Delay in rat lung alveolarization after the combined exposure of maternal hyperglycemia and postnatal hyperoxia

Koskinen, Anna; Lukkarinen, Heikki; Laine, Jukka; Ahotupa, Markku; Kääpä, Pietari; Soukka, Hanna

doi:10.1002/ppul.22837

Cited by 6 publications

(4 citation statements)

References 40 publications

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“…Although not yet in widespread use, this model was used to demonstrate the therapeutic potential of umbilical cord mononuclear cells to promote proper lung alveolarization (assessed by stereology, using airspace volume density and surface density of septa as surrogates for alveolarization) (239), and, on the basis the expression of surfactant protein and other genes, this model is considered to closely mimic the clinical situation (120). This concept of fetal priming has also been observed in the rodent hyperoxia model using maternal diabetes as a first hit, in which streptozotocin-induced diabetes in rats before pregnancy appeared to modulate the effects of hyperoxia on septal wall thickness in pup lungs, although the precise implications of this are not clear (173). In terms of other new models, the observation that maternal deprivation (that is, separation of mother and pups) in rats also led to a pronounced blunting of lung development (assessed by MLI), ostensibly mediated by dipeptidyl peptidase IV, suggests that maternal deprivation may represent a new (stress-induced) rat model of BPD (150).…”

Section: Animal Models Of Arrested Alveolarizationmentioning

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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Section: Animal Models Of Arrested Alveolarizationmentioning

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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“…Delayed pneumocyte differentiation and lung maturation were observed in the offspring in rodent models of diabetes during pregnancy 9‐12 . The possible mechanism for their pathogenesis is that phosphatidylglycerol production may be inhibited in gestational diabetes, resulting in reduced surfactants and increased susceptibility to respiratory distress syndrome, which may also explain the increased risk of persistent wheezing in human infants born to women with GDM 13‐18 …”

Section: Introductionmentioning

confidence: 99%

Association between maternal diabetes mellitus and allergic diseases in children — A systematic review and meta‐analysis

Wang

et al. 2021

Pediatric Allergy Immunology

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Background Existing knowledge suggests that gestational diabetes mellitus was inconsistently associated with offspring allergic diseases. The aim of this study was to identify the association between maternal diabetes mellitus and the risk of offspring allergic diseases by systematic review. Methods We searched and retrieved three databases (PubMed, Web of Science, and Cochrane Library) for articles on the association between maternal diabetes mellitus and offspring allergic diseases published before December 31, 2019. Stata software version 16.0 was used for statistical analysis. Results Eight published studies were included in this meta‐analysis. The pooled effect estimates showed the association between maternal diabetes mellitus and allergic outcomes, including asthma (OR: 1.13, 95% CI: 1.01‐1.27), wheezing (OR: 1.13, 95% CI: 1.07‐1.21), and atopic dermatitis (OR: 1.43, 95% CI: 1.22‐1.57). Maternal diabetes mellitus was not associated with the risk of allergic sensitization, with a pooled effect estimate of 1.07 (95% CI: 0.45, 2.58). Conclusion Maternal diabetes mellitus may increase the risk of allergic diseases in their children. However, this finding should be validated with future large‐sample epidemiological studies covering a wider spectrum of allergic diseases.

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“…Maternal diabetes is associated with perinatal risk factors including congenital malformations and respiratory distress syndrome RDS but has not previously been linked to BPD or CLDi. In rat models, fetal exposure to hyperglycemia leads to the functional, biochemical, and morphological perturbation of maturation of the lung as well as causing thinning of alveolar septa in association with increased apoptosis and proliferation …”

Section: Discussionmentioning

confidence: 99%

Determinants of chronic lung disease severity in the first year of life; A population based study

et al. 2015

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We received survey responses from 43/88 pediatric pulmonologists from 28/53 North American training centers who are experts in CLDi. Strong agreement between ranking (72-100%) of respiratory system parameters and weighting (out of 100 points weighting was within 20 points) was observed with severity of CLDi. Data from 940 CLDi premature infants <30 weeks GA were obtained. Infants with severe CLDi scores at 4-9 months CGA (relative to a zero score) showed positive associations with being male, odds ratio[OR] = 2.45[confidence interval (CI) 1.26-4.77]), >30 ventilator days, OR = 3.82 (1.30-11.2), postnatal steroids OR = 3.94 (1.94-7.84), and a surprising inverse association with retinopathy of prematurity stage 3-4, OR = 0.24 (0.09-0.67) CONCLUSIONS: The CLDi clinical severity score allowed for standardized assessment of pulmonary morbidity, and evaluation of risk factors in the NICU for CLDi following NICU discharge. These observations point to risk factors associated with CLDi outcomes at 4-9 months CGA.

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Delay in rat lung alveolarization after the combined exposure of maternal hyperglycemia and postnatal hyperoxia

Abstract: Our results thus indicate that the hyperglycemic priming of the fetal lung modifies the deleterious effect of hyperoxia on alveolarization in neonatal rats.

Cited by 6 publications

References 40 publications

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

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

Association between maternal diabetes mellitus and allergic diseases in children — A systematic review and meta‐analysis

Determinants of chronic lung disease severity in the first year of life; A population based study

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