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Amniotic fluid stem cells provide considerable advantages in epidermal regeneration: B7H4 creates a moderate inflammation microenvironment to promote wound repair.

Sun Q, Li F, Li H, Chen RH, Gu YZ, Chen Y, Liang HS, You XR, Ding SS, Gao L, Wang YL, Qin MD, Zhang XG - Sci Rep (2015)

Bottom Line: Co-localization of GFP/K14 and GFP/K10 in the repaired epidermis demonstrated that hAFS cells can differentiate into keratinocytes.During wound repair, hAFS cells did not directly secrete repair-related factors, such as bFGF, VEGF, CXCL12, TGF-β1 and KGF, and provided a moderate inflammation reaction with lower expression of IL-1β, IL-6, TNF-α, Cox2 and Mac3.Furthermore, with their uniquely high proliferation rate, hAFS cells offer a promising alternative for epidermal regeneration.

View Article: PubMed Central - PubMed

Affiliation: 1] The Stem Cell and Biomedical Material Key Laboratory of Jiangsu Province (the State Key Laboratory Incubation Base), Soochow University, Suzhou, Jiangsu Province, P.R. China [2] Department of Immunology, School of Biology and Basic Medical Sciences, Soochow University, Suzhou, Jiangsu Province, P.R. China.

ABSTRACT
The current treatments for severe skin injury all involve skin grafting. However, there is a worldwide shortage of donor skin tissue. In this study, we examined the advantages of using human amniotic fluid stem (hAFS) cells in skin wound healing. In vitro, hAFS cells differentiate into keratinocytes (termed hAFS-K). Like keratinocytes, hAFS-K cells express the markers K5, K14, K10 and involucrin; display typical cellular structure, including a tonofibril-rich cytoplasm; and construct a completely pluristratified epithelium in 3D culture. In vivo, in a mouse excisional wound model, GFP-positive hAFS cells participate in wound repair. Co-localization of GFP/K14 and GFP/K10 in the repaired epidermis demonstrated that hAFS cells can differentiate into keratinocytes. Real-time PCR results confirmed that hAFS cells can initiate and promote early-stage repair of skin damage. During wound repair, hAFS cells did not directly secrete repair-related factors, such as bFGF, VEGF, CXCL12, TGF-β1 and KGF, and provided a moderate inflammation reaction with lower expression of IL-1β, IL-6, TNF-α, Cox2 and Mac3. In hAFS cells, the negative co-stimulatory molecule B7H4 regulates low immunogenicity, which can provide a modest inflammatory reaction microenvironment for wound repair. Furthermore, with their uniquely high proliferation rate, hAFS cells offer a promising alternative for epidermal regeneration.

No MeSH data available.


Related in: MedlinePlus

hAFS cells indirectly promote wound healing in vivo(a) Real-time PCR analysis of mRNA expression of repair-related factors (bFGF, VEGF, TGF-β1, KGF, CXCL12, and CXCR4) at days 7, 14, 21 in hAFS cell-treated wounds, the fibroblast group and a sham control group. (b) Real-time PCR analysis of mRNA expression of inflammatory factors (TNF-α, Cox2, Mac3, IL-6, IL-1β) at days 1, 4, 7, 14 and 21 in hAFS cell-treated wounds in the fibroblast and sham control groups. Both mouse and human sequences were quantified in each case. There was no expression of human bFGF, VEGF, CXCL12, TGF-β1, KGF, TNF-α, Cox2, Mac3, IL-6, or IL-1β in either hAFS-, fibroblast- or sham-treated wounds. The data are presented as the mean ± SD of three independent experiments. Analysis was performed with GraphPad Prism; *p < 0.05.
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f5: hAFS cells indirectly promote wound healing in vivo(a) Real-time PCR analysis of mRNA expression of repair-related factors (bFGF, VEGF, TGF-β1, KGF, CXCL12, and CXCR4) at days 7, 14, 21 in hAFS cell-treated wounds, the fibroblast group and a sham control group. (b) Real-time PCR analysis of mRNA expression of inflammatory factors (TNF-α, Cox2, Mac3, IL-6, IL-1β) at days 1, 4, 7, 14 and 21 in hAFS cell-treated wounds in the fibroblast and sham control groups. Both mouse and human sequences were quantified in each case. There was no expression of human bFGF, VEGF, CXCL12, TGF-β1, KGF, TNF-α, Cox2, Mac3, IL-6, or IL-1β in either hAFS-, fibroblast- or sham-treated wounds. The data are presented as the mean ± SD of three independent experiments. Analysis was performed with GraphPad Prism; *p < 0.05.

Mentions: To explore the role of hAFS cells in skin repair, 11 mouse and human factors including repair-related and inflammatory factors were analysed with species-specific primers. There was no expression of human bFGF, VEGF, CXCL12, TGF-β1, KGF, TNF-α, Il-1β, Il-6, Cox2 or Mac3 in hAFS-treated, fibroblast groups or sham group wounds. As shown in Fig. 5a, the mRNA levels of mouse bFGF were highest in the hAFS cell group at day 7 and much higher than in the fibroblast and sham group but then reduced gradually through days 14 and 21. This pattern indicates that hAFS cells initiate the expression of bFGF at an early stage. In contrast, the expression of mouse bFGF in the fibroblast and sham groups reached a maximum at day 21 before the repair was complete. A similar pattern was observed for mouse VEGF, CXCL12, TGF-β1 and KGF at day 7 (Fig. 5a). Both mouse and human CXCR4 were detected, suggesting that both mouse and human AFS cells were involved in wound repair. During the course of wound healing, both mouse and human CXCR4 mRNA levels decreased, possibly because the stem cells leave the wound site after repair (Fig. 5a). Thus, these data suggest that, although no human bFGF, VEGF, KGF, TGF-β1 or CXCL12 were detected, hAFS cells were involved in the initiation of skin repair in the mouse model.


Amniotic fluid stem cells provide considerable advantages in epidermal regeneration: B7H4 creates a moderate inflammation microenvironment to promote wound repair.

Sun Q, Li F, Li H, Chen RH, Gu YZ, Chen Y, Liang HS, You XR, Ding SS, Gao L, Wang YL, Qin MD, Zhang XG - Sci Rep (2015)

hAFS cells indirectly promote wound healing in vivo(a) Real-time PCR analysis of mRNA expression of repair-related factors (bFGF, VEGF, TGF-β1, KGF, CXCL12, and CXCR4) at days 7, 14, 21 in hAFS cell-treated wounds, the fibroblast group and a sham control group. (b) Real-time PCR analysis of mRNA expression of inflammatory factors (TNF-α, Cox2, Mac3, IL-6, IL-1β) at days 1, 4, 7, 14 and 21 in hAFS cell-treated wounds in the fibroblast and sham control groups. Both mouse and human sequences were quantified in each case. There was no expression of human bFGF, VEGF, CXCL12, TGF-β1, KGF, TNF-α, Cox2, Mac3, IL-6, or IL-1β in either hAFS-, fibroblast- or sham-treated wounds. The data are presented as the mean ± SD of three independent experiments. Analysis was performed with GraphPad Prism; *p < 0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4477371&req=5

f5: hAFS cells indirectly promote wound healing in vivo(a) Real-time PCR analysis of mRNA expression of repair-related factors (bFGF, VEGF, TGF-β1, KGF, CXCL12, and CXCR4) at days 7, 14, 21 in hAFS cell-treated wounds, the fibroblast group and a sham control group. (b) Real-time PCR analysis of mRNA expression of inflammatory factors (TNF-α, Cox2, Mac3, IL-6, IL-1β) at days 1, 4, 7, 14 and 21 in hAFS cell-treated wounds in the fibroblast and sham control groups. Both mouse and human sequences were quantified in each case. There was no expression of human bFGF, VEGF, CXCL12, TGF-β1, KGF, TNF-α, Cox2, Mac3, IL-6, or IL-1β in either hAFS-, fibroblast- or sham-treated wounds. The data are presented as the mean ± SD of three independent experiments. Analysis was performed with GraphPad Prism; *p < 0.05.
Mentions: To explore the role of hAFS cells in skin repair, 11 mouse and human factors including repair-related and inflammatory factors were analysed with species-specific primers. There was no expression of human bFGF, VEGF, CXCL12, TGF-β1, KGF, TNF-α, Il-1β, Il-6, Cox2 or Mac3 in hAFS-treated, fibroblast groups or sham group wounds. As shown in Fig. 5a, the mRNA levels of mouse bFGF were highest in the hAFS cell group at day 7 and much higher than in the fibroblast and sham group but then reduced gradually through days 14 and 21. This pattern indicates that hAFS cells initiate the expression of bFGF at an early stage. In contrast, the expression of mouse bFGF in the fibroblast and sham groups reached a maximum at day 21 before the repair was complete. A similar pattern was observed for mouse VEGF, CXCL12, TGF-β1 and KGF at day 7 (Fig. 5a). Both mouse and human CXCR4 were detected, suggesting that both mouse and human AFS cells were involved in wound repair. During the course of wound healing, both mouse and human CXCR4 mRNA levels decreased, possibly because the stem cells leave the wound site after repair (Fig. 5a). Thus, these data suggest that, although no human bFGF, VEGF, KGF, TGF-β1 or CXCL12 were detected, hAFS cells were involved in the initiation of skin repair in the mouse model.

Bottom Line: Co-localization of GFP/K14 and GFP/K10 in the repaired epidermis demonstrated that hAFS cells can differentiate into keratinocytes.During wound repair, hAFS cells did not directly secrete repair-related factors, such as bFGF, VEGF, CXCL12, TGF-β1 and KGF, and provided a moderate inflammation reaction with lower expression of IL-1β, IL-6, TNF-α, Cox2 and Mac3.Furthermore, with their uniquely high proliferation rate, hAFS cells offer a promising alternative for epidermal regeneration.

View Article: PubMed Central - PubMed

Affiliation: 1] The Stem Cell and Biomedical Material Key Laboratory of Jiangsu Province (the State Key Laboratory Incubation Base), Soochow University, Suzhou, Jiangsu Province, P.R. China [2] Department of Immunology, School of Biology and Basic Medical Sciences, Soochow University, Suzhou, Jiangsu Province, P.R. China.

ABSTRACT
The current treatments for severe skin injury all involve skin grafting. However, there is a worldwide shortage of donor skin tissue. In this study, we examined the advantages of using human amniotic fluid stem (hAFS) cells in skin wound healing. In vitro, hAFS cells differentiate into keratinocytes (termed hAFS-K). Like keratinocytes, hAFS-K cells express the markers K5, K14, K10 and involucrin; display typical cellular structure, including a tonofibril-rich cytoplasm; and construct a completely pluristratified epithelium in 3D culture. In vivo, in a mouse excisional wound model, GFP-positive hAFS cells participate in wound repair. Co-localization of GFP/K14 and GFP/K10 in the repaired epidermis demonstrated that hAFS cells can differentiate into keratinocytes. Real-time PCR results confirmed that hAFS cells can initiate and promote early-stage repair of skin damage. During wound repair, hAFS cells did not directly secrete repair-related factors, such as bFGF, VEGF, CXCL12, TGF-β1 and KGF, and provided a moderate inflammation reaction with lower expression of IL-1β, IL-6, TNF-α, Cox2 and Mac3. In hAFS cells, the negative co-stimulatory molecule B7H4 regulates low immunogenicity, which can provide a modest inflammatory reaction microenvironment for wound repair. Furthermore, with their uniquely high proliferation rate, hAFS cells offer a promising alternative for epidermal regeneration.

No MeSH data available.


Related in: MedlinePlus