Recent Publications – May 25, 2009

Openers of SKCa and IKCa channels enhance agonist-evoked nitric oxide synthesis and arteriolar vasodilation.
Jianzhong Sheng, Srikanth Ella, Michael Davis, Michael Hill, Andrew Braun
FASEB Journal 23(4): 1138-1145

This study demonstrates that direct manipulation of select endothelial ion channels is capable of lowering blood pressure in animal models and may thus represent a novel therapeutic strategy in the treatment of hypertensive states associated with vascular disorders.

Andrew Braun:


Blockade of K(ATP) channels reduces endothelial hyperpolarization and leukocyte recruitment upon reperfusion after hypoxia.
Figura M, Chilton L, Liacini A, Viskovic MM, Phan V, Knight D, Millar TM, Patel K, Kubes P, Giles WR, Tibbles LA
Am J Transplant. 2009 Apr;9(4):687-96. Epub 2009 Mar 9.

Injury of kidney transplants at the time of transplantation can occur due to lack of oxygen when the graft is obtained from the donor, stored, and during the implantation into the recipient. This ischemic damage can result in short term graft dysfunction and long term graft loss. We examined the earliest stages of this damage in blood vessel lining (endothelial) cells, and found that lack of oxygen can affect channels in the cell membrane and lead to changes in the endothelial cells that promote inflammation and leukocyte recruitment. These changes can be altered using a common drug called glybenclamide (glyburide). This may be important in preventing transplant injury, and may also be a mechanism in other ischemic injuries like heart attacks and stroke.

Lee Anne Tibbles: Office ph# 403-220-2064


Antagonistic interactions among Plexins regulate the timing of intersegmental vessel formation.
Lamont RE, Lamont EJ, Childs SJ.
Dev Biol. 2009 May 5. [Epub ahead of print]
PMID: 19422817 [PubMed – as supplied by publisher]

In this article we show that zebrafish semaphorin3e (sema3e) is expressed by endothelial cells of the dorsal aorta, primary motoneurons, and endodermal cells. Further, loss of Sema3e leads to delayed exit of angioblasts from the dorsal aorta in ISV formation. Through transplant analysis, we show that Sema3e acts autonomously and non-autonomously in angioblasts to modulate interactions among themselves. The semaphorin receptors, PlexinD1 and PlexinB2, are expressed by zebrafish angioblasts. Loss of plxnB2 results in delayed ISV sprouting identical to that seen in sema3e morphants, while loss of plexinD1 in out of bounds (obd) mutants results in precocious ISV sprouting. Loss of either sema3e or plxnB2 in obd mutants generates an intermediate phenotype, suggesting that PlxnD1 and Sema3e/PlxnB2 antagonize each other to control timing of ISV sprouting. Consistent with this observation, we show that PlxnB2 acts cell autonomously in endothelial cells. This suggests a model where multiple semaphorin-plexin interactions control angioblast sprouting behaviour.

Sarah Childs:



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