10.25376/hra.7971245.v1
Steven J. Forrester
Steven
J. Forrester
Qian Xu
Qian
Xu
Daniel Kikuchi
Daniel
Kikuchi
Derick Okwan-Duodu
Derick
Okwan-Duodu
Ana Carolina Campos
Ana Carolina
Campos
Elizabeth Faidley
Elizabeth
Faidley
Guogang Zhang
Guogang
Zhang
Bernard Lassègue
Bernard
Lassègue
Ruxana T. Sadikot
Ruxana
T. Sadikot
Kathy K. Griendling
Kathy
K. Griendling
Marina S. Hernandes
Marina
S. Hernandes
Supplemental 1.pdf
Health Research Alliance
2019
Poldip2; acute respiratory distress syndrome; inflammation; leukocyte
Animal Physiology - Systems
Cell Biology
2019-04-09 15:49:29
Figure
https://hra.figshare.com/articles/figure/Supplemental_1_pdf/7971245
<div>Acute respiratory distress syndrome (ARDS) in a deadly disease that can be brought on</div><div>by endotoxins such as lipopolysaccharide (LPS). ARDS is characterized by vascular permeability,</div><div>a severe inflammatory response, lung leukocyte infiltration, and resultant lung</div><div>edema. Polymerase δ-interacting protein 2 (Poldip2) is a novel regulator of blood–brain barrier</div><div>permeability; however, its role in regulating lung permeability and vascular inflammation</div><div>is unknown. Here, the role of Poldip2 in regulating vascular permeability and inflammation</div><div>in a mouse model of ARDS was assessed. Heterozygous deletion of Poldip2 was</div><div>found to reduce LPS-induced mortality within 20 h, lung inflammatory signaling, and leukocyte</div><div>infiltration. Moreover, reduced Poldip2-suppressed LP-induced vascular cell adhesion</div><div>molecule (VCAM)-1 induction, leukocyte recruitment, and mitochondrial reactive oxygen</div><div>species (ROS) production in vitro. These data indicate that Poldip2 is an important regulator</div><div>of the debilitating consequences of ARDS, potentially through the regulation of mitochondrial</div><div>ROS-induced inflammatory signaling. Consequently, inhibition of Poldip2 may be</div><div>a viable option for therapeutic discovery moving forward.</div>