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PubMed2005

Heterologous regulation of chemokine receptor signaling by the lipid phosphatase SHIP in lymphocytes.

The SH2 domain-containing inositol polyphosphate 5-phosphatase (SHIP) is known to play an important role in the negative regulation by FcgammaRIIB of PI3K-dependent signaling cascades activated by the B cell antigen receptor (BCR) as well as several tyrosine-kinase coupled cytokine receptors. However, to date the role of SHIP in the regulation of PI3K-dependent signals elicited by G-protein-coupled receptors (GPCR) such as chemokine receptors has not been investigated. In this study, we report that ligation of the G-protein-coupled chemokine receptor CXCR4 by SDF-1/CXCL12 has no effect on the tyrosine phosphorylation of SHIP in the murine B cell lymphoma A20. However, co-ligation of the B cell antigen receptor and FcgammaRIIB inhibits the PI3K-dependent phosphorylation of PKB and ERK1/2 in response to CXCL12. We have also utilised a constitutively active membrane-localised SHIP mutant expressed in the Jurkat leukaemic T cell line (which do not normally express SHIP), in order to investigate the effect of this mutant on CXCL12 stimulated PI3K-dependent signaling events. Experiments have revealed that CXCL12-mediated PKB phosphorylation, chemotaxis and lipid accumulation are inhibited in the presence of this SHIP mutant. Thus, it appears that heterologous activation of SHIP by non-G-protein-coupled receptor-mediated routes can impinge on PI3K-dependent signaling pathways activated by independently ligated G-protein-coupled chemokine receptors.

Animals↗

PubMed1997

The phosphatidylinositol polyphosphate 5-phosphatase SHIP and the protein tyrosine phosphatase SHP-2 form a complex in hematopoietic cells which can be regulated by BCR/ABL and growth factors.

We report here that interleukin-3 (IL-3) and erythropoietin (EPO) induce formation of a complex composed of two SH2-containing phosphatases, the tyrosine phosphatase SHP-2 and the SH2 containing inositol 5-phosphatase (SHIP). Both SHP-2 and SHIP are known to be involved in growth factor signal transduction, but their potential interaction in the same pathway is novel. SHIP has previously been shown to associate with SHC, and potentially to be involved in regulating apoptosis. In contrast, in some model systems, SHP-2 has been demonstrated to positively regulate cell growth. Both phosphatases in the complex were tyrosine phosphorylated, and the amount of SHIP coprecipitating with SHP-2 was inversely related to the amount of SHIP coprecipitating with SHC. In hematopoietic cells transformed by the BCR/ABL oncogene, this phosphatase complex was found to be constitutively present with both components heavily tyrosine phosphorylated. Also, other proteins were detected in the complex, including BCR/ABL itself and c-CBL. However, transformation by BCR/ABL was associated with a reduced SHIP protein expression, which could further affect the accumulation of various inositol polyphosphates in these leukemic cells. These data suggest that the function of SHIP and SHP-2 in normal cells are linked and that BCR/ABL alters the function of this signaling complex.

Animals↗

PubMed2002

The SH2-containing inositol 5-phosphatase (SHIP)-1 is implicated in the control of cell-cell junction and induces dissociation and dispersion of MDCK cells.

Hepatocyte growth factor (HGF) induces the breakdown of cell junction and the dispersion of colonies of epithelial cells, providing a model system for the investigation of the molecular mechanisms of one of the important aspects of tumorogenesis. We have previously reported that the SH2-domain-containing inositol 5'phosphatase (SHIP)-1 binds to c-Met, and potentiated HGF-mediated branching tubulogenesis. In this study, we describe the establishment of MDCK cell lines which express MycHis-tagged SHIP-1 at different levels. Expression of SHIP-1 in MDCK cells at a high level resulted in cell morphology characteristic of an epithelial-mesenchymal like transition; cells lost cortical actin, developed actin stress fibers and gained spontaneous motility without treatment of HGF. When the level of MycHis-tagged SHIP-expression was relatively low, transfectants partially lost cortical actin and phalloidin stained puncta appeared at cell-cell junctions even in the absence of HGF. The treatment of MAP kinase inhibitor, PD98059, did not influence SHIP-1 mediated alteration of adherens-junction of MDCK cells, while, phosphatidylinositol 3 (PI 3)- kinase inhibitor, LY294002, drastically reduced SHIP-1 mediated phenotype. Furthermore, expression of a mutant SHIP-1 lacking catalytic activity in MDCK cells did not alter the cortical actin distribution and HGF-mediated MAP and Akt kinase-phosphorylation, but suppressed HGF induced cell dispersion, suggesting that phosphatase activity is important for cytoskeleton rearrangement and cell dispersion.

Adherens Junctions↗

PubMed1997

Interleukin-3 induces the association of the inositol 5-phosphatase SHIP with SHP2.

We recently purified and cloned a 145-kDa protein that becomes tyrosine phosphorylated and associated with Shc in response to multiple cytokines. Based on its predicated amino acid sequence and its enzymatic activity, we have called this protein SHIP, for Src homology 2-containing inositol phosphatase. To gain further insight into the intracellular pathways that this putative signal transduction intermediate might regulate we have investigated whether SHIP binds to intracellular proteins other than Shc. The results presented herein demonstrate that following interleukin-3 stimulation, SHIP binds to the tyrosine phosphatase, SHP2 (also called Syp, PTP1D, SHPTP2, and PTP2C) and that Shc is not present in these SHIP-SHP2 complexes. Time course studies reveal that SHIP's association with SHP2 is transient and is maximal at 10 min of stimulation with interleukin-3. We further show that the association of SHIP with SHP2 occurs through the direct interaction of the SH2 domain of SHIP with a pYXN(I/V) sequence within SHP2.

Animals↗

PubMed1997

Effect of shipping and chromium supplementation on performance, immune response, and disease resistance of steers.

Forty-eight Angus crossbred steers (263 +/- 2 kg initial BW) were blocked by weight and randomly assigned within weight group to treatment. Treatments consisted of control or .4 mg of supplemental Cr as Cr-nicotinic acid complex/kg of DM. Steers were fed diets containing 90% corn silage (DM basis) and 10% of a soybean meal-mineral-vitamin supplement. After 56 d on the dietary treatment, half of the steers in each treatment were transported 343 km and unloaded in an unfamiliar location. The next day, d 58, shipped steers were returned to the feedlot (50 km). On d 58 after shipped steers were returned to the feedlot, all steers were inoculated with infectious bovine rhinotracheitis virus (IBRV) intranasally. Average daily gain from d 0 to 80 was increased (P < .10) by supplemental Cr. There was a shipping x time interaction for serum cortisol concentrations. Shipping increased (P < .02) serum cortisol on d 58, but 7 d after transport there were no effects of shipping on serum cortisol. Transportation increased (P < .05) the ratio of neutrophils to lymphocytes. Supplemental Cr did not affect rectal temperature after the IBRV challenge or the antibody response to IBRV or porcine red blood cells. Immunoglobulin G antibody response to porcine red blood cells was decreased (P < .09) by shipping. Supplemental Cr as Cr-nicotinic acid improved ADG of growing steers, regardless of whether they had been stressed by shipping. Supplemental Cr did not affect any of the immune responses that were measured.

Animals↗

PubMed2000

SHIP inhibits Akt activation in B cells through regulation of Akt membrane localization.

Activation of the serine/threonine kinase Akt and the regulation of its activation are recognized as critical in controlling proliferative/survival signals via many hematopoietic receptors. In B lymphocytes, the B-cell receptor (BCR)-mediated activation of Akt is attenuated by co-cross-linking of BCR with the inhibitory receptor Fc gamma RIIB1, and the binding of the SH2 domain-containing inositol phosphatase, SHIP, to Fc gamma RIIB1. Because SHIP dephosphorylates phosphatidylinositol 3,4,5-trisphosphate (PIP3) and activation of Akt requires PIP3, the destruction of this phospholipid has been proposed as the mechanism for Akt inhibition. However, upstream kinases that activate Akt, such as PDK1, also require PIP3 for activation. In this report, we addressed whether SHIP inhibits Akt directly at the level of Akt recruitment to the membrane, indirectly through PDK recruitment/phosphorylation of Akt, or both. We generated stable B-cell lines expressing a regulatable, but constitutively membrane-bound Akt that still required PDK-dependent phosphorylation for activation. Several lines of evidence suggested that activation of this membrane-targeted Akt is not inhibited by Fc gamma RIIB1/SHIP and that PDK is not a target for SHIP-mediated inhibition. These data demonstrate that SHIP inhibits Akt primarily through regulation of Akt membrane localization. We also observed during these studies that Fc gamma RIIB1/SHIP does not inhibit p70(S6k) activation, even though several other PIP3-dependent events were down-regulated. Because the enhanced activation of Akt in the absence of SHIP correlates with hyperproliferation in the myeloid lineage, our data have implications for SHIP and Akt-dependent regulation of proliferation in the hematopoietic lineage. (Blood. 2000;96:1449-1456)

Animals↗

PubMed2004

[Mutation analysis of SHIP gene in acute leukemia].

OBJECTIVE: The SH2 domain containing inositol 5'-phosphatase (SHIP) is predominately expressed in hematopoietic cells, and is a crucial negative regulator in the development of hematopoietic cells. This paper is to evaluate the role of the SHIP gene in human leukemogenesis. METHODS: Expression of SHIP gene in bone marrow and/or peripheral blood from 32 patients with acute myeloid leukemia (AML), 9 with acute lymphoblastic leukemia (ALL), as well as human hematopoietic cell lines was analyzed by reverse transcription-polymerase chain reaction (RT-PCR), single strand conformational polymorphism (SSCP) and DNA sequencing. RESULTS: RT-PCR showed that all samples expressed SHIP gene. Mutations of SHIP gene were detected in 7 (22%) of 32 AML patients and one (12%) of 9 ALL patients. Interestingly, two missense mutations that had been observed in a AML patient at diagnosis disappeared after complete remission (CR). In addition, in vitro Akt phosphorylation was prolonged and increased following IL-3 stimulation of this patient's cells. CONCLUSION: Our data demonstrate for the first time the mutation of SHIP gene in acute leukemia and suggest a possible role of the mutation of this gene in the development of acute leukemia. SHIP may serve as a tumor suppressor by negatively regulating the PI3K/Akt signaling pathway in hematopoietic cells.

Blotting, Western↗

PubMed2005

Dok1 and SHIP act as negative regulators of v-Abl-induced pre-B cell transformation, proliferation and Ras/Erk activation.

The v-Abl tyrosine kinase activates several signaling pathways during transformation of bone marrow cells in mice. Because the SH2-containing inositol 5'-phosphatase (SHIP) and Downstream of tyrosine kinase 1 (Dok1) have been shown to interact with Abl, the effect of SHIP and Dok1 deficiency on v-Abl transformation was investigated. Bone marrow cells from either Dok1- or SHIP-deficient mice are more susceptible to transformation by v-Abl. v-Abl-transformed preB cells from these knockout mice show Abl kinase-dependent hyperproliferation and moderate resistance to apoptosis. Elevated activation of Ras, Raf-1, and Erk, but not of Akt, was observed in either SHIP(-/-) or Dok1(-/-) v-Abl-transformed cells. This activation is sensitive to treatment with STI571. Furthermore, treatment of these cells with either a farnesyltransferase inhibitor or a MEK1/2 inhibitor abrogates the increased proliferation of SHIP(-/-) or Dok1(-/-) cells in a dose-dependent manner. Complementation of SHIP(-/-) or Dok1(-/-) cells abrogates their hyperproliferation and intracellular Erk activation. These data indicate that both SHIP and Dok1 functionally regulate the activation of Ras-Erk pathway by v-Abl and affect the mitogenic activity of v-Abl transformed bone marrow cells.

Animals↗

PubMed1997

The course of shipped livers used as full size, reduced or split grafts.

A total of 110 transplants, 66 in adults (8 retransplants) and 30 in children (6 retransplants) were analysed according to the origin of the graft (shipped n = 39-non-shipped i.e. self procured n = 71) and the way they were transplanted (as full size grafts (FS) n = 82, reduced size grafts (RED) n = 23 or split grafts (SG) n = 5). Twenty-nine transplants were performed for urgent and 81 for elective indications. There was a statistically higher incidence of 2 or more risk factors in the donors that were selfprocured (non shipped) than in donors from shipped livers (p = 0.025). The overall 3 months graft survival was 79.5% for shipped livers versus 69% for non-shipped livers and patients survival was 89.2% versus 79.0% respectively after 3 months and 82.9% versus 74.4% after 40 months. From these results that were analysed with risk factors of the donors, cold ischaemia time and liver function tests in recipients, transplanted for acute and elective indications, it is concluded that shipping of grafts is a practical and safe procedure even if size reduction or the use of SG is intended.

Adult↗

PubMed1998

The SH2-containing inositol polyphosphate 5-phosphatase, ship, is expressed during hematopoiesis and spermatogenesis.

Ship is a recently identified SH2-containing inositol polyphosphate 5-phosphatase that has been implicated as an important signaling molecule in cell-culture systems. To understand the physiologic function of Ship in vivo, we performed expression studies of Ship during mouse development. Results of this study demonstrate the expression of ship to be in late primitive-streak stage embryos (7.5 days postcoitus [dpc]), when hematopoiesis is thought to begin, and the expression is restricted to the hematopoietic lineage in mouse embryo. In adult mice, Ship expression continues to be in the majority of cells from hematopoietic origin, including granulocytes, monocytes, and lymphocytes, and is also found in the spermatids of the testis. Furthermore, the level of Ship expression is developmentally regulated during T-cell maturation. These results suggest a possible role for Ship in the differentiation and maintenance of the hematopoietic lineages and in spermatogenesis.

Animals↗

PubMed2024

SHIP-1 Differentially Regulates IgE-Induced IL-10 and Antiviral Responses in Human Monocytes.

IgE-mediated stimulation of monocytes regulates multiple cellular functions including cellular maturation, cytokine release, antiviral responses, and T-cell differentiation. Expression of the high-affinity IgE receptor, FcεRI, is closely linked to serum IgE levels and atopic disease. The signaling molecules regulating FcεRI effector functions have been well studied in mast cells and basophils; however, less is known about the signaling and regulatory mechanisms in monocytes. This study sought to identify regulators of IgE-mediated cytokine release in human monocytes. SHIP-1 was identified as a negative regulator of IgE-induced IL-10 production. It was also determined that IgE-mediated stimulation and SHIP-1 inhibition decreased antiviral IP-10 production after liposomal poly(I:C) stimulation, indicating differential regulation by SHIP-1 in IgE-driven and antiviral response pathways. SHIP-1 and NF-κB were activated following IgE-mediated stimulation of monocytes, and NF-κB activation was related to both SHIP-1 and FcεRIα cellular expression levels. To our knowledge, this is the first study to identify a role for SHIP-1 in regulating IgE-mediated and antiviral responses in human monocytes. Given the importance of monocytes in inflammation and immune responses, a better understanding of the signaling and regulatory mechanisms downstream of the FcεRI receptor could lead to new therapeutic targets in allergic disease.

Humans↗

PubMed2006

Epidemiology of gastroenteritis on cruise ships, 2001-2004.

BACKGROUND: The incidence of diarrheal disease among cruise ship passengers declined from 29.2 cases per 100,000 passenger days in 1990 to 16.3 per 100,000 passenger days in 2000. In 2002, the Vessel Sanitation Program of the Centers for Disease Control and Prevention reported 29 outbreaks (3% or more passengers ill) of acute gastroenteritis on cruise ships, an increase from 3 the previous year. This analysis of gastroenteritis on cruise ships, conducted in 2005, details the increase in outbreak incidence rates during 2001 through 2004. METHODS: Using Gastrointestinal Illness Surveillance System data, investigators evaluated incidence rates of gastroenteritis on cruise ships calling on U.S. ports, carrying 13 or more passengers, by cruise length and reporting region during the study period. The investigators also evaluated the association between inspection scores, and gastroenteritis incidence and the frequency of outbreaks in 2001 through 2004. RESULTS: During the study period, the background and outbreak-associated incidence rates of passengers with acute gastroenteritis per cruise were 25.6 and 85, respectively. Acute gastroenteritis outbreaks per 1000 cruises increased overall from 0.65 in 2001 to 5.46 in 2004; outbreaks increased from 2 in 2001 to a median of 15 per year in 2002-2004. Median ship inspection scores remained relatively constant during the study period (median 95 on a 100-point scale), and were not significantly associated with either gastroenteritis incidence rates (risk ratio, 1.00; 95% confidence interval, 0.98-1.02) or outbreak frequency (Spearman's coefficient, 0.01, p=0.84). CONCLUSIONS: Despite good performance on environment health sanitation inspections by cruise ships, the expectation of passenger cases of gastroenteritis on an average 7-day cruise increased from two cases during 1990-2000 to three cases during the study period. This increase, likely attributable to noroviruses, highlights the inability of environmental programs to fully predict and prevent risk factors common to person-to-person and fomite spread of disease.

Acute Disease↗

PubMed1994

Working on a moving surface--a biomechanical analysis of musculo-skeletal load due to ship motions in combination with work.

Ship motions are recognized by fishermen as a cause of high musculo-skeletal load. In the present study, the motions of a Swedish trawler at sea were registered over three degrees of freedom. Simultaneously, the working postures of a fisherman on board were registered in the sagittal plane during five different working situations: (1) standing erect in still conditions; (2) holding a load of 21 kg in still conditions; (3) standing erect during motion of the ship; (4) standing during motion of the ship, holding a load of 21 kg; and (5) repeatedly lifting and lowering a 21 kg load during motion of the ship. All registrations were sampled using a computer where data were processed in a two-dimensional, dynamic biomechanics model, developed for this particular purpose. Vertical and horizontal forces as well as moments were calculated for seven major joint systems of the body, as was compression at the L4/L5 vertebral level. In situation (3), ship motions were mainly counteracted by motions in the lower extremity and lumbar back, thus inducing increased strain in these parts of the body; other parts of the body were little affected. Holding a load considerably increased the load on most joints. Lifting the load further increased the musculo-skeletal strain and also increased the range of moments in each joint as well as the range of lumbar compression. Moment at the C7 vertebral level was relatively unaffected by ship motions and by handling external loads.

Biomechanical Phenomena↗

PubMed1999

Measurements of mineral oil mist, hydrocarbon vapor, and noise in engine rooms of ships.

The purpose of this study was to determine the concentrations of oil mist and hydrocarbon vapor to which marine engineers are currently exposed. Measurements were also taken of the sound level in the engine room and the control rooms. Area mist concentration measurements were performed in 21 ferries, 2 cargo ships, and 1 westamaran (an express ship with two keels). Measurements were also performed for four different tasks where exposures above area level were expected. The area level of oil mist in the engine rooms of the different ships varied from not detectable to 0.53 mg/m3 (mean 0.24 mg/m3). The levels of hydrocarbons in the different ships varied from 0.2 to 14.5 mg/m3. The sound level varied from 96 to 108 dB(A) in the engine rooms, and from 70 to 90 dB(A) in the control room. When compared to other studies, it is supposed that the exposure to noise and mineral oil mist in the engine rooms of ships may represent a risk of adverse health effects for workers on Norwegian ships. The sound level may cause neurogenic hearing loss when appropriate hearing protection is not used.

Air Pollutants↗

PubMed2001

A small outbreak of Legionnaires' disease in a cargo ship under repair.

It was reported that two mechanics working on a cargo ship under repair in the port of Barcelona had died after having fever. An investigation was made into the possibility of any additional cases and the presence of Legionella pneumophila in the ship they were repairing and in their hotel. The contaminated water system was treated with sodium hypochlorite. Both patients died after having been repeatedly diagnosed as having influenza. The two cases occurred among those who had been working with the pump of the ship's water system, while no cases were observed among the other workers (p = 0.02). Various serogroups of L. pneumophila were isolated from the ship's water pump and distribution system. However, organism of serogroup 1, subgroup Pontiac (Knoxville) were identified with identical deoxyribonucleic acid (DNA) patterns in the lung tissue of one patient and in the cooling water circuit valve of the ship's water pump. The first postintervention control water samples showed no further growth of legionella, but serogroups 4 and 8 were identified 8 months later. This legionellosis outbreak, although small, was highly lethal, probably due to the high levels of bacteria to which the patients were exposed and also because of the failure of correct diagnosis. International recommendations on prevention and control of legionellosis, which include ships under repair, are required.

Adult↗

PubMed1999

Critical incident stress debriefing (CISD) in a shipping company.

Critical incident stress debriefing (CISD) is a method used successfully to reduce suffering from stress-related ailments such as insomnia, depression, anger, headaches etc. The resources of the shipping company are very limited and, thus, networking with existing organizations and specialists is necessary to carry out CISD effectively. The present company model has been adopted to take into account various situations and levels of disaster. The model has been adopted at three levels of events:Level 1. Serious accidents on shore, sudden deaths, severe events and threats. Events involving one or only few persons. Level 2. Life-threatening occupational accidents on board ship, suicide of a workmate, sudden death and fire on board ship. Events involving one person or limited group of persons. Level 3. Disasters at sea. Severe events involving all or nearly all persons on board ship. Actions at different levels: Level 1: A leaflet describing CISD, situations where it would be appropriate and where it is available, is given to each sailor. The victim is encouraged to seek CISD from public health care centres, most of which have their own services in Finland. Level 2. Training of about 8 hours is carried out by an experienced crisis psychologist for supervisors and officers on board ship. After the training they are able to identify stressful situations. At each harbour, the shipping company has made agreements with experienced crisis psychologists to act as specialists and contact persons on shore. These nominated psychologists will initiate CISD actions when necessary. If they need extra manpower they will turn to other psychologists. Level 3. In such serious accidents, the company's own resources alone are insufficient to provide effective CISD. All available public and private resources will he needed (health care organizations, Red Cross, Church etc.).

Crisis Intervention↗

PubMed1979

Study on the possibility of adopting a complex method in Blattella germanica (L.) control on board ships.

Campaings to control the German cockroach, Blattela germanica, were conducted at 14-day intervals over a period of 5.5 months on two merchant vessels of similar size and type. On one ship only the chemical "Gertoks", carbamate insecticide containing 1% propoxur was applied, and on the second ship two preparations simultaneously, a chemical and a biological--"Biotrol 25 W" containing Bacillus thuringiensis. - In order to assess the success of the control, the extent of infestation in the accomodation was determined immediately before and 24 h after the spraying. - The susceptibility of the cockroaches caught on the ships, to the two preparations applied, was also determined. It was found that "Gertoks" was an efficient preparation, the biopreparation "Biotrol 25 W" being less efficient. - A certain increase in resistance of the cockroaches to both preparations, was noted. - The above observations indicate that a considerable drop in numbers of population of cockroaches can be achieved if the ship's crew carry out systematic thorough spraying of ships quarters infested by cockroaches, with Gertoks". They also confirm previous suggestions that complex method in B. germanica control on board ships is possible, using chemical and biological preparations containing Bac. thuringiensis spores simultaneously.

Animals↗

PubMed2004

LPS-induced upregulation of SHIP is essential for endotoxin tolerance.

An initial exposure to lipopolysaccharide (LPS) induces a transient state of hyporesponsiveness to a subsequent challenge with LPS. The mechanism underlying this phenomenon, termed endotoxin tolerance, remains poorly understood despite a recent resurgence of interest in this area. We demonstrate herein that SHIP(-/-) bone marrow-derived macrophages (BMmphis) and mast cells (BMMCs) do not display endotoxin tolerance. Moreover, an initial LPS treatment of wild-type BMmphis or BMMCs increases the level of SHIP, but not SHIP2 or PTEN, and this increase is critical for the hyporesponsiveness to subsequent LPS stimulation. Interestingly, this increase in SHIP protein is mediated by the LPS-induced production of autocrine-acting TGFbeta and neutralizing antibodies to TGFbeta block LPS-induced endotoxin tolerance. In vivo studies with SHIP(+/+) and SHIP(-/-) mice confirm these in vitro findings and show a correlation between the duration of endotoxin tolerance and elevated SHIP levels.

Animals↗