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Proteintech primary antibodies against gdf15
Primary Antibodies Against Gdf15, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 61 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/primary+antibodies+against+gdf15/GDF15+Antibody/pm39147013-54-67-94
Average 94 stars, based on 61 article reviews

primary antibodies against gdf15 - by Bioz Stars, 2026-09

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Article Title: GDF15 attenuates sepsis-induced myocardial dysfunction by inhibiting cardiomyocytes ferroptosis via the SOCS1/GPX4 signaling pathway.
Article Snippet: This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record.. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article.. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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GDF15 expression in DCs. (A) A time course of GDF15 expression in DCs. DCs (10 6 cell/well) were cultured from bone marrow progenitors in the presence of IL-4 and granulocyte/macrophage colony stimulating factor (GM-CSF). Cultured DCs were collected on day 2, 4, 6, and 8 for RNA extraction. The level of GDF15 mRNA was detected by qRT-PCR and GAPDH was used as loading control. Relative quantity of GDF15 mRNA was the expression of GDF15 in Day 2 DCs. n = 4, One way ANOVA was conducted for statistical analysis. (B) rhGDF15 increased GDF15 expression in DCs. BM-derived DCs were cultured and a variety of concentrations of rhGDF15 were added on day 4. Twenty-four hours after treatment, GDF15 expression in DCs was detected using qRT-PCR. GDF15 expression was normalized with control DCs without rhGDF15 treatment. n = 4, One way ANOVA was conducted for statistical analysis. (C) The up-regulation of GDF15 in DCs by rhGDF15 was time related. BM-derived DCs were treated with 2.5 ng/ml rhGDF15 on day 5. n = 3, the student T -test was conducted for statistical analysis. GDF15 expression in DCs was detected 4 h and 12 h after addition of rhGDF15 by qRT-PCR. The expression of GDF15 in DCs treated for 4 h was used as a normalizer. (D) GDF15 protein expressed in DCs. Total protein was extracted from day 2 and 6 in vitro cultured DCs. GDF15 expression at the protein levels was determined by western blotting using GDF15 Abs. β-Actin was used as a loading control. Images were representatives of n = 3, * P < 0.05.

Journal: Frontiers in Immunology

Article Title: GDF15 Regulates Malat-1 Circular RNA and Inactivates NFκB Signaling Leading to Immune Tolerogenic DCs for Preventing Alloimmune Rejection in Heart Transplantation

doi: 10.3389/fimmu.2018.02407

Figure Lengend Snippet: GDF15 expression in DCs. (A) A time course of GDF15 expression in DCs. DCs (10 6 cell/well) were cultured from bone marrow progenitors in the presence of IL-4 and granulocyte/macrophage colony stimulating factor (GM-CSF). Cultured DCs were collected on day 2, 4, 6, and 8 for RNA extraction. The level of GDF15 mRNA was detected by qRT-PCR and GAPDH was used as loading control. Relative quantity of GDF15 mRNA was the expression of GDF15 in Day 2 DCs. n = 4, One way ANOVA was conducted for statistical analysis. (B) rhGDF15 increased GDF15 expression in DCs. BM-derived DCs were cultured and a variety of concentrations of rhGDF15 were added on day 4. Twenty-four hours after treatment, GDF15 expression in DCs was detected using qRT-PCR. GDF15 expression was normalized with control DCs without rhGDF15 treatment. n = 4, One way ANOVA was conducted for statistical analysis. (C) The up-regulation of GDF15 in DCs by rhGDF15 was time related. BM-derived DCs were treated with 2.5 ng/ml rhGDF15 on day 5. n = 3, the student T -test was conducted for statistical analysis. GDF15 expression in DCs was detected 4 h and 12 h after addition of rhGDF15 by qRT-PCR. The expression of GDF15 in DCs treated for 4 h was used as a normalizer. (D) GDF15 protein expressed in DCs. Total protein was extracted from day 2 and 6 in vitro cultured DCs. GDF15 expression at the protein levels was determined by western blotting using GDF15 Abs. β-Actin was used as a loading control. Images were representatives of n = 3, * P < 0.05.

Article Snippet: Transferred membranes were blocked with 5% fat-free milk powder in TBST for 30 min at room temperature and then blotted with the primary antibodies against mouse or human GDF15,TGFβ RI, and TGFβ RII (1:1,000 dilution, Sigma), phosphorylated Rel A p65, (1:1,000 dilution, Cell Signaling Technology, Danvers, MA), total Rel A p65 (1:1,000 dilution, Cell Signaling Technology), and β-actin (1:4,000 dilution, Santa Cruz Biotechnologies, San Diego, CA) at 4°C for overnight.

Techniques: Expressing, Cell Culture, RNA Extraction, Quantitative RT-PCR, Derivative Assay, In Vitro, Western Blot

Knockout of GDF15 promoted DC maturation. (A) GDF15 KO DCs promoted DC maturation. BM-derived DCs were cultured from GDF15 KO and WT mice. On day 6, DCs were stimulated with 50 ng/ml LPS for 3 h. DC maturation was detected by measuring the expression of MHCII, CD40, CD83, and CD86 using flow cytometry. Images were representatives of n = 4. (B) GDF15 silenced GDF15 expression in DCs. Day 5 DCs cultured from WT mice were transfected with GDF15 siRNA for 24 h. GDF15 expression was determined by qRT-PCR (left) and Western blotting (right). n = 3, the student T -test was conducted for statistical analysis of qRT-PCR results. (C) GDF15 siRNA increased the expression of CD83 and CD86 in DCs. DCs were transfected with GDF15 siRNA. 24 h after transfection, CD83 and CD86 expression was detected by flow cytometry. Data were representatives of n = 3. (D) GDF15-Ad increased GDF15 expression in DCs. Day 4 DCs were infected with 100MOI of adenovirus expressing human GDF15 qRT-PCR (left, n = 3) and Western blotting (right). Data were representatives of n = 3. (E) GDF15-Ad decreased CD40 expression in DCs measured by flow cytometry. n = 3, the student T -test was conducted for statistical analysis. * P < 0.05.

Journal: Frontiers in Immunology

Article Title: GDF15 Regulates Malat-1 Circular RNA and Inactivates NFκB Signaling Leading to Immune Tolerogenic DCs for Preventing Alloimmune Rejection in Heart Transplantation

doi: 10.3389/fimmu.2018.02407

Figure Lengend Snippet: Knockout of GDF15 promoted DC maturation. (A) GDF15 KO DCs promoted DC maturation. BM-derived DCs were cultured from GDF15 KO and WT mice. On day 6, DCs were stimulated with 50 ng/ml LPS for 3 h. DC maturation was detected by measuring the expression of MHCII, CD40, CD83, and CD86 using flow cytometry. Images were representatives of n = 4. (B) GDF15 silenced GDF15 expression in DCs. Day 5 DCs cultured from WT mice were transfected with GDF15 siRNA for 24 h. GDF15 expression was determined by qRT-PCR (left) and Western blotting (right). n = 3, the student T -test was conducted for statistical analysis of qRT-PCR results. (C) GDF15 siRNA increased the expression of CD83 and CD86 in DCs. DCs were transfected with GDF15 siRNA. 24 h after transfection, CD83 and CD86 expression was detected by flow cytometry. Data were representatives of n = 3. (D) GDF15-Ad increased GDF15 expression in DCs. Day 4 DCs were infected with 100MOI of adenovirus expressing human GDF15 qRT-PCR (left, n = 3) and Western blotting (right). Data were representatives of n = 3. (E) GDF15-Ad decreased CD40 expression in DCs measured by flow cytometry. n = 3, the student T -test was conducted for statistical analysis. * P < 0.05.

Techniques: Knock-Out, Derivative Assay, Cell Culture, Expressing, Flow Cytometry, Transfection, Quantitative RT-PCR, Western Blot, Infection

GDF15 impaired DC's capacity to activate T cells. (A) GDF15 KO DCs increased T cell proliferation. BM-derived DCs were cultured from WT or GDF15 KO mice. On day 6, an MLR was performed in which different cultured DCs were used as stimulators and allogeneic (BALB/c) CFSE-labeled T cells were used as responders. Proliferation was measured by CFSE dilution. Data were representatives of n = 3. (B) GDF15-Ad DCs inhibited T cell proliferation. BM-derived DCs were infected with GDF15-Ad on day 2 and an MLR was conducted to measure T cell proliferation . Data were representatives of n = 4. (C) GDF15 decreased the expression of proinflammatory genes. RNA was extracted from DCs treated with GDF15–Ad or Null-Ad. Expression of IL2 and IL-12 was detected by qRT-PCR and IFNγ in the culture medium was detected by ELISA. n = 3, the student T -test was conducted for statistical analysis. (D) GDF15 increased immunosuppressive cytokines IL10 and TGF-β. The expression of TGF-β and IL10 in the cells was detected by qRT-PCR and expression of IL10 in culture medium was detected by ELISA. n = 3, the student T -test was conducted for statistical analysis. * p < 0.05.

Journal: Frontiers in Immunology

Article Title: GDF15 Regulates Malat-1 Circular RNA and Inactivates NFκB Signaling Leading to Immune Tolerogenic DCs for Preventing Alloimmune Rejection in Heart Transplantation

doi: 10.3389/fimmu.2018.02407

Figure Lengend Snippet: GDF15 impaired DC's capacity to activate T cells. (A) GDF15 KO DCs increased T cell proliferation. BM-derived DCs were cultured from WT or GDF15 KO mice. On day 6, an MLR was performed in which different cultured DCs were used as stimulators and allogeneic (BALB/c) CFSE-labeled T cells were used as responders. Proliferation was measured by CFSE dilution. Data were representatives of n = 3. (B) GDF15-Ad DCs inhibited T cell proliferation. BM-derived DCs were infected with GDF15-Ad on day 2 and an MLR was conducted to measure T cell proliferation . Data were representatives of n = 4. (C) GDF15 decreased the expression of proinflammatory genes. RNA was extracted from DCs treated with GDF15–Ad or Null-Ad. Expression of IL2 and IL-12 was detected by qRT-PCR and IFNγ in the culture medium was detected by ELISA. n = 3, the student T -test was conducted for statistical analysis. (D) GDF15 increased immunosuppressive cytokines IL10 and TGF-β. The expression of TGF-β and IL10 in the cells was detected by qRT-PCR and expression of IL10 in culture medium was detected by ELISA. n = 3, the student T -test was conducted for statistical analysis. * p < 0.05.

Techniques: Derivative Assay, Cell Culture, Labeling, Infection, Expressing, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay

GDF15 enhanced DCs ability to generate Tregs. (A) The effect of GDF15 on Tregs. DCs were cultured from WT mice and treated with rhGDF15 or GDF15 siRNA, or control GL2 siRNA. rhGDF15 treated DCs and GDF15 silenced DCs or untreated DCs or GL2 siRNA transfected DCs were co-cultured with allogeneic naïve T cells from BABL/c mice at the ratio of 1:10 for 5 days. CD4 + CD25 + FoxP3 + cells were detected by flow cytometry. Representative images (upper) and summarized data (lower) from n = 5 experiments. The student t -test was conducted to compare data between rhGDF15 treated DCs and untreated DCs and between GDF15 siRNA and GL2 siRNA. * P < 0.05. (B) GDF15 increased the expression of IDO 1 and IDO2. DCs were cultured and treated with rhGDF15, GDF15 expression adenovirus (GDF15-Ad), or control null adenovirus (Null-Ad). Expression of IDO 1 and IDO2 in DCs was detected s by qRT-PCR, n = 3, the student t -test was conducted to compare data between rhGDF15 treated DCs and untreated DCs and between GDF15-Ad and Null-Ad. * P < 0.05. (C) Deficiency of IDO in DCs eliminated the effect of GDF15 on Treg generation. DCs were cultured from IDO KO mice and treated with rhGDF15 or GDF15 siRNA, then subjected to co-cultured with allogeneic T cells for 5 days. CD4 + CD25 + FoxP3 + cells were detected by flow cytometry. * P < 0.05. (D) GDF15 up-regulated immune inhibitory ligands. DCs were cultured and treated with GDF15-Ad or Null- Adenovirus. Expression of GDF15, Galectin 9, PD-L1 and TIM-3 was detected by qRT-PCR. Control adenovirus infected DCs were used as a normalizer. n = 3, the student t -test was conducted to compare data between Null-Ad and GDF15-Ad.* P < 0.05.

Journal: Frontiers in Immunology

Article Title: GDF15 Regulates Malat-1 Circular RNA and Inactivates NFκB Signaling Leading to Immune Tolerogenic DCs for Preventing Alloimmune Rejection in Heart Transplantation

doi: 10.3389/fimmu.2018.02407

Figure Lengend Snippet: GDF15 enhanced DCs ability to generate Tregs. (A) The effect of GDF15 on Tregs. DCs were cultured from WT mice and treated with rhGDF15 or GDF15 siRNA, or control GL2 siRNA. rhGDF15 treated DCs and GDF15 silenced DCs or untreated DCs or GL2 siRNA transfected DCs were co-cultured with allogeneic naïve T cells from BABL/c mice at the ratio of 1:10 for 5 days. CD4 + CD25 + FoxP3 + cells were detected by flow cytometry. Representative images (upper) and summarized data (lower) from n = 5 experiments. The student t -test was conducted to compare data between rhGDF15 treated DCs and untreated DCs and between GDF15 siRNA and GL2 siRNA. * P < 0.05. (B) GDF15 increased the expression of IDO 1 and IDO2. DCs were cultured and treated with rhGDF15, GDF15 expression adenovirus (GDF15-Ad), or control null adenovirus (Null-Ad). Expression of IDO 1 and IDO2 in DCs was detected s by qRT-PCR, n = 3, the student t -test was conducted to compare data between rhGDF15 treated DCs and untreated DCs and between GDF15-Ad and Null-Ad. * P < 0.05. (C) Deficiency of IDO in DCs eliminated the effect of GDF15 on Treg generation. DCs were cultured from IDO KO mice and treated with rhGDF15 or GDF15 siRNA, then subjected to co-cultured with allogeneic T cells for 5 days. CD4 + CD25 + FoxP3 + cells were detected by flow cytometry. * P < 0.05. (D) GDF15 up-regulated immune inhibitory ligands. DCs were cultured and treated with GDF15-Ad or Null- Adenovirus. Expression of GDF15, Galectin 9, PD-L1 and TIM-3 was detected by qRT-PCR. Control adenovirus infected DCs were used as a normalizer. n = 3, the student t -test was conducted to compare data between Null-Ad and GDF15-Ad.* P < 0.05.

Techniques: Cell Culture, Transfection, Flow Cytometry, Expressing, Quantitative RT-PCR, Infection

GDF15 reduced circ_Malat-1 expression and inhibited the NFκB pathway. (A) circ_Malat-1 expression in DCs. BM derived DCs were cultured from WT mice and treated with 50 ng/ml CD40 L or 10 ng/ML LPS for 24 h.Untreated DCs were used as control. RNA was extracted and circ_Malat-1 expression was detected by RT-PCR. Left: regular PCR, representative images for n = 3; Right: qPCR, n = 3, One way ANOVA was conducted for statistical analysis * P < 0.05. (B) GDF15 negatively regulated circ_Malat-1 expression. The expression of circ_Malat 1 was detected in GDF15 KO DCs, WT DCs or GDF15-Ad or control Null-Ad treated DCs by qRT-PCR. n = 3, One way ANOVA was conducted for statistical analysis * P < 0.05. (C) Representative DNA sequence from DNA sequencing of RT-PCR products. circ_Malat-1 was amplified using divergent primers and the PCR products was then subjected to DNA sequencing using forward primer of circ_Malat-1. Arrow: pointing to the junction of circ_Malat-1. The sequencing containing the circ_Malat-1 conjunction sequence gcatatcg gttt caaggt ctcc ccacaa was presented. The central conjunction sequence was underlined. (D) The expression of Rel A and Rel B by qRT-PCR. DCs were treated with GDF5-Ad, or Null-Ad. The expression of Rel A and Rel B were measured by qRT-PCR 48 h after infection. One way ANOVA was conducted for statistical analysis n = 3 * P < 0.05. (E) . GDF15 inhibited the NFkB signaling pathway . Phosphorylated p65 and total p-65 protein was detected by western blotting using phosphorylated p65A Abs and p65 Abs. Representative of image of western blotting (upper) and relative quantity of protein (low) from n = 4 experiments. Samples treated with LPS and samples without LPS treatment were loaded separately by other samples for PAGE.

Journal: Frontiers in Immunology

Article Title: GDF15 Regulates Malat-1 Circular RNA and Inactivates NFκB Signaling Leading to Immune Tolerogenic DCs for Preventing Alloimmune Rejection in Heart Transplantation

doi: 10.3389/fimmu.2018.02407

Figure Lengend Snippet: GDF15 reduced circ_Malat-1 expression and inhibited the NFκB pathway. (A) circ_Malat-1 expression in DCs. BM derived DCs were cultured from WT mice and treated with 50 ng/ml CD40 L or 10 ng/ML LPS for 24 h.Untreated DCs were used as control. RNA was extracted and circ_Malat-1 expression was detected by RT-PCR. Left: regular PCR, representative images for n = 3; Right: qPCR, n = 3, One way ANOVA was conducted for statistical analysis * P < 0.05. (B) GDF15 negatively regulated circ_Malat-1 expression. The expression of circ_Malat 1 was detected in GDF15 KO DCs, WT DCs or GDF15-Ad or control Null-Ad treated DCs by qRT-PCR. n = 3, One way ANOVA was conducted for statistical analysis * P < 0.05. (C) Representative DNA sequence from DNA sequencing of RT-PCR products. circ_Malat-1 was amplified using divergent primers and the PCR products was then subjected to DNA sequencing using forward primer of circ_Malat-1. Arrow: pointing to the junction of circ_Malat-1. The sequencing containing the circ_Malat-1 conjunction sequence gcatatcg gttt caaggt ctcc ccacaa was presented. The central conjunction sequence was underlined. (D) The expression of Rel A and Rel B by qRT-PCR. DCs were treated with GDF5-Ad, or Null-Ad. The expression of Rel A and Rel B were measured by qRT-PCR 48 h after infection. One way ANOVA was conducted for statistical analysis n = 3 * P < 0.05. (E) . GDF15 inhibited the NFkB signaling pathway . Phosphorylated p65 and total p-65 protein was detected by western blotting using phosphorylated p65A Abs and p65 Abs. Representative of image of western blotting (upper) and relative quantity of protein (low) from n = 4 experiments. Samples treated with LPS and samples without LPS treatment were loaded separately by other samples for PAGE.

Techniques: Expressing, Derivative Assay, Cell Culture, Reverse Transcription Polymerase Chain Reaction, Quantitative RT-PCR, Sequencing, DNA Sequencing, Amplification, Infection, Western Blot

GDF15 regulated DCs by using TGFβ receptors. (A) Expression of GFRAL and TGF-β RI and RII. RNA was extracted from DCs and the expression of GFRAL and TGF-β RI and RII was detected by RT-PCR. PCR products were run on 1.5% agarose gel and visualized with EB. (B) TGF-β receptor I and II reversed the inhibitory function of GDF15 in DC maturation. DCs cultured from WT mice and treated with rhGDF15 on day 4. Ly210976 (5 mg/ml) and Ly 364947 (10 mg/ml) was added to rhgDF15 treated DCs on day 5, respectively. 24 h later, DCs maturation was determined by measuring expression of MHCII, CD40, CD80, CD83, CD86, and CCR7 flow cytometry. Data were representatives of three independent experiments. (C) IP assays. Total protein was extracted from the above DCs treated with GDF15-Ad or control Adenovirus and an IP assay was employed to pull down GDF15 bound protein using GDF15 Abs and control Ig Abs. IP protein was subjected to western blotting with TGFβ RI and RII Abs respectively. Representative of image of n = 4 experiments. PCR products for TGF-β RII from Splenocytes (SP) and two DC samples (DC1 and DC 2) were loaded separately by other genes products on an agarose gel and the image shown was modified by deletion of other genes' bands between TGF-β RII's bands.

Journal: Frontiers in Immunology

Article Title: GDF15 Regulates Malat-1 Circular RNA and Inactivates NFκB Signaling Leading to Immune Tolerogenic DCs for Preventing Alloimmune Rejection in Heart Transplantation

doi: 10.3389/fimmu.2018.02407

Figure Lengend Snippet: GDF15 regulated DCs by using TGFβ receptors. (A) Expression of GFRAL and TGF-β RI and RII. RNA was extracted from DCs and the expression of GFRAL and TGF-β RI and RII was detected by RT-PCR. PCR products were run on 1.5% agarose gel and visualized with EB. (B) TGF-β receptor I and II reversed the inhibitory function of GDF15 in DC maturation. DCs cultured from WT mice and treated with rhGDF15 on day 4. Ly210976 (5 mg/ml) and Ly 364947 (10 mg/ml) was added to rhgDF15 treated DCs on day 5, respectively. 24 h later, DCs maturation was determined by measuring expression of MHCII, CD40, CD80, CD83, CD86, and CCR7 flow cytometry. Data were representatives of three independent experiments. (C) IP assays. Total protein was extracted from the above DCs treated with GDF15-Ad or control Adenovirus and an IP assay was employed to pull down GDF15 bound protein using GDF15 Abs and control Ig Abs. IP protein was subjected to western blotting with TGFβ RI and RII Abs respectively. Representative of image of n = 4 experiments. PCR products for TGF-β RII from Splenocytes (SP) and two DC samples (DC1 and DC 2) were loaded separately by other genes products on an agarose gel and the image shown was modified by deletion of other genes' bands between TGF-β RII's bands.

Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Agarose Gel Electrophoresis, Cell Culture, Flow Cytometry, Western Blot, Modification

GDF15 regulated DCs prevent allograft rejection in heart transplantation and augment tolerance induction and T cell exhaustion. (A) Allograft survival. Donor derived (C57BL/6) DCs were cultured and treated with GDF15-Ad or Null-Ad on day 2. 1 million day 7 DCs were i.v. injected into recipient BABL/c mice 7 days prior to heart transplantation. Allogeneic heart transplantation was conducted between C57BL/6 and BABL/c mice. Recipient mice daily received 1 g/kg rapamycin for 7 days from day 0 post transplantation. The cessation of heartbeat was defined as rejection. n = 6. (B) CD4 + CD25 + Foxp3 + Tregs in splenic cells. At the end of experiments, mice splenic cells were isolated from recipient mice on day 100 to detect CD4 + CD25 + Foxp3 + Tregs by flow cytometry. Representative images (upper) and relative quantity of FoxP3 protein from n = 3 * P < 0.05. (C) Inhibitory receptor expression. RNA was extracted from the above rejected and tolerant recipient mice. Gene expression of inhibitory receptors PD-1, TIM3, BTLA and galectin 9 was detected by qRT-PCR. n = 3, the student t -test was conducted for statistical analysis * P < 0.05.

Journal: Frontiers in Immunology

Article Title: GDF15 Regulates Malat-1 Circular RNA and Inactivates NFκB Signaling Leading to Immune Tolerogenic DCs for Preventing Alloimmune Rejection in Heart Transplantation

doi: 10.3389/fimmu.2018.02407

Figure Lengend Snippet: GDF15 regulated DCs prevent allograft rejection in heart transplantation and augment tolerance induction and T cell exhaustion. (A) Allograft survival. Donor derived (C57BL/6) DCs were cultured and treated with GDF15-Ad or Null-Ad on day 2. 1 million day 7 DCs were i.v. injected into recipient BABL/c mice 7 days prior to heart transplantation. Allogeneic heart transplantation was conducted between C57BL/6 and BABL/c mice. Recipient mice daily received 1 g/kg rapamycin for 7 days from day 0 post transplantation. The cessation of heartbeat was defined as rejection. n = 6. (B) CD4 + CD25 + Foxp3 + Tregs in splenic cells. At the end of experiments, mice splenic cells were isolated from recipient mice on day 100 to detect CD4 + CD25 + Foxp3 + Tregs by flow cytometry. Representative images (upper) and relative quantity of FoxP3 protein from n = 3 * P < 0.05. (C) Inhibitory receptor expression. RNA was extracted from the above rejected and tolerant recipient mice. Gene expression of inhibitory receptors PD-1, TIM3, BTLA and galectin 9 was detected by qRT-PCR. n = 3, the student t -test was conducted for statistical analysis * P < 0.05.

Techniques: Transplantation Assay, Derivative Assay, Cell Culture, Injection, Isolation, Flow Cytometry, Expressing, Quantitative RT-PCR

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