Hyperoxia-induced changes in estradiol metabolism in postnatal airway smooth muscle

Martin, Yvette N.; Manlove, L.; Dong, Jie; Carey, William A.; Thompson, Michael A.; Pabelick, Christina M.; Pandya, Hitesh; Martin, Richard J.; Wigle, Dennis A.; Prakash, Y. S.

doi:10.1152/ajplung.00266.2014

Cited by 14 publications

(10 citation statements)

References 21 publications

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“…The proliferation of human fASM cells has been previously demonstrated (Hartman et al, ; Martin et al, ; Vogel et al, ). The presence of R568 significantly increased fASM cell proliferation even at zero [Ca 2+ ] o , whereas NPS2143 significantly blunted proliferation at different [Ca 2+ ] o (Figure a).…”

Section: Resultsmentioning

confidence: 86%

Calcium sensing receptor in developing human airway smooth muscle

Roesler

Wicher

Ravix

et al. 2019

Journal Cellular Physiology

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Airway smooth muscle (ASM) regulation of airway structure and contractility is critical in fetal/neonatal physiology in health and disease. Fetal lungs experience higher Ca2+ environment that may impact extracellular Ca2+ ([Ca2+]o) sensing receptor (CaSR). Well‐known in the parathyroid gland, CaSR is also expressed in late embryonic lung mesenchyme. Using cells from 18‐22 week human fetal lungs, we tested the hypothesis that CaSR regulates intracellular Ca2+ ([Ca2+]i) in fetal ASM (fASM). Compared with adult ASM, CaSR expression was higher in fASM, while fluorescence Ca2+ imaging showed that [Ca2+]i was more sensitive to altered [Ca2+]o. The fASM [Ca2+]i responses to histamine were also more sensitive to [Ca2+]o (0–2 mM) compared with an adult, enhanced by calcimimetic R568 but blunted by calcilytic NPS2143. [Ca2+]i was enhanced by endogenous CaSR agonist spermine (again higher sensitivity compared with adult). Inhibition of phospholipase C (U73122; siRNA) or inositol 1,4,5‐triphosphate receptor (Xestospongin C) blunted [Ca2+]o sensitivity and R568 effects. NPS2143 potentiated U73122 effects. Store‐operated Ca2+ entry was potentiated by R568. Traction force microscopy showed responsiveness of fASM cellular contractility to [Ca2+]o and NPS2143. Separately, fASM proliferation showed sensitivity to [Ca2+]o and NPS2143. These results demonstrate functional CaSR in developing ASM that modulates airway contractility and proliferation.

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Section: Resultsmentioning

confidence: 86%

Calcium sensing receptor in developing human airway smooth muscle

Roesler

Wicher

Ravix

et al. 2019

Journal Cellular Physiology

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“…Wang and coworkers (355) described the differential impact of elevated oxygen levels on smooth muscle mass and collagen deposition in the developing airways in mice exposed to 40% O 2 or 70% O 2 from P1 to P7, followed by recovery in room air between P8 and P21. Other reports, for example those documenting the impact of cigarette smoke on mitochondrial function (24,25) and the proliferation and ECM production (347) in airway smooth muscle cells, as well as the impact of hyperoxia on estradiol metabolism in postnatal airway smooth muscle (219), highlight the potential relevance of perturbations to airway development to lung maturation. Furthermore, Chen and colleagues (67) provide evidence that endogenous retinoic acid, a key player in lung development, restricts airway smooth muscle cell differentiation during formation of the airways.…”

Section: A Role For the Small Airways?mentioning

confidence: 99%

Recent advances in the mechanisms of lung alveolarization and the pathogenesis of bronchopulmonary dysplasia

Silva

Nardiello

Pozarska

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

120

117

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Alveolarization is the process by which the alveoli, the principal gas exchange units of the lung, are formed. Along with the maturation of the pulmonary vasculature, alveolarization is the objective of late lung development. The terminal airspaces that were formed during early lung development are divided by the process of secondary septation, progressively generating an increasing number of alveoli that are of smaller size, which substantially increases the surface area over which gas exchange can take place. Disturbances to alveolarization occur in bronchopulmonary dysplasia (BPD), which can be complicated by perturbations to the pulmonary vasculature that are associated with the development of pulmonary hypertension. Disturbances to lung development may also occur in persistent pulmonary hypertension of the newborn in term newborn infants, as well as in patients with congenital diaphragmatic hernia. These disturbances can lead to the formation of lungs with fewer and larger alveoli and a dysmorphic pulmonary vasculature. Consequently, affected lungs exhibit a reduced capacity for gas exchange, with important implications for morbidity and mortality in the immediate postnatal period and respiratory health consequences that may persist into adulthood. It is the objective of this Perspectives article to update the reader about recent developments in our understanding of the molecular mechanisms of alveolarization and the pathogenesis of BPD.

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“…Microarray data set GSE25286 was downloaded from Gene Expression Omnibus [GEO: GSE25286], including 3 BPD samples and 2 healthy controls [ 28 ], The GLP1261 [Mouse430_2] Affymetrix Mouse Genome 430 2.0 Array (Affymetrix, Santa Clara, CA, USA) and the annotation information of probes were used to detect the gene expression.…”

Section: Methodsmentioning

confidence: 99%

Overexpression of AGT promotes bronchopulmonary dysplasis via the JAK/STAT signal pathway

2017

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Angiotensinogen (AGT) is involved in the production of angiotensin II which is the main mediator of action of the rennin-angiotensin system (RAS), whereas the RAS mediates the regulation of sodium homeostasis, blood pressure, and inflammation. The present study aimed to investigate the roles of the AGT in the progression of broncopulmonary dysplasia in premature newborns. By bioinformatics analysis, AGT was found to be the major node in molecular interaction networks of BPD mouse model. Quantitative PCR and western blot analyses were applied to examine AGT expression in A549 cells which were treated with the hyperoxic condition. The AGT inhibitor Valsartan and the AGT agonist ANGII were employed to investigate the roles of AGT in cell growth and the inflammation. Results show that hyperoxic treatment induced upregulation of AGT expression in A549 cells. Overexpression of AGT resulted in the inflammation via the JAK/STAT signal pathway, ultimately suppressed the proliferation of the A549 cell. In conclusion, increased expression of AGT was demonstrated to be associated with the development and progression of BPD, and may be regarded as a promising therapeutic target for BPD.

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Hyperoxia-induced changes in estradiol metabolism in postnatal airway smooth muscle

Cited by 14 publications

References 21 publications

Calcium sensing receptor in developing human airway smooth muscle

Calcium sensing receptor in developing human airway smooth muscle

Recent advances in the mechanisms of lung alveolarization and the pathogenesis of bronchopulmonary dysplasia

Overexpression of AGT promotes bronchopulmonary dysplasis via the JAK/STAT signal pathway

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