Effect of Fetal Membrane-Derived Mesenchymal Stem Cell Transplantation in Rats With Acute and Chronic Pancreatitis

Kawakubo, Kazumichi; Ohnishi, Shunsuke; Fujita, Hideomi; Kuwatani, Masaki; Onishi, Reizo; Masamune, Atsushi; Takeda, Hiroshi; Sakamoto, Naoya

doi:10.1097/mpa.0000000000000541

Cited by 28 publications

(28 citation statements)

References 42 publications

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“…Zhou et al reported that umbilical cord-derived MSCs reduce pancreatic fibrosis in a dibutyltin dichloride-induced rat model of CP by suppressing inflammatory cytokines in the pancreas [38]. We have demonstrated that human amnionderived MSCs decrease monocyte chemotactic protein-1 (MCP-1) expression in the pancreas [33]. Pancreatic stellate cells are responsible for fibrosis in CP.…”

Section: Msc Therapy For Chronic Pancreatitismentioning

confidence: 88%

“…Another study also showed that MSCs reduce damage to the small intestinal capillary endothelial barrier by increasing AQP-1 expression in the small intestine [31]. Another mechanism of MSCs for suppressing inflammation in AP is the anti-apoptosis effect [32,33]. MSCs promote repair and angiogenesis via the stromal cell derived factor (SDF)-1a/C-X-C chemokine receptor type 4 (CXCR4) axis [34].…”

Section: Mesenchymal Stem Cellsmentioning

confidence: 99%

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Mesenchymal stem cell therapy for acute and chronic pancreatitis

et al. 2017

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Mesenchymal stem cells (MSCs) have attracted attention as a cell source for regenerative medicine. In particular, MSCs have an anti-inflammatory effect by secreting several kinds of bioactive molecules. MSC therapy is now being applied to various gastrointestinal diseases, such as graft-versus-host disease, inflammatory bowel disease, and liver cirrhosis. Therefore, MSC therapy has the potential to be a novel treatment for acute and chronic pancreatitis by suppressing inflammation. Several studies have investigated the effect of MSC therapy on acute and chronic pancreatitis, but the underlying mechanisms remain unknown. In this review, we summarize the present status of MSC therapy for acute and chronic pancreatitis.

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Section: Msc Therapy For Chronic Pancreatitismentioning

confidence: 88%

Section: Mesenchymal Stem Cellsmentioning

confidence: 99%

Mesenchymal stem cell therapy for acute and chronic pancreatitis

et al. 2017

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“…HAMSCs had an increased proliferative capacity, higher colony-forming efficiency, fewer apoptotic cells, and similar cell-junction formation capabilities and pump functionality compared with primary HCECs ( 21 , 22 ). Amniotic membrane can restrict dedifferentiation of human retinal pigment epithelial cells (RPE cells) in culture, promoting RPE65, CRALBP, VEGF, CD68, and tyrosinase gene expression in RPE cells ( 23 ). Experiments have demonstrated the ability of HAMSCs to migrate into brain, prevents the degeneration of nigral dopmineneurons in rats with 6-hydroxydopami-ne lesions ( 24 ).…”

Section: Discussionmentioning

confidence: 99%

Human amnion-derived mesenchymal stem cells protect against UVA irradiation-induced human dermal fibroblast senescence, in vitro

Zhang

Yuchi

Sun

et al. 2017

Molecular Medicine Reports

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Abstract. The aim of the present study was to determine if human amnion-derived mesenchymal stem cells (HAMSCs) exert a protective effect on ultraviolet A (UVA) irradiation-induced human dermal fibroblast (HDF) senescence. A senescence model was constructed as follows: HDFs (10 4 -10 6 cells/well) were cultured in a six-well plate in vitro and then exposed to UVA irradiation at 9 J/cm 2 for 30 min. Following the irradiation period, HDFs were co-cultured with HAMSCs, which were seeded on transwells. A total of 72 h following the co-culturing, senescence-associated β-galactosidase staining was performed and reactive oxygen species (ROS) content and mitochondrial membrane potential (Δψm) were detected in the HDFs via flow cytometric analysis. The results demonstrated that the percentage of HDFs, detected via staining with X-gal, were markedly decreased when co-cultured with human HAMSCs, compared with the group that were not co-cultured. The ROS content was decreased and the mitochondrial membrane potential (Δψm) recovered in cells treated with UVA and HAMSCs, compared with that of cells treated with UVA alone. Reverse transcription-quantitative polymerase chain reaction revealed the significant effects of HAMSCs on the HDF senescence marker genes p53 and matrix metalloproteinase-1 mRNA expression. In addition to this, western blot analysis verified the effects of HAMSCs on UVA induced senescence, providing a foundation for novel regenerative therapeutic methods. Furthermore, the results suggested that activation of the extracellular-signal regulated kinase 1/2 mitogen activated protein kinase signal transduction pathway, is essential for the HAMSC-mediated UVA protective effects. The decrease in ROS content additionally indicated that HAMSCs may exhibit the potential to treat oxidative stress-mediated UVA skin senescence in the future.

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“…Although human fetal membrane is usually discarded as medical waste after delivery, fetal tissues have been found to be rich sources of mesenchymal stem cells. [19,20] We have demonstrated that systemic administration of fetal membrane-or amnion-derived mesenchymal stem cells (AMSCs) improved rats with hindlimb ischemia, [21] myocarditis, [22,23] glomerulonephritis, [24] ischemia/reperfusion-induced acute kidney injury, [25] severe colitis, [26] radiation proctitis, [27] pancreatitis, [28] and liver fibrosis, [29] possibly through secretory factors from transplanted AMSCs.…”

Section: Introductionmentioning

confidence: 99%