Maturational changes induced by 1 alpha,25-dihydroxyvitamin D3 in type II cells from fetal rat lung explants

Marin, L.; Dufour, Marie Noëlle; Nguyen, Thi M.‐D.; Tordet, C.; Garabedian, M.

doi:10.1152/ajplung.1993.265.1.l45

Cited by 35 publications

(36 citation statements)

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“…Fibroblasts are recognized as influencing surfactant biosynthesis through paracrine actions. Before parturition, fibroblasts secrete a polypeptide that stimulates the rate-limiting enzyme for surfactant synthesis by the ATII cells (34,60,70). Perinatal lung maturation is a highly regulated process, and alveolar epithelialmesenchymal interactions play a critical role (90,96).…”

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confidence: 99%

The impact of vitamin D on fetal and neonatal lung maturation. A systematic review

Lykkedegn

Sørensen

Beck-Nielsen

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

122

104

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-Respiratory distress syndrome (RDS) and bronchopulmonary dysplasia (BPD) are major complications to preterm birth. Hypovitaminosis D is prevalent in pregnancy. We systematically reviewed the evidence of the impact of vitamin D on lung development, surfactant synthesis, RDS, and BPD searching PubMed, Embase, and Cochrane databases with the terms vitamin D AND (surfactant OR lung maturation OR lung development OR respiratory distress syndrome OR fetal lung OR prematurity OR bronchopulmonary dysplasia). Three human studies, ten animal studies, two laboratory studies, and one combined animal and laboratory study were included. Human evidence was sparse, allowing no conclusions. BPD was not associated with vitamin D receptor polymorphism in a fully adjusted analysis. Animal and laboratory studies showed substantial positive effects of vitamin D on the alveolar type II cell, fibroblast proliferation, surfactant synthesis, and alveolarization. These data support the hypothesis of hypovitaminosis D as a frequent, modifiable risk factor of RDS and BPD, which should be tested in randomized controlled trials on pregnant women, those with threatening preterm delivery, or in the preterm neonates. Future experimental and human studies should aim to identify optimal time windows, vitamin D doses, and cut-off levels for 25-hydroxyvitamin D in interventions against RDS, BPD, and later adverse respiratory outcomes. vitamin D; fetus; lung; surfactant; preterm; neonate THE IMPORTANCE OF VITAMIN D in nonskeletal fetal and childhood health has become increasingly recognized in the last decades (19,65). The impact of vitamin D on early lung development and maturation and lung diseases of early life is an emerging field of research. Hypovitaminosis D during pregnancy is associated with reduced placental development and weight, leading to a presumed risk of preterm birth (24,25), which per se may lead to respiratory distress syndrome (RDS) and bronchopulmonary dysplasia (BPD). Moreover, vitamin D is suggested to play a role in the embryogenesis and in cellular growth and differentiation, including lung development and regulation of lung maturation in the fetus (23,29,38,70,71,108), whereby hypovitaminosis D could be hypothesized to aggravate premature neonatal lung diseases.Vitamin D is involved in the development of the innate and adaptive immune system, and, because of its unique capacity to bind to the vitamin D receptor (VDR) and thereby to serve as a transcriptional factor, vitamin D can regulate gene expression and exert widespread immunomodulatory effects including proliferation, differentiation, and complex regulation (19, 56, 58 -61, 64, 65, 68, 69, 105). Evidence suggests that vitamin D may stimulate regulatory T cell development and T cell function to suppress inappropriate Th1 and Th2 responses to environmental exposure (i.e., allergens, infection load), leading to a more balanced immune response inhibiting autoimmune diseases (with Th1 dominance) and allergic diseases (Th2 dominance) (55). Vitamin D could therefore be inv...

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mentioning

confidence: 99%

The impact of vitamin D on fetal and neonatal lung maturation. A systematic review

Lykkedegn

Sørensen

Beck-Nielsen

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

122

104

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“…In fetal rat lung, 1,25(OH) 2 D 3 increases the synthesis and secretion of surfactant lipids (34,35) and accelerates the appearance of the morphological features of alveolar type II cells (34). Rat alveolar type II cells have been shown to contain the nuclear hormone receptor for 1,25(OH) 2 D 3 , which is responsible for many of its physiological effects (38).…”

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confidence: 99%

Regulation of human pulmonary surfactant protein gene expression by 1α,25-dihydroxyvitamin D₃

Phokela¹,

Peleg²,

Moya³

et al. 2005

American Journal of Physiology-Lung Cellular and Molecular Phys

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[1,25(OH)2D3] has been reported to stimulate lung maturity, alveolar type II cell differentiation, and pulmonary surfactant synthesis in rat lung. We hypothesized that 1,25(OH) 2D3 stimulates expression of surfactant protein-A (SP-A), SP-B, and SP-C in human fetal lung and type II cells. We found that immunoreactive vitamin D receptor was detectable in fetal lung tissue and type II cells only when incubated with 1,25(OH)2D3. 1,25(OH)2D3 significantly decreased SP-A mRNA in human fetal lung tissue but did not significantly decrease SP-A protein in the tissue. In type II cells, 1,25(OH)2D3 alone had no significant effect on SP-A mRNA or protein levels but reduced SP-A mRNA and protein in a dose-dependent manner when the cells were incubated with cAMP. SP-A mRNA levels in NCI-H441 cells, a nonciliated bronchiolar epithelial (Clara) cell line, were decreased in a dose-dependent manner in the absence or presence of cAMP. 1,25(OH)2D3 had no significant effect on SP-B mRNA levels in lung tissue but increased SP-B mRNA and protein levels in type II cells incubated in the absence or presence of cAMP. Expression of SP-C mRNA was unaffected by 1,25(OH)2D3 in lung tissue incubated Ϯ cAMP. These results suggest that regulation of surfactant protein gene expression in human lung and type II cells by 1,25(OH)2D3 is not coordinated; 1,25(OH)2D3 decreases SP-A mRNA and protein levels in both fetal lung tissue and type II cells, increases SP-B mRNA and protein levels only in type II cells, and has no effect on SP-C mRNA levels. alveolar type II cell; steroid hormone PULMONARY SURFACTANT IS a unique complex of phospholipids and proteins that maintains alveolar integrity by reducing surface tension at the alveolar air-liquid interface (15) and participates in host defense and the control of inflammation in the lung (16). Surfactant is composed of 90% lipids and 10% proteins by weight. Phosphatidylcholine, mostly dipalmitoyl phosphatidylcholine, constitutes 70 -80% of the lipid portion of surfactant. Several distinct lung-specific proteins make up the protein component of surfactant, surfactant protein-A (SP-A), SP-B, SP-C, and SP-D (23). Whereas the lipid portion of surfactant is largely responsible for its surface activity, the highly hydrophobic proteins SP-B and SP-C also play a direct role in influencing the surface tension-reducing properties of surfactant (54). On the other hand, SP-A and SP-D are hydrophilic members of the collectin family of proteins (25) that play important roles in the control of host defense and inflammation in the lung (16). Pulmonary alveolar type II epithelial cells that are positioned in the corners of the alveoli carry out the highly specialized functions of synthesizing, secreting, and reutilizing surfactant (36, 49). Surfactant synthesis is initiated in alveolar type II cells only after 75% of gestation is complete (43). Infants born before this period of gestation lack sufficient surfactant and are predisposed to develop respiratory distress syndrome, one of the leading causes of neonatal morbi...

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“…[25][26][27][28][29] Specific binding sites for 1,25(OH)2D3 localized to type II pneumocytes have been found in fetal rat lungs and it has been shown that vitamin D accelerates type II pneumocyte maturation, increases the surfactant synthesis and secretion and has a critical role in epithelialmesenchymal interaction during lung growth. 17,18 In probable pathophysiology of TTN, immaturity of epithelial sodium channels (ENaC) is now believed to be major factor in failure of lung fluid resorption. A surge in catecholamines and endogenous steroids increase the expression and activity of ENaC.…”

Section: Discussionmentioning

confidence: 99%

“…16 Moreover, in fetal rat lung, vitamin D increases the synthesis and secretion of surfactant lipids and proteins in alveolar type II cells. 17,18 As role of vitamin D in TTN has not been studied much, so we conducted present study in our hospital to find the association between serum vitamin D levels and TTN.…”

Section: 13mentioning

confidence: 98%

Association of serum vitamin D levels and transient tachypnea of newborn: a case control study

Singh

Sood

Narang

et al. 2017

Int J Contemp Pediatr

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Background: Transient tachypnea of newborn (TTN) is a common cause of respiratory distress in newborns with estimated incidence of 1-2% of all newborns. Although a self-limiting transient condition but it may cause severe morbidities. This study was conducted to find association of serum vitamin D levels in neonates who develop TTN as compared to normal healthy neonates.Methods: With thorough history with structured questionnaire and lab tests, serum vitamin D levels of 45 neonates who develop TTN were compared with 56 healthy neonates in control group.Results: Out of 45 neonates who develop TTN 39(86.7%) were deficient in vitamin D as compared to control group where 33(58.9%) out of 56 healthy neonates were deficient in vitamin D.Conclusions: Lower vitamin D levels at birth in term neonates is associated with increased risk of developing TTN and vitamin D may have a role in its pathogenesis.

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Maturational changes induced by 1 alpha,25-dihydroxyvitamin D3 in type II cells from fetal rat lung explants

Cited by 35 publications

References 0 publications

The impact of vitamin D on fetal and neonatal lung maturation. A systematic review

The impact of vitamin D on fetal and neonatal lung maturation. A systematic review

Regulation of human pulmonary surfactant protein gene expression by 1α,25-dihydroxyvitamin D₃

Association of serum vitamin D levels and transient tachypnea of newborn: a case control study

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Maturational changes induced by 1 alpha,25-dihydroxyvitamin D3 in type II cells from fetal rat lung explants

Cited by 35 publications

References 0 publications

The impact of vitamin D on fetal and neonatal lung maturation. A systematic review

The impact of vitamin D on fetal and neonatal lung maturation. A systematic review

Regulation of human pulmonary surfactant protein gene expression by 1α,25-dihydroxyvitamin D3

Association of serum vitamin D levels and transient tachypnea of newborn: a case control study

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Regulation of human pulmonary surfactant protein gene expression by 1α,25-dihydroxyvitamin D₃