Stimulation of MAP kinase pathways after maternal IL-1β exposure induces fetal lung fluid absorption in guinea pigs

Bhattacharjee, Reshma; Li, Tianbo; Koshy, Shyny; Beard, LaMonta L.; Sharma, Kapil; Carter, Ethan P.; Garat, Chrystelle; Folkesson, Hans G.

doi:10.1186/1465-9921-8-27

Cited by 4 publications

(6 citation statements)

References 33 publications

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“…In some studies, dopamine and isoproterenol as well as growth factors up-regulate Na,K-ATPase expression via activating MEK and ERK [15,19,20]. In our earlier study [16], MEK and ERK activation did not change lung ENaC expression, but stimulated lung fluid absorption in fetal guinea pigs. It has been suggested that MAP kinase activation during high V t ventilation leads to type II cell hyperplasia [40].…”

Section: Discussionmentioning

confidence: 92%

“…We [16] and others [15,19] have shown that these proteins can be important for lung fluid absorption. In some studies, dopamine and isoproterenol as well as growth factors up-regulate Na,K-ATPase expression via activating MEK and ERK [15,19,20].…”

Section: Discussionmentioning

confidence: 97%

“…Because our laboratory [16] and others [21,22] have shown that MAP kinases may be involved in regulating lung fluid absorption, pMEK and pERK expression were studied in GD67 fetal guinea pig lungs after ventilation with the low and higher V t (N = 6 in each group). Ventilation with higher V t…”

Section: Pmek and Perk Expressionmentioning

confidence: 99%

“…In our earlier study on MAP kinase (MAPK) regulation of fetal lung fluid absorption, we demonstrated that the MAPK/extracellular signal-regulated kinase (ERK) kinase (MEK)/ERK MAP kinase pathway may have been involved in regulation of lung fluid absorption near term in the guinea pig [16]. MAP kinases such as ERK and c-Jun N-terminal kinase (JNK) have been shown to be activated by stress responses [17,18].…”

mentioning

confidence: 98%

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Lung fluid absorption is induced in preterm guinea pigs ventilated with low tidal volumes

Koshy

Beard

Kuzenko

et al. 2010

Experimental Lung Research

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The objective of this study was to determine if low tidal volume (V(t)) ventilation was beneficial when ventilating preterm fetuses. The authors ventilated preterm guinea pig fetuses at gestation day (GD) 67, 3 days before birth, newborn, and 10-day-old (PD10) guinea pigs with low V(t) (6 mL/kg body weight [bw]) and compared them to age-matched fetuses/animals ventilated with higher potentially injurious V(t) (12 mL/kg bw). Lung fluid absorption was measured after intratracheal instillation of 5% albumin in 0.9% NaCl. Low V(t) ventilation stimulated lung fluid absorption when compared to higher V(t) in all groups. The increased lung fluid absorption in low V(t)-ventilated fetuses was associated with increased α epithelial Na channel (αEnaC) mRNA. However, αENaC and βENaC protein was unchanged over the 1-hour study. Because stretch induces mitogen-activated protein (MAP) kinase expression and MAP kinases may affect lung fluid absorption, the authors investigated if MAP kinase (MAPK) expression was affected by V(t). Extracellular signal-regulated kinase (ERK) and MAPK/ERK kinase (MEK) were phosphorylated in the higher V(t)-ventilated guinea pig fetuses. This suggested that a reduced activation of MAP kinases might explain the increased lung fluid absorption in the low V(t)-ventilated fetuses. Thus these data suggest that low V(t) ventilation increases fetal lung fluid absorption and thus may be preferential to use clinically.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 97%

Section: Pmek and Perk Expressionmentioning

confidence: 99%

mentioning

confidence: 98%

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Lung fluid absorption is induced in preterm guinea pigs ventilated with low tidal volumes

Koshy

Beard

Kuzenko

et al. 2010

Experimental Lung Research

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“…It has also been demonstrated that stretch‐induced release of MAP kinases may be involved in regulating fetal lung fluid absorption (Koshy et al, in press). MAP kinases have, in several studies, been proposed to regulate lung fluid absorption in both positive and negative ways (Pesce et al, 2000; Guerrero et al, 2001; Frank et al, 2003; Upadhyay et al, 2003; Lin et al, 2005; Roux et al, 2005; Bhattacharjee et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Fetal Lung Epithelial Ion Channels Relocate in the Cell Membrane During Late Gestation

Beard¹,

Li²,

Hu³

et al. 2011

The Anatomical Record

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Near the end of gestation, the direction of ion and fluid flow across the alveolar epithelium rapidly changes from secretion to absorption. Thus, the relative cell membrane location of epithelial Na channels (ENaCs) and cystic fibrosis transmembrane regulator (CFTR) Cl channels during late fetal lung development and after maternal interleukin-1b (IL1b) pretreatment was the focus of our study. Western blot analysis after sucrose gradient separation of caveolin-1-(Cav-1)-rich membrane regions (CRR) and Cav-1-poor membrane (non-CRR) revealed primary CRR ENaC localization at gestation day (GD) 61 in guinea pigs. Correlating with the natural induction of distal lung fluid absorption, ENaC appeared in the non-CRR cell membrane regions at GD68. Conversely, CFTR was present in the non-CRR cell membrane regions at GD61 and in the CRRs at GD68. IL-1b-induced conversion to distal lung fluid absorption at GD61 was associated with ENaC non-CRR presence and CFTR CRR presence, suggesting that relative ENaC and CFTR locations induced distal lung fluid absorption and decreased fluid secretion. Instilling fetal lungs with the CRR-disrupting agent methyl-b-cyclodextrin resulted in the conversion from lung fluid secretion to absorption and ENaC non-CRR presence at GD61. Coimmunoprecipitation of Cav-1 with a-and b-ENaC demonstrated reduced coimmunoprecipitation with increased GD and after IL-1b pretreatment. On the other hand, coimmunoprecipitation of Cav-1 with CFTR demonstrated increased coimmunoprecipitation with increasing GD and after IL-1b pretreatment. This concept may provide novel molecular mechanisms for the rapid transition from fetal distal lung fluid secretion to absorption in near-term lungs.

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IL-1 promotes α-epithelial Sodium Channel (α-ENaC) expression in murine lung epithelial cells: involvement of NF-κB

Mustafa

Hernandez

Johnson‐Pais

et al. 2019

J. Cell Commun. Signal.

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Intra‐amniotic exposure to proinflammatory cytokines such as interleukin‐1 (IL‐1) correlates with a decreased incidence of respiratory distress syndrome (RDS) in infants following premature birth. At birth, inadequate absorption of fluid from the fetal lung contributes to the onset RDS. Lung fluid clearance is coupled to Na+ transport via epithelial sodium channels (ENaC). In this study, we assessed the effects of IL‐1 on the expression of ENaC, particularly the α‐subunit which is critical for fetal lung fluid clearance at birth. Cultured mouse lung epithelial (MLE‐12) cells were treated with either IL‐1α or IL‐1β to determine their effects on α‐ENaC expression. Changes in IL‐1‐induced α‐ENaC levels in the presence of IL‐1 receptor antagonist (IL‐1ra), cycloheximide, NF‐κB inhibitor, and MAP kinase inhibitors were investigated. IL‐1α and IL‐1β independently induced a significant increase of α‐ENaC mRNA and protein after 24 h compared to untreated cells. IL‐1‐dependent increases in α‐ENaC protein were mitigated by IL‐1ra and cycloheximide. IL‐1 exposure induced NF‐κB binding activity. Attenuation of IL‐1‐induced NF‐κB activation by its inhibitor SN50 decreased α‐ENaC protein abundance. Inhibition of ERK 1,2 MAPK significantly decreased both IL‐1α and β‐induced α‐ENaC protein expression whereas inhibition of p38 MAPK only blocked IL‐1β‐induced α‐ENaC protein levels. In contrast, IL‐1‐induced α‐ENaC protein levels were unaffected by a c‐Jun N‐terminal kinase (JNK) inhibitor. Our results suggest that in MLE‐12 cells, IL‐1‐induced elevation of α‐ENaC is mediated via NF‐κB activation and in part involves stimulation of the ERK 1,2 and p38 MAPK signaling pathways.

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Stimulation of MAP kinase pathways after maternal IL-1β exposure induces fetal lung fluid absorption in guinea pigs

Abstract: Background: We tested the hypothesis that maternal interleukin-1β (IL-1β) pretreatment and induction of fetal cortisol synthesis activates MAP kinases and thereby affects lung fluid absorption in preterm guinea pigs.

Cited by 4 publications

References 33 publications

Lung fluid absorption is induced in preterm guinea pigs ventilated with low tidal volumes

Lung fluid absorption is induced in preterm guinea pigs ventilated with low tidal volumes

Fetal Lung Epithelial Ion Channels Relocate in the Cell Membrane During Late Gestation

IL-1 promotes α-epithelial Sodium Channel (α-ENaC) expression in murine lung epithelial cells: involvement of NF-κB

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