4.5 Article

Molecular cloning and functional analysis of scavenger receptor zebrafish CL-P1

Journal

BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS
Volume 1810, Issue 12, Pages 1150-1159

Publisher

ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbagen.2011.09.016

Keywords

Collectin; Scavenger receptor; Innate immunity; Zebrafish; Embryogenesis

Funding

  1. Japanese Ministry of Education, Culture, Sports, Science, and Technology [16390161, 19390227]
  2. Japan Society for the Promotion of Sciences
  3. Japan Health Sciences Foundation [KH21011]
  4. Smoking Research Foundation
  5. Hokkaido Heart Association
  6. Takeda Science Foundation
  7. Grants-in-Aid for Scientific Research [22590259, 22390113, 16390161, 19390227] Funding Source: KAKEN

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Background: Scavenger receptors are generally expressed in macrophages and vascular endothelial cells and some scavenger receptors are thought to contribute to the development of atherosclerosis. Methods: We cloned the cDNA of a zebrafish CL-P1 (collectin placenta 1) and performed a knockdown study using its antisense morpholino oligonucleotides (MO). Results: Zebrafish CL-P1 (zCL-P1) is 51% identical to human CL-P1 in its amino acid sequence. Microbes and OxLDL bound to zCL-P1 cDNA transfected cells. zCL-P1 mRNA expression gradually increased after 6 hours post-fertilization (hpf), reached its highest level at 24 hpf, and then decreased, which is similar to the gene expression pattern of Tie-2. The knockdown of zCL-P1 led to an increase in the number of zebrafish embryos with severe morphological abnormalities such as short body lengths and defects in the dorsal aorta at 48 hpf. Simultaneous injection of both MO and synthetic zCL-P1 or zVEGF mRNA rescued the abnormal phenotype. Conclusions: In vivo knockdown study shows that zCL-P1 is implicated in vasculogenesis and those of our in vitro study support its role as a scavenger receptor. General significance: These results suggest that zCL-P1 might be essential for vasculogenesis during the early embryonic phase in bone fish. (C) 2011 Elsevier B.V. All rights reserved.

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