Search

Your search keyword '"Powell, Henry C."' showing total 346 results
Start Over Author "Powell, Henry C."
346 results on '"Powell, Henry C."'

3. Thyroid hormone receptor repression is linked to type I pneumocyte-associated respiratory distress syndrome

Author

Pei, Liming, Leblanc, Mathias, Barish, Grant, Atkins, Annette, Nofsinger, Russell, Whyte, Jamie, Gold, David, He, Mingxiao, Kawamura, Kazuko, Li, Hai-Ri, Downes, Michael, Yu, Ruth T., Powell, Henry C., Lingrel, Jerry B., and Evans, Ronald M.

Subjects
Physiological aspects, Genetic aspects, Research, Risk factors, Respiratory distress syndrome -- Genetic aspects -- Health aspects -- Risk factors -- Research, Hormone receptors -- Physiological aspects -- Genetic aspects -- Research, Thyroid hormones -- Physiological aspects -- Genetic aspects -- Research
Abstract

At birth, the neonate undergoes a profound metabolic transition and has a dramatically enhanced dependence on postnatal oxidative metabolism. Although this metabolic switch is a hallmark of the transition from [...], Although the lung is a defining feature of air-breathing animals, the pathway controlling the formation of type I pneumocytes, the cells that mediate gas exchange, is poorly understood. In contrast, the glucocorticoid receptor and its cognate ligand have long been known to promote type II pneumocyte maturation; prenatal administration of glucocorticoids is commonly used to attenuate the severity of infant respiratory distress syndrome (RDS). Here we show that knock-in mutations of the nuclear co-repressor SMRT (silencing mediator of retinoid and thyroid hormone receptors) in C57BL/6 mice ([SMRT.sup.mRID]) produces a previously unidentified respiratory distress syndrome caused by prematurity of the type I pneumocyte. Though unresponsive to glucocorticoids, treatment with anti-thyroid hormone drugs (propylthiouracil or methimazole) completely rescues SMRT-induced RDS, suggesting an unrecognized and essential role for the thyroid hormone receptor (TR) in lung development. We show that TR and SMRT control type I pneumocyte differentiation through Klf2, which, in turn, seems to directly activate the type I pneumocyte gene program. Conversely, mice without lung Klf2 lack mature type I pneumocytes and die shortly after birth, closely recapitulating the [SMRT.sup.mRID] phenotype. These results identify TR as a second nuclear receptor involved in lung development, specifically type I pneumocyte differentiation, and suggest a possible new type of therapeutic option in the treatment of RDS that is unresponsive to glucocorticoids.

Published
2011
Full Text
View/download PDF

15. Mast cell degranulation and blood-nerve barrier permeability in rat sciatic nerve after 7 days of hyperglycemia

Author

Kalichman, Michael W., Powell, Henry C., Calcutt, Nigel A., and Mizisin, Andrew P.

Subjects
Hyperglycemia -- Research, Mast cells -- Physiological aspects, Permeability -- Physiological aspects, Biological sciences
Abstract

A study of the relationship between altered blood-nerve barrier permeability and hyperglycemia in rats 7 days postexperimental diabetes reveals increased water content and permeability to mannitol in the nerves of galactose-fed rats. Vasoconstriction index and degranulating perivascular mast cell number increase more in galactose-fed animals than in diabetic and control animals, as revealed by electron microscopy, indicating that permeability changes that occur 7 days post-galactose intoxication are mediated by mast cells.

Published
1995

Catalog

Books, media, physical & digital resources
See catalog results