PMID- 29484847
OWN - NLM
STAT- MEDLINE
DCOM- 20190221
LR  - 20240315
IS  - 2051-817X (Electronic)
IS  - 2051-817X (Linking)
VI  - 6
IP  - 5
DP  - 2018 Mar
TI  - Lung epithelial-specific TRIP-1 overexpression maintains epithelial integrity 
      during hyperoxia exposure.
LID - 10.14814/phy2.13585 [doi]
LID - e13585
AB  - The onset and degree of injury occurring in animals that develop hyperoxic acute 
      lung injury (HALI) is dependent on age at exposure, suggesting that 
      developmentally regulated pathways/factors must underlie initiation of the 
      epithelial injury and subsequent repair. Type II TGFbeta receptor interacting 
      protein-1 (TRIP-1) is a negative regulator of TGFbeta signaling, which we have 
      previously shown is a developmentally regulated protein with modulatory effects 
      on epithelial-fibroblastic signaling. The aim of this study was to assess if type 
      II alveolar epithelial cells overexpressing TRIP-1 are protected against 
      hyperoxia-induced epithelial injury, and in turn HALI. Rat lung epithelial cells 
      (RLE) overexpressing TRIP-1 or LacZ were exposed to 85% oxygen for 4 days. A 
      surfactant protein C (SPC)-driven TRIP-1 overexpression mouse (TRIP-1(AECTg+) ) 
      was generated and exposed to hyperoxia (>95% for 4 days) at 4 weeks of age to 
      assess the effects TRIP-1 overexpression has on HALI. RLE overexpressing TRIP-1 
      resisted hyperoxia-induced apoptosis. Mice overexpressing TRIP-1 in their lung 
      type II alveolar epithelial cells (TRIP-1(AECTg+) ) showed normal lung 
      development, increased phospho-AKT level and E-cadherin, along with resistance to 
      HALI, as evidence by less TGFbeta activation, apoptosis, alveolar macrophage influx, 
      KC expression. Taken together, these findings point to existence of a TRIP-1 
      mediated molecular pathway affording protection against epithelial/acute lung 
      injury.
CI  - (c) 2018 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on 
      behalf of The Physiological Society and the American Physiological Society.
FAU - Nyp, Michael F
AU  - Nyp MF
AUID- ORCID: 0000-0001-5127-670X
AD  - Division of Neonatology, Department of Pediatrics, Children's Mercy Kansas City, 
      Kansas City, Missouri.
AD  - Department of Pediatrics, University of Missouri Kansas City, Kansas City, 
      Missouri.
FAU - Mabry, Sherry M
AU  - Mabry SM
AD  - Division of Neonatology, Department of Pediatrics, Children's Mercy Kansas City, 
      Kansas City, Missouri.
AD  - Department of Pediatrics, University of Missouri Kansas City, Kansas City, 
      Missouri.
FAU - Navarro, Angels
AU  - Navarro A
AD  - Division of Neonatology, Department of Pediatrics, Children's Mercy Kansas City, 
      Kansas City, Missouri.
AD  - Department of Pediatrics, University of Missouri Kansas City, Kansas City, 
      Missouri.
FAU - Menden, Heather
AU  - Menden H
AD  - Division of Neonatology, Department of Pediatrics, Children's Mercy Kansas City, 
      Kansas City, Missouri.
AD  - Department of Pediatrics, University of Missouri Kansas City, Kansas City, 
      Missouri.
FAU - Perez, Ricardo E
AU  - Perez RE
AD  - Department of Anatomy and Cell Biology, Rush University, Chicago, Illinois.
FAU - Sampath, Venkatesh
AU  - Sampath V
AD  - Division of Neonatology, Department of Pediatrics, Children's Mercy Kansas City, 
      Kansas City, Missouri.
AD  - Department of Pediatrics, University of Missouri Kansas City, Kansas City, 
      Missouri.
FAU - Ekekezie, Ikechukwu I
AU  - Ekekezie II
AD  - Division of Neonatology, Department of Pediatrics, Children's Mercy Kansas City, 
      Kansas City, Missouri.
AD  - Department of Pediatrics, University of Missouri Kansas City, Kansas City, 
      Missouri.
LA  - eng
GR  - R01 HL128374/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Physiol Rep
JT  - Physiological reports
JID - 101607800
RN  - 0 (Eukaryotic Initiation Factors)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (TRIP-1 protein, mouse)
SB  - IM
MH  - Acute Lung Injury/etiology/*metabolism
MH  - Alveolar Epithelial Cells/metabolism
MH  - Animals
MH  - Apoptosis
MH  - Cell Line
MH  - Eukaryotic Initiation Factors/genetics/*metabolism
MH  - Humans
MH  - Hypoxia/*complications
MH  - Intracellular Signaling Peptides and Proteins/genetics/*metabolism
MH  - Lung/cytology/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Rats
PMC - PMC5827472
OTO - NOTNLM
OT  - Airway and lung biology
OT  - TGFbeta
OT  - TRIP-1
OT  - hyperoxic acute lung injury
EDAT- 2018/02/28 06:00
MHDA- 2019/02/23 06:00
PMCR- 2018/02/27
CRDT- 2018/02/28 06:00
PHST- 2017/08/18 00:00 [received]
PHST- 2017/12/20 00:00 [revised]
PHST- 2017/12/27 00:00 [accepted]
PHST- 2018/02/28 06:00 [entrez]
PHST- 2018/02/28 06:00 [pubmed]
PHST- 2019/02/23 06:00 [medline]
PHST- 2018/02/27 00:00 [pmc-release]
AID - PHY213585 [pii]
AID - 10.14814/phy2.13585 [doi]
PST - ppublish
SO  - Physiol Rep. 2018 Mar;6(5):e13585. doi: 10.14814/phy2.13585.