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Protective Effect of Anti-P-Selectin Monoclonal Antibody in Lipopolysaccharide-Induced Lung Hemorrhage (1999)

Ohnishi, Masako ; Imanishi, Noriaki ; Tojo, Shinichiro J.

Springer

Inflammation 23 (1999), S. 461-469

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ISSN: 1573-2576

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Abstract Excessive leukocyte accumulation is involved in the pathogenesis of the sepsis-induced acute lung injury. Selectins are essential to the interaction between leukocytes and endothelial cells. In this report, we investigated the role of selectins in the severe lung injury induced by lipopolysaccharide (LPS). Significant lung hemorrhage was observed 24 h after the intravenous administration of LPS (1 mg/kg). First, we evaluated the effect of sialyl Lewis X-oligosaccharide (SLeX-OS), a derivative of sialyl Lewis X which is one of the ligands for E-, P- and L-selectins. The treatment with SLeX-OS (26.5 mg/kg iv bolus + 19.8 mg/kg iv infusion) resulted in a decrease of lung hemorrhage by 49.5% (P 〈 0.05 versus the control group). Second, we tested the effect of anti-P-selectin monoclonal antibody (MAb), PB1.3, to investigate the role of P-selectin. The bolus administration of PB1.3 at a dose of 5 mg/kg attenuated the lung hemorrhage by 74.6% (P 〈 0.05 versus the control group). In addition, we also detected an increase of soluble P-selectin in plasma 24 h after the injection of LPS. These results suggest that P-selectin has a substantial role in the pathogenesis of the lung injury induced by LPS.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1023/A:1021917110651

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Regulation of larval cuticle protein gene expression in Drosophila melanogaster (1989)

Kimbrell, Deborah A. ; Tojo, Shinichiro J. ; Alexander, Sherry ; [et al.]

Chichester [u.a.] : Wiley-Blackwell

Developmental Genetics 10 (1989), S. 198-209

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ISSN: 0192-253X

Keywords: Gene cluster ; Transposon ; Enhancer ; Life and Medical Sciences ; Genetics

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Biology

Notes: Genes that encode 3rd instar larval cuticle proteins (LCP's) of Drosophila melanogaster are located in at least two chromosomal sites. The genes encoding four of the five predominant LCP's are located in a cluster at the chromosomal region 44D. They are organized in pairs that are transcribed divergently, and expressed with different timing during the third larval instar. Towards understanding the basis of gene regulation within the 44D cluster, we have analyzed genetic variants, including the 2-3 variant, which has an insertion of a copia-like transposable element, H.M.S. Beagle, within the 44D cluster. The Beagle element appears to inactivate the LCP-3 gene by inserting into its TATA box, but also may cause the precocious expression of two other LCP genes, LCP-1 and LCP-f2, in the cluster. The long terminal repeat (LTR) of the Beagle element apparently contains a sequence, perhaps an enhancer-like element, which causes altered expression of these genes. We have also investigated the cis-regulatory elements involved in expression of the LCP-2 gene in wild-type larvae. We have identified two upstream regions that may contain separate cisregulatory elements. The region between -252 bp and -515 bp may be essential for any expression of LCP-2. Additionally, the region between -515 bp and -795 bp appears to be required for the normal level of expression of the LCP-2 gene.

Additional Material: 7 Ill.