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659 results on '"Rehan, Virender"'

157. Comparison of protective effects of electroacupuncture and moxibustion at Zusanli(ST 36) on perinatal nicotine exposure-induced lung phenotype in rat offspring

Author

Ge, Yunpeng, Liu, Yitian, Zhao, Guozhen, Sakurai, Reiko, Xie, Yana, Shi, Tianyu, Fang, Yang, Wang, Jiajia, Rehan, Virender K., and Ji, Bo

Abstract

To compare the effects of electroacupuncture (EA) and moxibustion at Zusanli(ST 36) on the lung phenotype of rat offspring exposed to nicotine during the perinatal period.

Published
2023
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198. Metyrapone Alleviates Deleterious Effects of Maternal Food Restriction on Lung Development and Growth of Rat Offspring.

Author

Paek, David S., Sakurai, Reiko, Saraswat, Aditi, Li, Yishi, Khorram, Omid, Torday, John S., and Rehan, Virender K.

Subjects
BRONCHOPULMONARY dysplasia, MALNUTRITION in pregnancy, FETAL growth retardation, METOPIRONE, LUNG development, GLUCOCORTICOIDS, MATERNAL health, LABORATORY rats, DISEASE risk factors
Abstract

Maternal food restriction (MFR) causes intrauterine growth restriction, a known risk factor for developing chronic lung disease. However, it is unknown whether this negative outcome is gender specific or preventable by blocking the MFR-induced hyperglucocorticoidism. Using a well-established rat model, we used metyrapone (MTP), an inhibitor of glucocorticoid synthesis, to study the MFR-induced lung changes on postnatal day (p) 21 in a gender-specific manner. From embryonic day 10 until delivery, pregnant dams were fed either an ad libitum diet or a 50% caloric restricted diet with or without MTP supplementation. Postnatally, the offspring were fed ad libitum from healthy dams until p21. Morphometric, Western blot, and immunohistochemical analysis of the lungs demonstrated that MTP mitigated the MFR-mediated decrease in alveolar count, decrease in adipogenic protein peroxisome proliferator-activated receptor γ, increase in myogenic proteins (fibronectin, α-smooth muscle actin, and calponin), increase in Wnt signaling intermediates (lymphoid enhancer-binding factor 1 and β-catenin), and increase in glucocorticoid receptor (GR) levels. The MFR-induced lung phenotype and the effects of MTP were similar in both genders. To elucidate the mechanism of MFR-induced shift of the adipogenic-to-myogenic phenotype, lung fibroblasts were used to independently study the effects of (1) nutrient restriction and (2) excess steroid exposure. Nutrient deprivation increased myogenic proteins, Wnt signaling intermediates, and GR, all changes blocked by protein supplementation. MTP also blocked, likely by normalizing nicotinamide adenine dinucleotide phosphate levels, the corticosterone-induced increase in myogenic proteins, but had no effect on GR levels. In summary, protein restriction and increased glucocorticoid levels appear to be the key players in MFR-induced lung disease, affecting both genders. [ABSTRACT FROM AUTHOR]

Published
2015
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199. The Lung Alveolar Lipofibroblast: An Evolutionary Strategy Against Neonatal Hyperoxic Lung Injury.

Author

Rehan, Virender K. and Torday, John S.

Subjects
*PREMATURE infant diseases, *HYPEROXIA, *RESPIRATORY insufficiency, *REACTIVE oxygen species, *PGC-1 protein, *SURFACE active agents
Abstract

Significance: Oxygen, the main mode of support for premature infants with immature lungs, can cause toxicity by producing reactive oxygen species (ROS) that disrupt homeostasis; yet, these same molecules were entrained to promote vertebrate lung phylogeny. By providing a deeper understanding of this paradox, we propose physiologically rational strategies to prevent chronic lung disease (CLD) of prematurity. Recent Advances: To prevent neonatal hyperoxic lung damage biologically, we have exploited the alveolar defense mechanism(s) that evolutionarily evolved to combat increased atmospheric oxygen during the vertebrate water to land transition. Critical Issues: Over the course of vertebrate lung evolution, ROS promoted the formation of lipofibroblasts, specialized adepithelial cells, which protect the alveoli against oxidant injury; peroxisome proliferator-activated receptor gamma (PPARγ), the master switch for lipofibroblast differentiation, prevents such oxidant lung injury, both by directly promoting mesodermal differentiation and its antioxidant defenses, and indirectly by stimulating the developmental epithelial-mesenchymal paracrine interactions that have physiologically determined lung surfactant production in accord with the lung's phylogenetic adaptation to atmospheric oxygen, preventing Respiratory Distress Syndrome at birth. Future Directions: The molecular strategy (PPARγ agonists) to prevent CLD of prematurity, proposed by us, although seems to be robust, effective, and safe under experimental conditions, it awaits detailed pharmacokinetic and pharmacodynamic studies for its safe and effective clinical translation to human infants. Antioxid. Redox Signal. 21, 1893-1904. [ABSTRACT FROM AUTHOR]

Published
2014
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