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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 Stem+Cells+Dev
2015 ; 24
(5
): 587-96
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Corticosterone mediates the inhibitory effect of restraint stress on the
migration of mesenchymal stem cell to carbon tetrachloride-induced fibrotic liver
by downregulating CXCR4/7 expression
#MMPMID25268050
Zhang S
; Lv C
; Yang X
; Han Z
; Zhang S
; Zhang J
; Zong C
; Gao L
; Li L
; Zhao Q
; Li R
; Yang Y
; Yu F
; Li X
; Zhang P
; Wei L
Stem Cells Dev
2015[Mar]; 24
(5
): 587-96
PMID25268050
show ga
Recent studies have revealed that mesenchymal stem cells (MSCs) have a great
potential in therapeutic applications. The low efficiency of MSC recruitment and
homing to sites of diseased organ tissue, however, remains a major hurdle in
their application for treatment of diseases. Stress is commonly associated with
various diseases. At the present time, little information is available about the
effect of stress on MSC function. Here, we employed a carbon tetrachloride
(CCl4)-induced mouse liver fibrosis model to investigate whether constraint
stress affects the migration of MSCs to fibrotic liver. MSC homing to the
fibrotic liver was significantly inhibited in mice with restraint stress.
Restraint stress induced an elevation of corticosterone level in the serum.
Blocking glucocorticoid signaling with either corticosterone-synthesis inhibitor
metyrapone (MET) or glucocorticoid receptor antagonist RU486 attenuated restraint
stress-induced inhibition of MSCs migration. The serum concentration of stromal
cell-derived factor-1 (SDF-1) increased in mice treated with CCl4. Restraint
stress had no influence on expression of SDF-1 and hepatocyte growth factor (HGF)
in the fibrotic liver. Culture with the serum of CCl4-treated mice or SDF-1
promoted MSC migration, which was suppressed by corticosterone. Exposure of MSCs
to corticosterone decreased their expression of C-X-C chemokine receptor type 4
(CXCR4) and C-X-C chemokine receptor type 7 (CXCR7). These results demonstrate
that the inhibitory effect of corticosterone on MSC migration might be mediated
via decreasing the expression of CXCR4 and CXCR7 in MSCs. Interventions targeting
the interaction between corticosterone and its receptor improve migration and
homing of MSCs in hosts receiving transplantation of these cells.