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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Cell+Mol+Med
2016 ; 20
(3
): 506-17
Nephropedia Template TP
gab.com Text
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English Wikipedia
Progranulin deficiency leads to severe inflammation, lung injury and cell death
in a mouse model of endotoxic shock
#MMPMID26757107
Yu Y
; Xu X
; Liu L
; Mao S
; Feng T
; Lu Y
; Cheng Y
; Wang H
; Zhao W
; Tang W
J Cell Mol Med
2016[Mar]; 20
(3
): 506-17
PMID26757107
show ga
Progranulin (PGRN) is a crucial secreted growth factor involved in various kinds
of physiologic and disease processes and often has a protective role in
inflammatory diseases. This study was designed to investigate the protective
effects of PGRN on endotoxic shock in a mouse model of PGRN deficiency. After
lipopolysaccharide (LPS) injection to induce endotoxic shock in mice, PGRN levels
were induced in wild-type (WT) mice at 6 and 24 hrs. Survival rate analysis,
haematoxylin and eosin staining, immunohistochemical staining, enzyme-linked
immunosorbent assay and in situ terminal deoxynucleotidyl transferase-mediated
uridine triphosphate nick-end labelling assay were used to reveal the
susceptibility, lung injury, inflammatory cell infiltration, production of
inflammatory mediators and lung cell death in mice after LPS injection.
PGRN-deficient (Grn(-/-) ) mice were highly susceptible to LPS-induced endotoxic
shock, with decreased survival, severe lung injury, increased production of
pro-inflammatory mediators, and inflammatory cell infiltration and apoptotic
death in the lung. Additionally, recombinant PGRN (rPGRN) administration before
LPS stimulation ameliorated the survival of and abnormalities in both WT and
Grn(-/-) mice. Altogether, these findings indicate that PGRN may be a novel
biologic agent with therapeutic potential for endotoxic shock probably by
inhibiting LPS-induced systemic and local inflammation in mice for treating
endotoxic shock.
|Animals
[MESH]
|Apoptosis/immunology
[MESH]
|Cytokines/blood
[MESH]
|Granulins
[MESH]
|Inflammation/metabolism
[MESH]
|Intercellular Signaling Peptides and Proteins/*genetics/metabolism
[MESH]