1 and Cdc42 are required for Fcgamma receptor- mediated phagocytosis and for membrane ruffling mediated by structurally distinct receptors in macrophages.

Animals↗