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Stay current with NHLBI Lab e-Notes, an e-newsletter highlighting research supported by the National Heart, Lung, and Blood Institute of the NIH.

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Synectin Regulates Artery Development and Growth

Coronary angiogram images of artery network in normal and synectin deficient mice.

Compared to the highly complex artery network in normal mice (top panel), the vessels of synectin deficient animals (lower panel) have fewer branches.

Image courtesy of Michael Simons.


Researchers at Dartmouth Medical School have identified a key difference in the way arteries and veins form blood vessel networks.  According to the team, a protein called synectin regulates the density and branching patterns of arteries, but not veins.  Compared with normal animals, the artery systems in synectin deficient zebrafish and mice are significantly smaller and less complex.  The impaired motility of synectin depleted cells in response to certain growth cues may underlie the defects.  The researchers speculate that abnormal synectin levels could help explain why some patients with clogged arteries grow extra vessels to help blood bypass blockages, while others do not.

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Pubmed Abstract

Scientists Curb Protein Involved in Cystic Fibrosis


The proteasome (depicted in the cartoon above) degrades damaged proteins such as the mutated chloride transporter produced by most CF patients.

The proteasome (depicted in the cartoon above) degrades damaged proteins such as the mutated chloride transporter produced by most CF patients.
Image credit: U.S. Department of Energy Genomics:GTL Program,

Johns Hopkins researchers have silenced an overactive protein that may contribute to cystic fibrosis (CF), a genetic disorder that disrupts the transport of chloride salt in and out of cells.  This chloride trafficking helps keep healthy lungs moist but defects in the process lead to the characteristic thick mucus buildup, lung infections, and lung damage of CF.  p97/valosin-containing protein (VCP)—the rogue protein identified by the researchers—is part of the cell’s quality control system.  p97/VCP targets a damaged version of a chloride transporter protein produced by most CF patients for destruction by the proteasome, the cell’s waste disposal.  By turning off p97/VCP in laboratory cells using a technique called RNA interference, or blocking the proteasome with a drug, the team restored chloride transport function to the cells. Although development and testing could take years, the findings could eventually lead to new treatments for CF.

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PubMed Abstract


Circulation by Suction in Early Heart

Picture of a young zebrafish.

Because they are transparent during development, scientists often use zebrafish to study organ formation. Image courtesy of Shawn Burgess.


With its complex valves and chambers, the vertebrate heart looks very different from its embryonic precursor—a tube-shaped organ long thought to squeeze blood from one end to the other like a peristaltic pump.  But according to a new study by researchers at the California Institute of Technology, embryo heart tubes work as suction pumps.  By imaging heart wall movement and blood flow in transparent zebrafish embryos, the team showed that contracting cells at one end of the heart tube generate wave motions that allow suction to pull blood through the tube.  This sucking action differs from the peristaltic movements that push material forward through other tube-like organs such as the intestine.  The team’s findings suggest that the adult heart’s mechanics—pumping blood out through arteries by contracting and then relaxing to take in more blood from         veins—originate very early in development.

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PubMed Abstract

Researchers Engineer Blood-Compatible Nanomaterials


Cartoon depicting uncoated and heparin-coated carbon nanotubes.

Blood components stick to the uncoated carbon nanotube in the top panel, but not to the heparin-coated nanotube depicted in the lower panel.
Image courtesy of Saravanababu Murugesan and Robert J. Linhardt.

Medical devices could soon employ blood-compatible nanomaterials engineered by scientists at Rensselaer Polytechnic Institute.  Blood components often stick to materials used in medical devices and can cause blood clots in patients undergoing treatments such as kidney dialysis.  The researchers nearly eliminated clot formation by coating nanoscale materials with heparin—a widely used anticoagulant.  They also demonstrated that heparin-coated membranes with nanometer-sized (billionths of a meter) pores can work like an artificial kidney, or dialyzer, by filtering wastes from blood while maintaining blood flow.  In theory, heparin-coated biomaterials could eliminate the need for systemic anticoagulant treatment during certain medical procedures and the side-effects that are associated with anticoagulant treatment such as excessive bleeding.       

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PubMed Abstract





NHLBI Lab e-Notes is produced by the Office of Science and Technology of the National Heart, Lung, and Blood Institute, part of the National Institutes of Health.  The NHLBI supported all of the work described in this digest.  Some of the material in this newsletter was summarized from university or national lab news releases.  For more information about NHLBI Lab e-Notes, please contact the editor at To unsubscribe click here.



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