Mesenchymal stem cells improve mouse non-heart-beating liver graft survival by inhibiting Kupffer cell apoptosis via TLR4-ERK1/2-Fas/FasL-caspase3 pathway regulation View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-10-27

AUTHORS

Yang Tian, Jingcheng Wang, Wei Wang, Yuan Ding, Zhongquan Sun, Qiyi Zhang, Yan Wang, Haiyang Xie, Sheng Yan, Shusen Zheng

ABSTRACT

BackgroundLiver transplantation is the optimal treatment option for end-stage liver disease, but organ shortages dramatically restrict its application. Donation after cardiac death (DCD) is an alternative approach that may expand the donor pool, but it faces challenges such as graft dysfunction, early graft loss, and cholangiopathy. Moreover, DCD liver grafts are no longer eligible for transplantation after their warm ischaemic time exceeds 30 min. Mesenchymal stem cells (MSCs) have been proposed as a promising therapy for treatment of certain liver diseases, but the role of MSCs in DCD liver graft function remains elusive.MethodsIn this study, we established an arterialized mouse non-heart-beating (NHB) liver transplantation model, and compared survival rates, cytokine and chemokine expression, histology, and the results of in vitro co-culture experiments in animals with or without MSC infusion.ResultsMSCs markedly ameliorated NHB liver graft injury and improved survival post-transplantation. Additionally, MSCs suppressed Kupffer cell apoptosis, Th1/Th17 immune responses, chemokine expression, and inflammatory cell infiltration. In vitro, PGE2 secreted by MSCs inhibited Kupffer cell apoptosis via TLR4-ERK1/2-caspase3 pathway regulation.ConclusionOur study uncovers a protective role for MSCs and elucidates the underlying immunomodulatory mechanism in an NHB liver transplantation model. Our results suggest that MSCs are uniquely positioned for use in future clinical studies owing to their ability to protect DCD liver grafts, particularly in patients for whom DCD organs are not an option according to current criteria. More... »

PAGES

157

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/s13287-016-0416-y

DOI

http://dx.doi.org/10.1186/s13287-016-0416-y

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1025910060

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/27788674


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36 schema:description BackgroundLiver transplantation is the optimal treatment option for end-stage liver disease, but organ shortages dramatically restrict its application. Donation after cardiac death (DCD) is an alternative approach that may expand the donor pool, but it faces challenges such as graft dysfunction, early graft loss, and cholangiopathy. Moreover, DCD liver grafts are no longer eligible for transplantation after their warm ischaemic time exceeds 30 min. Mesenchymal stem cells (MSCs) have been proposed as a promising therapy for treatment of certain liver diseases, but the role of MSCs in DCD liver graft function remains elusive.MethodsIn this study, we established an arterialized mouse non-heart-beating (NHB) liver transplantation model, and compared survival rates, cytokine and chemokine expression, histology, and the results of in vitro co-culture experiments in animals with or without MSC infusion.ResultsMSCs markedly ameliorated NHB liver graft injury and improved survival post-transplantation. Additionally, MSCs suppressed Kupffer cell apoptosis, Th1/Th17 immune responses, chemokine expression, and inflammatory cell infiltration. In vitro, PGE2 secreted by MSCs inhibited Kupffer cell apoptosis via TLR4-ERK1/2-caspase3 pathway regulation.ConclusionOur study uncovers a protective role for MSCs and elucidates the underlying immunomodulatory mechanism in an NHB liver transplantation model. Our results suggest that MSCs are uniquely positioned for use in future clinical studies owing to their ability to protect DCD liver grafts, particularly in patients for whom DCD organs are not an option according to current criteria.
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42 schema:keywords BackgroundLiver transplantation
43 ConclusionOur study
44 DCD liver grafts
45 DCD organs
46 Kupffer cell apoptosis
47 MSC infusion
48 MethodsIn
49 PGE2
50 ResultsMSCs
51 Th1
52 ability
53 alternative approach
54 animals
55 apoptosis
56 applications
57 approach
58 cardiac death
59 cell apoptosis
60 cell infiltration
61 cells
62 certain liver diseases
63 challenges
64 chemokine expression
65 clinical studies
66 co-culture experiments
67 criteria
68 current criteria
69 cytokines
70 death
71 disease
72 donation
73 donor pool
74 dysfunction
75 early graft loss
76 end-stage liver disease
77 experiments
78 expression
79 function
80 future clinical studies
81 graft
82 graft dysfunction
83 graft function
84 graft injury
85 graft loss
86 graft survival
87 histology
88 immune response
89 immunomodulatory mechanisms
90 infiltration
91 inflammatory cell infiltration
92 infusion
93 injury
94 ischemic time
95 liver disease
96 liver graft function
97 liver graft injury
98 liver graft survival
99 liver grafts
100 liver transplantation model
101 loss
102 mechanism
103 mesenchymal stem cells
104 mice
105 min
106 model
107 optimal treatment options
108 options
109 organ shortage
110 organs
111 pathway regulation
112 patients
113 pool
114 promising therapy
115 protective role
116 rate
117 regulation
118 response
119 results
120 role
121 role of MSCs
122 shortage
123 stem cells
124 study
125 survival
126 survival rate
127 therapy
128 time
129 transplantation
130 transplantation model
131 treatment
132 treatment options
133 use
134 warm ischemic time
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