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Nitric oxide production by a murine macrophage cell line (RAW264.7 cells) stimulated with Aggregatibacter actinomycetemcomitans surface-associated material

Sosroseno W, Bird PS, Seymour GJ

Anaerobe, 2011 Oct;17(5):246-51.
PMID: 21736946 DOI: 10.1016/j.anaerobe.2011.06.006

Nitric oxide (NO) may play a crucial role in the pathogenesis of periodontal disease and, hence, the aim of the present study was to test the hypothesis that Aggregatibacter actinomycetemcomitans surface-associated material (SAM) stimulates inducible nitric oxide synthase (iNOS) activity and NO production by the murine macrophage cell line RAW264.7. Cells were stimulated with untreated or heat-treated A. actinomycetemcomitans SAM and with or without pre-treatment with L-N(6)-(1-Iminoethyl)-lysine (L-NIL) (an iNOS inhibitor), polymyxin B, interferon-gamma (IFN-γ) and Interleukin-4 (IL-4), IL-10, genistein [a protein tyrosine kinase (PTK) inhibitor], bisindolylmaleimide [a protein kinase C (PKC) inhibitor], bromophenacyl bromide (BPB) [a phospholipase A(2) (PLA2) inhibitor] or wortmannin [phosphatidylinositol 3-kinase (PI-3K) inhibitor]. The iNOS activity and nitrite production in the cell cultures were determined. Untreated but not heat-treated A. actinomycetemcomitans SAM-stimulated both iNOS activity and nitrite production in RAW264.7 cells. L-NIL, IL-4, IL-10, genistein, bisindolylmaleimide, or BPB, suppressed but IFN-γ enhanced both iNOS activity and nitrite production by A. actinomycetemcomitans SAM-stimulated cells. Wortmannin and polymyxin B failed to alter both iNOS activity or nitrite production by A. actinomycetemcomitans SAM treated cells. Therefore, the present study suggests that a heat-sensitive protein constituent(s) of A. actinomycetemcomitans SAM stimulates both iNOS activity and nitrite production by RAW264.7 cells in a cytokine, PTK, PKC, and PLA(2) but not PI-3K-dependent fashion.

Matched MeSH terms: Protein-Tyrosine Kinases/metabolism
Fulltext Primary oesophageal Ki (CD30)-positive ALK+ anaplastic large cell lymphoma of T-cell phenotype

Yaakup H, Sagap I, Fadilah SA

Singapore Med J, 2008 Oct;49(10):e289-92.
PMID: 18946602

Primary oesophageal lymphoma is a very rare entity, with fewer than 30 reported cases worldwide. It represents an important cause of dysphagia. Most of the oesophageal lymphomas are diffuse large B-cell type, with only one reported case of anaplastic large cell lymphoma (ALCL) of T-cell phenotype. Primary oesophageal lymphomas that are not associated with an immunocompromised state tend to affect elderly patients. We describe the first case of primary oesophageal Ki (CD30)-positive ALK+ALCL of T-cell phenotype in a 34-year-old immunocompetent woman, who presented with a two-year history of dysphagia. She was treated with chemotherapy and endoscopic oesophageal dilations and stenting, resulting in complete remission of the lymphoma and resolution of the dysphagia. She then underwent autologous peripheral blood haematopoietic stem cell transplantation and remained disease-free two years after the diagnosis.

Matched MeSH terms: Protein-Tyrosine Kinases/biosynthesis*; Receptor Protein-Tyrosine Kinases
Fulltext Anaplastic Large Cell Lymphoma Presenting as a Soft Tissue Mass – A Case Report

Siti-Aishah, M.A., Salwati, S., Idrus, M., Rahimah, R., Salmi, A., Leong, C.F., et al.

Medicine & Health, 2008;3(1):69-74.
MyJurnal

Anaplastic large cell lymphoma (ALCL) is a rare tumour, accounting for approximately 3% of adult non-Hodgkin lymphomas.1 Primary systemic ALCL frequently involves both lymph nodes and extranodal sites. A 44-year-old woman presented with a firm, mobile mass in the left iliac fossa region. Ultrasound findings showed a well defined inhomogenous soft tissue mass, measuring 4x4x2.6cm in the deep subcutaneous region. Histopathological examination revealed that the mass was infiltrated by large lymphoid cells with marked nuclear atypia including kidney-shaped nuclei. These neoplastic cells expressed anaplastic lymphoma kinase (ALK) (both nuclear & cytoplasmic staining), CD30 and EMA but not for T-cell (CD45RO and CD3), and B-cell (CD20 & CD79α) markers. Fluorescence in situ hybridization (FISH) analysis showed a t(2;5)(p23;q35) chromosomal translocation. Subsequently the patient developed shortness of the breath and a thoracic computed tomography (CT) scan showed a mass encasing the right upper lobe bronchus. She also had bilateral axillary lymph nodes, measuring 1 cm in diameter (biopsy was not done). The mediastinum and endobronchial region did not show any abnormalities. She received 6 cycles of CHOP chemotherapy and remained disease free 2 years after diagnosis. ALCL, rarely present as a soft tissue tumour and this disease should be included as a differential diagnosis of any soft tissue mass.

Matched MeSH terms: Receptor Protein-Tyrosine Kinases
Fulltext High intracellular Zn2+ ions modulate the VHR, ZAP-70 and ERK activities of LNCaP prostate cancer cells

Wong PF, Abubakar S

Cell Mol Biol Lett, 2008;13(3):375-90.
PMID: 18311544 DOI: 10.2478/s11658-008-0009-6

Malignant prostate tissues have markedly reduced zinc (Zn(2+)) contents in comparison to non-malignant tissues. In this study, we restored a high intracellular Zn(2+) level to LNCaP prostate cancer cells by culturing the cells in a growth medium supplemented with a supraphysiological concentration of Zn(2+) (10 microg/ml) over 5 weeks. The intracellular Zn(2+) level increased in the Zn(2+)-treated cells, and there was a marked increase in the presence of zincosomes, a Zn(2+)-specific intracellular organelle. The proliferation rate of the Zn(2+)-treated cells was markedly reduced. There was also a significant increase (36.6% +/- 6.4%) in the total tyrosine phosphorylated proteins. Vaccinia H1-related (VHR) phosphatase, zeta chain-associated protein-70 (ZAP-70) kinase and phosphorylated extracellular signal-regulated protein kinase 1 and 2 (p-ERK 1 and 2) were also present in higher abundance. Treatment with TPEN, which chelates Zn(2+), reduced the abundance of VHR phosphatase and ZAP-70 kinase, but increased the abundance of p-ERK 1. However, the TPEN treatment restored the Zn(2+)-treated LNCaP cell proliferation to a rate comparable to that of the non Zn(2+)-treated cells. These results highlight the importance of a high intracellular Zn(2+) content and the VHR/ZAP-70-associated pathways in the modulation of LNCaP prostate cancer cell growth.

Matched MeSH terms: Protein-Tyrosine Kinases/metabolism
EGFR Intron 1 polymorphism in Asian Populations and its correlation with EGFR gene expression and amplification in breast tumor tissues

Zhou Q, Cheung YB, Jada SR, Lim WT, Kuo WL, Gray JW, et al.

Cancer Biol Ther, 2006 Nov;5(11):1445-9.
PMID: 17102595

AIM: The purpose of this study was to test the hypothesis if longer CA dinucleotide repeats are more common in the Asian population and also to gain insights into the interplay between the CA dinucleotide repeats and the frequencies of EGFR gene expression and amplifications as this might have therapeutic implications with regards to treatment with tyrosine kinase inhibitors.
MATERIALS AND METHODS: The EGFR intron 1 polymorphism was analysed in three distinct healthy Asian subjects, namely, Chinese (N = 96), Malays (N = 98) and Indians (N = 100). Comparative genomic hybridisation was performed to investigate for changes in DNA copy number in relation to the polymorphic CA dinucleotide repeats in breast tumor tissues (N = 22).
RESULTS: The frequency of short alleles with 14 and 15 CA repeats were most common in the Asian populations and significantly higher than those reported for Caucasians. The frequency of 20 CA repeats was 5%, almost 13-fold lower than previous reports. EGFR amplifications were detected in 23% and 11% of breast tumor tissues harboring short and long CA repeats, respectively.
CONCLUSION: Our results show that the frequency of alleles encoding for short CA dinucleotide repeats is common in Asian populations. EGFR expression and amplification levels were also higher in Asian breast tumor tissues with short CA dinucleotide repeats. These findings suggest that the EGFR intron 1 polymorphism may influence response to treatment with tyrosine kinase inhibitors in breast cancer patients and further studies are warranted.

Matched MeSH terms: Protein-Tyrosine Kinases/antagonists & inhibitors
Immunohistochemical localisation of RET and p53 mutant protein of thyroid lesions in a North-Eastern Malaysian population and its prognostic implications

Omar E, Madhavan M, Othman NH

Pathology, 2004 Apr;36(2):152-9.
PMID: 15203751

To investigate RET and p53 expression in local thyroid lesions, in order to shed light on the pathogenesis of papillary carcinoma and explain the high prevalence of this condition among the nodular hyperplasia (multi-nodular goitre) cases.

Matched MeSH terms: Receptor Protein-Tyrosine Kinases/metabolism*
Intracellular proteins involved in Porphyromonas gingivalis-induced opsonophagocytic activities of a murine macrophage cell line (RAW264.7 cells)

Sosroseno W, Bird PS, Seymour GJ

J Microbiol Immunol Infect, 2003 Dec;36(4):229-35.
PMID: 14723250

The aim of this study was to determine the role of intracellular proteins in phagocytosis of opsonized Porphyromonas gingivalis by RAW264.7 cells, a murine macrophage-like cell line. This periodontopathogen was grown anaerobically and opsonized with an IgG2a murine monoclonal anti-P. gingivalis lipopolysaccharide antibody. RAW264.7 cells were preincubated with protein tyrosine kinase inhibitors (staurosporine and genistein), protein kinase C inhibitors (phorbol myristic acetate and bisindolylmaleimide), a serine/threonine phosphatase inhibitor (okadaic acid), a phosphatidylinositol 3-kinase inhibitor (worthmannin), phospholipase A2 inhibitors (bromophenacyl bromide and nordihydroguaiaretic acid), phospholipase C inhibitors (p-chloromercuriphenyl sulfonate and neomycin sulfate), an actin-filament depolymerizer (cytochalasin D), and a microtubule disrupting agent (colchicine). Inhibitor-treated macrophages were then incubated with the opsonized P. gingivalis and the phagocytosed cells determined microscopically. The results showed the percentage of the phagocytosed organisms decreased when the cells were preincubated with protein tyrosine kinase, protein kinase C, protein phosphatase and phosphatidylinositol 3-kinase inhibitors. Of interest, preincubation with phorbol myristic acetate for 30 min increased the ability of RAW264.7 cells to phagocytose the opsonized organisms. Phospholipase A2 and phospholipase C inhibitors only slightly reduced the number of phagocytosed organisms. The results indicated that opsonophagocytosis of P. gingivalis by RAW264.7 cells might be determined by the activation of protein tyrosine kinase, protein kinase C, protein phosphatases, and phosphatidylinositol 3-kinase inhibitor. Both phospholipase A2 and phospholipase C would appear to be involved to a lesser extent. The opsonophagocytosis of this periodontopathogen would also appear to be dependent upon actin and microtubule polymerization.

Matched MeSH terms: Protein-Tyrosine Kinases/antagonists & inhibitors; Protein-Tyrosine Kinases/physiology*
Common ALK gene rearrangement in Asian CD30+ anaplastic large cell lymphoma: an immunohistochemical and fluorescence in situ hybridisation (FISH) study on paraffin-embedded tissue

Tai YC, Kim LH, Peh SC

Pathology, 2003 Oct;35(5):436-43.
PMID: 14555389

AIMS: The most common recurrent genetic aberration in anaplastic large cell lymphoma (ALCL) is translocation involving the ALK gene that results in ectopic expression of ALK protein in lymphoid tissue. This study aims to investigate the frequency of ALK gene rearrangement in a series of Asian ALCL.
METHODS: ALK gene rearrangement was detected by immunostaining of ALK protein and fluorescence in situ hybridisation (FISH) targeting at the 2p23 region.
RESULTS: The expression of ALK protein was detected in 24/34 (71%) of the cases, and it was significantly higher in childhood cases (100%) when compared to adult cases (47%). The analyses by FISH were consistent with the results from immunostaining of ALK protein, but the analyses were only successful in 15/34 (44%) cases. FISH analyses detected extra copies of ALK gene in three cases, including one case that expressed ALK protein and showed 2p23 rearrangement.
CONCLUSIONS: The current series revealed a high frequency of ALK gene rearrangement, especially in the children. Immunostaining of ALK protein is a reliable indication of ALK gene rearrangement, and is superior to FISH. However, FISH analysis is useful in detecting other genetic aberrations that are not related to ALK gene rearrangement.

Matched MeSH terms: Protein-Tyrosine Kinases/genetics*; Protein-Tyrosine Kinases/metabolism; Receptor Protein-Tyrosine Kinases
Fulltext Immunohistochemical localization of RET rearrangements in a Malaysian papillary thyroid carcinoma population

Omar E, Othman NH

Med J Malaysia, 2003 Aug;58(3):461-2.
PMID: 14750392
Matched MeSH terms: Receptor Protein-Tyrosine Kinases/genetics*
Nitric oxide production by a murine macrophage cell line (RAW264.7) stimulated with lipopolysaccharide from Actinobacillus actinomycetemcomitans

Sosroseno W, Barid I, Herminajeng E, Susilowati H

Oral Microbiol. Immunol., 2002 Apr;17(2):72-8.
PMID: 11929552

The aim of this study was to determine whether Actinobacillus actinomycetemcomitans lipopolysaccharide (LPS-A. actinomycetemcomitans) could stimulate a murine macrophage cell line (RAW264.7 cells) to produce nitric oxide (NO). The cells were treated with LPS-A. actinomycetemcomitans or Escherichia coli LPS (LPS-Ec) for 24 h. The effects of N(G)-monomethyl-L-arginine (NMMA), polymyxin B and cytokines (IFN-gamma, TNF-alpha, IL-4 and IL-12) on the production of NO were also determined. The role of protein tyrosine kinase, protein kinase C and microtubulin organization on NO production were assessed by incubating RAW264.7 cells with genistein, bisindolylmaleide and colchicine prior to LPS-A. actinomycetemcomitans stimulation, respectively. NO levels from the culture supernatants were determined by the Griess reaction. The results showed that LPS-A. actinomycetemcomitans stimulated NO production by RAW264.7 cells in a dose-dependent manner, but was slightly less potent than LPS-Ec. NMMA and polymyxin B blocked the production of NO. IFN-gamma and IL-12 potentiated but IL-4 depressed NO production by LPS-A. actinomycetemcomitans-stimulated RAW264.7 cells. TNF-alpha had no effects on NO production. Genistein and bisindolylmalemaide, but not colchicine, reduced the production of NO in a dose-dependent mechanism. The results of the present study suggest that A. actinomycetemcomitans LPS, via the activation of protein tyrosine kinase and protein kinase C and the regulatory control of cytokines, stimulates NO production by murine macrophages.

Matched MeSH terms: Protein-Tyrosine Kinases/antagonists & inhibitors