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Biochim Biophys Acta. 2000 Nov 30;1543(1):159-73.
Structural characterisation of human proteinosis surfactant protein A.

Berg T, Leth-Larsen R, Holmskov U, Hojrup P.

Department of Molecular Biology, Univesity of Southern Denmark, Odense University, DK-5230 Odense M. Denmark.

Human surfactant protein-A (SP-A) has been purified from a proteinosis patient and characterised by a combination of automated Edman degradation and mass spectrometry. The complete protein sequence was characterised. The major part of SP-A was shown to consist of SP-A2 gene product, and only a small amount of SP-A1 gene product was shown to be present. A cysteine extension to the N-terminal was indicated by sequence data, but was not definitely proven. All proline residues in the Y position of Gly-X-Y in the collagen-like region were at least partially modified to hydroxy-proline, but no lysine residues were found to be modified. A complex N-linked glycosylation was found on Asn-187 showing great heterogeneity as variants from a mono-antennary to penta-antennary glycosylation with varying amounts of attached pentose were identified. The disulfide bridges in the carbohydrate recognition domain were identified to be in the 1-4, 2-3 pattern common for collectins. Interchain disulfide bridges were discovered between two Cys-48 residues and cysteine residues in the N-terminal region. However, the exact disulfide bridge connections within the bouquet-like ultrastructure could not be established.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11087951&dopt=Abstract

Endocrinology. 2000 Nov;141(11):3956-64.
Inhibition of osteoblast differentiation by tumor necrosis factor-alpha.

Gilbert L, He X, Farmer P, Boden S, Kozlowski M, Rubin J, Nanes MS.

Division of Endocrinology and Metabolism, Emory University School of Medicine and Veterans Affairs Medical Center, Atlanta, Georgia 30033, USA.

Tumor necrosis factor-alpha (TNF-alpha) has a key role in skeletal disease in which it promotes reduced bone formation by mature osteoblasts and increased osteoclastic resorption. Here we show that TNF inhibits differentiation of osteoblasts from precursor cells. TNF-alpha treatment of fetal calvaria precursor cells, which spontaneously differentiate to the osteoblast phenotype over 21 days, inhibited differentiation as shown by reduced formation of multilayered, mineralizing nodules and decreased secretion of the skeletal-specific matrix protein osteocalcin. The effect of TNF was dose dependent with an IC50 of 0.6 ng/ml, indicating a high sensitivity of these precursor cells. Addition of TNF-alpha from days 2-21, 2-14, 7-14, and 7-10 inhibited nodule formation but addition of TNF after day 14 had no effect. Partial inhibition of differentiation was observed with addition of TNF on only days 7-8, suggesting that TNF could act during a critical period of phenotype selection. Growth of cells on collagen-coated plates did not prevent TNF inhibition of differentiation, suggesting that inhibition of collagen deposition into matrix by proliferating cells could not, alone, explain the effect of TNF. Northern analysis revealed that TNF inhibited the expression of insulin-like growth factor I (IGF-I). TNF had no effect on expression of the osteogenic bone morphogenic proteins (BMPs-2, -4, and -6), or skeletal LIM protein (LMP-1), as determined by semiquantitative RT-PCR. Addition of IGF-I or BMP-6 to fetal calvaria precursor cell cultures enhanced differentiation but could not overcome TNF inhibition, suggesting that TNF acted downstream of these proteins in the differentiation pathway. The clonal osteoblastic cell line, MC3T3-E1-14, which acquires the osteoblast phenotype spontaneously in postconfluent culture, was also studied. TNF inhibited differentiation of MC3T3-E1-14 cells as shown by failure of mineralized matrix formation in the presence of calcium and phosphate. TNF was not cytotoxic to either cell type as shown by continued attachment and metabolism in culture, trypan blue exclusion, and Alamar Blue cytotoxicity assay. These results demonstrate that TNF-alpha is a potent inhibitor of osteoblast differentiation and suggest that TNF acts distal to IGF-I, BMPs, and LMP-1 in the progression toward the osteoblast phenotype.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11089525&dopt=Abstract

Endocrinology. 2000 Nov;141(11):4313-6.
Parathyroid hormone-related peptide is a potent tumor angiogenic factor.

Akino K, Ohtsuru A, Kanda K, Yasuda A, Yamamoto T, Akino Y, Naito S, Kurokawa M, Iwahori N, Yamashita S.

Department of Anatomy, Nagasaki University School of Medicine, Japan.

Rat pituitary malignant tumor cells; mGH3, show hypervascularization in in vivo xenografts and overexpress parathyroid hormone-related peptide (PTHrP) compared to original GH3 cells. To elucidate whether PTHrP is involved in tumor-derived angiogenesis, we examined the effect of PTHrP on vascular endothelial cells both in vitro and in vivo. Results of in vivo diffusion chamber assay showed a clear hypervascularization on the outer surface of diffusion chambers containing mGH3 tumor cell implants but not in those containing GH3 cells. Co-incubation with antisense PTHrP oligonucleotide (10 microM), but not sense or mismatched PTHrP oligonucleotide, suppressed hypervascularization in diffusion chambers. To further examine the role of PTHrP on endothelial cell function, PTHrP(1-34) was added at various concentrations to cultured bovine endothelial cells (BAECs) harvested from the aorta. PTHrP(1-34) did not alter the proliferation or migration of endothelial cells, but rather dose-dependently increased capillary formation by endothelial cells on the collagen gel matrix. Furthermore, 0.1 mM of 8-bromo-cAMP caused a similar increase in tube formation, which was dose-dependently inhibited by H89, a protein kinase A inhibitor. Our results indicate for the first time that PTHrP is a potential paracrine factor acting via the PKA pathway to enhance angiogenesis through capillary tube formation by endothelial cells in malignant pituitary tumors.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11089567&dopt=Abstract

Clin Exp Metastasis. 1999;17(10):849-55.
Highly metastatic variant of a mouse colon carcinoma cell line, LM17 and its response to GM-CSF gene therapy.

Ikubo A, Aoki Y, Nagai E, Suzuki T.

Department of Microbiology, Molecular Genetics and Immunology, University of Kansas Medical Center, Kansas City 66160, USA.

In order to establish a highly metastatic variant of a mouse colon carcinoma cell line (CT26), BALB/c mice were first subcutaneously injected with CT26 cells. Several weeks later, metastatic tumors in lungs were resected, mechanically dispersed into a single cell suspension and cultured in vitro until cells reached confluency. These tumor cells were then subcutaneously injected into new mice. After repeating this procedure five times, a highly lung metastatic cell line, denoted as LM17, has been established. The LM17 cells grow in vitro with or without serum, whereas parental CT26 cells require serum for their growth. The LM17 cells adhere to type I collagen or fibronectin stronger than CT26 cells do. The LM17 cells invade through Matrigel-coated basement membrane in greater number than CT26 cells. By gelatin zymography, LM17 cells showed higher proteinase activity than CT26. Furthermore, subcutaneous injection of irradiated LM17 cells infected with adenovirus harboring mouse GM-CSF gene prevents the growth and lung metastasis of pre-existing subcutaneous tumor. The injection of irradiated GM-CSF-producing LM17 cells after the surgical removal of pre-existing tumor also protected the occurrence of lung metastasis. These results suggest that this highly metastatic LM17 cell line could be useful for analysis of the lung metastatic mechanism and as the mouse GM-CSF gene therapy model.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11089883&dopt=Abstract

Inflamm Res. 2000 Oct;49(10):535-40.
Effects of the non-peptide B2 receptor antagonist FR173657 in models of visceral and cutaneous inflammation.

Griesbacher T, Legat FJ.

Department of Experimental and Clinical Pharmacology, University of Graz, Austria. thomas.griesbachefunigraz.ac.at

OBJECTIVE: The non-peptide B2 receptor antagonist (E)-3-(6-acetamido-3-pyridyl)-N-[N-[2,4-dichloro-3-[(2-methyl-8-quinolin yl)oxymethyl]phenyl]-N-methylaminocarbonylmethyl]acrylamide (FR173657) was compared to the peptide antagonist icatibant in models of visceral and cutaneous inflammation. METHODS: Pancreatitis was induced by caerulein in anaesthetized Sprague-Dawley rats. Acute cystitis was induced by intravesical instillation of xylene or i.p. cyclophosphamide injection. Cutaneous inflammation was induced in anaesthetized guinea-pigs by s.c. injection of collagenase from Clostridium histolyticum. RESULTS: FR173657 inhibited oedema formation and tissue enzyme retention during pancreatitis at 500 nmol/kg and above after peroral administration, and from 30 nmol/kg after s.c. injection; icatibant was effective at 3 nmol/kg s. c. Protein extravasation in both cystitis models was abolished by s.c. FR173657 at 300 nmol/kg. Collagenase-induced oedema was attenuated equieffectively by FR173657 and icatibant at doses of 10 micomol/kg and 300 nmol/kg s.c., respectively. CONCLUSIONS: FR173657 inhibits kinin-mediated effects in visceral and cutaneous inflammation at doses that are about 10 times higher than those of icatibant. However, FR173657 is also active following oral administration.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11089906&dopt=Abstract

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