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R&D Systems igf 2

PTN regulates endometrial stromal cell decidualization through <t>the</t> <t>IGF-2</t> signaling axis. (A) PPI network of PTN, IGF-2, IGFBP1, LIF, PRL, and other decidualization-related genes. (B) The expression levels of PTN and its interacting partners (IGF-2, WNT4, PRL, IGFBP1, and LIF) in the RIF (left) and RPL (right) datasets. (C) Expressions of decidualization-related genes (including IGFBP1 , LIF , PRL , and WNT4 ) in NC or si PTN hESCs after treatment with control vehicle, cAMP, and IGF-2 via RT-qPCR (n = 9). (D) Immunoblotting for PTN, IGFBP1, and PRL expression levels with control vehicle, cAMP, and IGF-2. (E) ELISA for IGF-2 levels with control vehicle, cAMP, and IGF-2. (F) Schematic diagram of the experiments performed using the different treatments of hESCs. Data are presented as mean ± SEM and analyzed using t-test or one-way ANOVA test. * compared with NC treated with control vehicle, # compared with si PTN treated with control vehicle, $ compared with si PTN treated with control cAMP (NS, no significant difference; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ####p < 0.0001, $p < 0.05, $$p < 0.01, $$$p < 0.001, $$$$p< 0.0001). PPI, protein–protein interaction; RIF, recurrent implantation failure; RPL, recurrent pregnancy loss; hESCs, human endometrial stromal cells; cAMP, cyclic adenosine monophosphate.

Igf 2, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 48 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 48 article reviews

igf 2 - by Bioz Stars, 2026-05

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1) Product Images from "PTN/IGF-2 signaling modulates endometrial decidualization and immune cell trafficking to facilitate pregnancy maintenance"

Article Title: PTN/IGF-2 signaling modulates endometrial decidualization and immune cell trafficking to facilitate pregnancy maintenance

Journal: Frontiers in Immunology

doi: 10.3389/fimmu.2026.1790942

PTN regulates endometrial stromal cell decidualization through the IGF-2 signaling axis. (A) PPI network of PTN, IGF-2, IGFBP1, LIF, PRL, and other decidualization-related genes. (B) The expression levels of PTN and its interacting partners (IGF-2, WNT4, PRL, IGFBP1, and LIF) in the RIF (left) and RPL (right) datasets. (C) Expressions of decidualization-related genes (including IGFBP1 , LIF , PRL , and WNT4 ) in NC or si PTN hESCs after treatment with control vehicle, cAMP, and IGF-2 via RT-qPCR (n = 9). (D) Immunoblotting for PTN, IGFBP1, and PRL expression levels with control vehicle, cAMP, and IGF-2. (E) ELISA for IGF-2 levels with control vehicle, cAMP, and IGF-2. (F) Schematic diagram of the experiments performed using the different treatments of hESCs. Data are presented as mean ± SEM and analyzed using t-test or one-way ANOVA test. * compared with NC treated with control vehicle, # compared with si PTN treated with control vehicle, $ compared with si PTN treated with control cAMP (NS, no significant difference; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ####p < 0.0001, $p < 0.05, $$p < 0.01, $$$p < 0.001, $$$$p< 0.0001). PPI, protein–protein interaction; RIF, recurrent implantation failure; RPL, recurrent pregnancy loss; hESCs, human endometrial stromal cells; cAMP, cyclic adenosine monophosphate.

Figure Legend Snippet: PTN regulates endometrial stromal cell decidualization through the IGF-2 signaling axis. (A) PPI network of PTN, IGF-2, IGFBP1, LIF, PRL, and other decidualization-related genes. (B) The expression levels of PTN and its interacting partners (IGF-2, WNT4, PRL, IGFBP1, and LIF) in the RIF (left) and RPL (right) datasets. (C) Expressions of decidualization-related genes (including IGFBP1 , LIF , PRL , and WNT4 ) in NC or si PTN hESCs after treatment with control vehicle, cAMP, and IGF-2 via RT-qPCR (n = 9). (D) Immunoblotting for PTN, IGFBP1, and PRL expression levels with control vehicle, cAMP, and IGF-2. (E) ELISA for IGF-2 levels with control vehicle, cAMP, and IGF-2. (F) Schematic diagram of the experiments performed using the different treatments of hESCs. Data are presented as mean ± SEM and analyzed using t-test or one-way ANOVA test. * compared with NC treated with control vehicle, # compared with si PTN treated with control vehicle, $ compared with si PTN treated with control cAMP (NS, no significant difference; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ####p < 0.0001, $p < 0.05, $$p < 0.01, $$$p < 0.001, $$$$p< 0.0001). PPI, protein–protein interaction; RIF, recurrent implantation failure; RPL, recurrent pregnancy loss; hESCs, human endometrial stromal cells; cAMP, cyclic adenosine monophosphate.

Techniques Used: Expressing, Control, Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay

IGF-2 promotes decidualization and rescues decidualization defects caused by PTN deficiency. (A) Schematic diagram of the experiments performed using the different treatments of ESCs isolated from endometrium of RIF and RPL patients. (B, C) RT-qPCR analysis of levels of decidualization-related genes in ESCs isolated from endometrium of RIF (B) and RPL (C) patients after IGF-2 (50 ng/mL) treatment for 48 h (n = 9). (D) The flowchart depicts the steps involved in establishing a mouse model of intrauterine perfusion with siRNA-mediated knockdown of PTN and then supplemented with IGF-2 (50 ng/mL) through tail vein injection. (E) Expression of PTN after Ptn knockdown and supplemented with control vehicle or IGF-2 (50 ng/mL) in the mouse endometrium, measured by immunofluorescence, and quantitative analysis of immunofluorescence was performed (n = 6). (F) RT-qPCR analysis of levels of decidualization-related genes after Ptn knockdown and supplemented with control vehicle or IGF-2 (50 ng/mL) in the mouse endometrium (n = 6). Data are presented as mean ± SEM and analyzed using t-test or one-way ANOVA test. * compared with NC treated with control vehicle, # compared with si PTN treated with control vehicle (NS, no significant difference; *p < 0.05, **p < 0.01, ***p < 0.001, ****p< 0.0001, ## p < 0.01, ### p < 0.001, #### p < 0.0001). ESCs, endometrial stromal cells; PPI, protein–protein interaction; RIF, recurrent implantation failure.

Figure Legend Snippet: IGF-2 promotes decidualization and rescues decidualization defects caused by PTN deficiency. (A) Schematic diagram of the experiments performed using the different treatments of ESCs isolated from endometrium of RIF and RPL patients. (B, C) RT-qPCR analysis of levels of decidualization-related genes in ESCs isolated from endometrium of RIF (B) and RPL (C) patients after IGF-2 (50 ng/mL) treatment for 48 h (n = 9). (D) The flowchart depicts the steps involved in establishing a mouse model of intrauterine perfusion with siRNA-mediated knockdown of PTN and then supplemented with IGF-2 (50 ng/mL) through tail vein injection. (E) Expression of PTN after Ptn knockdown and supplemented with control vehicle or IGF-2 (50 ng/mL) in the mouse endometrium, measured by immunofluorescence, and quantitative analysis of immunofluorescence was performed (n = 6). (F) RT-qPCR analysis of levels of decidualization-related genes after Ptn knockdown and supplemented with control vehicle or IGF-2 (50 ng/mL) in the mouse endometrium (n = 6). Data are presented as mean ± SEM and analyzed using t-test or one-way ANOVA test. * compared with NC treated with control vehicle, # compared with si PTN treated with control vehicle (NS, no significant difference; *p < 0.05, **p < 0.01, ***p < 0.001, ****p< 0.0001, ## p < 0.01, ### p < 0.001, #### p < 0.0001). ESCs, endometrial stromal cells; PPI, protein–protein interaction; RIF, recurrent implantation failure.

Techniques Used: Isolation, Quantitative RT-PCR, Knockdown, Injection, Expressing, Control, Immunofluorescence

PTN deficiency induces endometrial immune imbalance and leads to adverse pregnancy outcomes, which can be partially reversed by IGF-2. (A) PPI network of PTN, IGF-2, CXCR4, CD4, CD8, CD56, and other immunoregulators. (B, C) Flow cytometry analysis (B) and statistical quantification (C) of cell populations of NK cells and T cells, and the expression levels of CD16, CXCR4, and GZMB in NK cell form the endometrial tissues of NC and si PTN mice treated with control vehicle or IGF-2 (50 ng/mL) (n = 6). (D) The flowchart depicts the steps involved in establishing a mouse model of intrauterine perfusion with siRNA-mediated knockdown of Ptn and then supplemented with IGF-2 (50 ng/mL) through tail vein injection for 2 days; then, these female mice were mated with fertile male mice; analysis of fertility, including pregnancy rate, IF, and fluorescence-activated cell sorting (FACS). were performed at gestational day 13.5. (E) Representative images of uteri from pregnant mice in the NC and si PTN mice treated with control vehicle or IGF-2 (50 ng/mL) at gestational day 13.5 (n = 6) (arrow shows the absorption site). (F) Pregnancy rate (%) in NC and si PTN mice treated with control vehicle or IGF-2 (50 ng/mL) (n = 15). (G) Quantification of embryo numbers (left) and absorption rate (right) per mouse in NC (n = 13) and si PTN mice treated with control vehicle (n = 6) or IGF-2 (50 ng/mL) (n = 11) at gestational day 13.5. Data are presented as mean ± SEM and analyzed using one-way ANOVA test or χ 2 test. * Compared with NC treated with control vehicle, # compared with si PTN treated with control vehicle (NS, no significant difference; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ## p < 0.01, ### p < 0.001, #### p < 0.0001). IF, immunofluorescence.

Figure Legend Snippet: PTN deficiency induces endometrial immune imbalance and leads to adverse pregnancy outcomes, which can be partially reversed by IGF-2. (A) PPI network of PTN, IGF-2, CXCR4, CD4, CD8, CD56, and other immunoregulators. (B, C) Flow cytometry analysis (B) and statistical quantification (C) of cell populations of NK cells and T cells, and the expression levels of CD16, CXCR4, and GZMB in NK cell form the endometrial tissues of NC and si PTN mice treated with control vehicle or IGF-2 (50 ng/mL) (n = 6). (D) The flowchart depicts the steps involved in establishing a mouse model of intrauterine perfusion with siRNA-mediated knockdown of Ptn and then supplemented with IGF-2 (50 ng/mL) through tail vein injection for 2 days; then, these female mice were mated with fertile male mice; analysis of fertility, including pregnancy rate, IF, and fluorescence-activated cell sorting (FACS). were performed at gestational day 13.5. (E) Representative images of uteri from pregnant mice in the NC and si PTN mice treated with control vehicle or IGF-2 (50 ng/mL) at gestational day 13.5 (n = 6) (arrow shows the absorption site). (F) Pregnancy rate (%) in NC and si PTN mice treated with control vehicle or IGF-2 (50 ng/mL) (n = 15). (G) Quantification of embryo numbers (left) and absorption rate (right) per mouse in NC (n = 13) and si PTN mice treated with control vehicle (n = 6) or IGF-2 (50 ng/mL) (n = 11) at gestational day 13.5. Data are presented as mean ± SEM and analyzed using one-way ANOVA test or χ 2 test. * Compared with NC treated with control vehicle, # compared with si PTN treated with control vehicle (NS, no significant difference; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ## p < 0.01, ### p < 0.001, #### p < 0.0001). IF, immunofluorescence.

Techniques Used: Flow Cytometry, Expressing, Control, Knockdown, Injection, Fluorescence, FACS, Immunofluorescence

Image Search Results

Lung cancer cells induced CAFs activation via IGF2 secretion (A) mRNA levels of IGF2 in cells were detected by qPCR. (B) IGF2 concentrations in cell culture medium were detected by ELISA. (C) NFs were treated with IGF2 (50 and 100 ng/mL) for 24 h. Cell morphology was observed under a microscope. (D) NFs were treated with IGF2. α-SMA and FAP expressions were detected by western blotting. (E) NFs were treated with IGF2. Cell proliferation was examined by CCK-8 kit after 48 h. (F and G) NFs were treated with IGF2. NFs migration was detected by trans-well assay after 24 h. (H) NFs were treated with CM or CM + IGF2 neutralizing antibody. Cell morphology was observed under a microscope. (I) NFs were treated with CM or CM + IGF2 neutralizing antibody. α-SMA and FAP expressions were detected by western blotting. (J) NFs were treated with CM or CM + IGF2 neutralizing antibody, and IGF2 (100 ng/mL). Cell proliferation was examined by CCK-8 kit after 48 h. (K and L) NFs were treated with CM or CM + IGF2 neutralizing antibody. NFs migration was detected by trans-well assay after 24 h. (M) The effect of IGF2 knockdown by RNAi. (N) IGF2 expression was knocked down in lung cancer cells, and then the CM was collected and used to culture NFs. α-SMA and FAP expressions were detected by western blotting. (O and P) IGF2 expression was knocked down in lung cancer cells by RNAi, and then the CM was collected and used to culture NFs. NFs migration was detected by trans-well assay after 24 h. Ab, neutralizing antibody. Scale bar, 100 μm. Data represents the mean ± SD from three independent experiments. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 .

Journal: iScience

Article Title: Reprogramming of fibroblasts into cancer-associated fibroblasts via IGF2-mediated autophagy promotes metastasis of lung cancer cells

doi: 10.1016/j.isci.2024.111269

Figure Lengend Snippet: Lung cancer cells induced CAFs activation via IGF2 secretion (A) mRNA levels of IGF2 in cells were detected by qPCR. (B) IGF2 concentrations in cell culture medium were detected by ELISA. (C) NFs were treated with IGF2 (50 and 100 ng/mL) for 24 h. Cell morphology was observed under a microscope. (D) NFs were treated with IGF2. α-SMA and FAP expressions were detected by western blotting. (E) NFs were treated with IGF2. Cell proliferation was examined by CCK-8 kit after 48 h. (F and G) NFs were treated with IGF2. NFs migration was detected by trans-well assay after 24 h. (H) NFs were treated with CM or CM + IGF2 neutralizing antibody. Cell morphology was observed under a microscope. (I) NFs were treated with CM or CM + IGF2 neutralizing antibody. α-SMA and FAP expressions were detected by western blotting. (J) NFs were treated with CM or CM + IGF2 neutralizing antibody, and IGF2 (100 ng/mL). Cell proliferation was examined by CCK-8 kit after 48 h. (K and L) NFs were treated with CM or CM + IGF2 neutralizing antibody. NFs migration was detected by trans-well assay after 24 h. (M) The effect of IGF2 knockdown by RNAi. (N) IGF2 expression was knocked down in lung cancer cells, and then the CM was collected and used to culture NFs. α-SMA and FAP expressions were detected by western blotting. (O and P) IGF2 expression was knocked down in lung cancer cells by RNAi, and then the CM was collected and used to culture NFs. NFs migration was detected by trans-well assay after 24 h. Ab, neutralizing antibody. Scale bar, 100 μm. Data represents the mean ± SD from three independent experiments. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 .

Article Snippet: Recombinant human IGF2 , Sino Biological , Cat#13032-HNAY.

Techniques: Activation Assay, Cell Culture, Enzyme-linked Immunosorbent Assay, Microscopy, Western Blot, CCK-8 Assay, Migration, Knockdown, Expressing

IGF2-induced autophagy mediated the effect of lung cancer cells on CAFs activation (A) NFs were treated with CM and then were stained with 0.5 μg/mL AO for 15 min. The acidic vesicular organelles (AVOs) formation was observed under a fluorescence microscope (scale bar, 20 μm). (B) NFs were treated with CM. The expression of LC-3II and ATG5 were detected by western blotting. (C) NFs were treated with IGF2 (50 or 100 mg/mL) for 24 h. The AVOs formation was examined by AO staining (scale bar, 20 μm). (D) NFs were treated with IGF2. The expression of LC-3II and ATG5 was detected by western blotting. (E) NFs were treated with IGF2 or IGF2 + 3-MA (5 mM). The AVOs formation was examined by AO staining (scale bar, 20 μm). (F) NFs were treated with IGF2 or IGF2 + 3-MA. Protein expressions were detected by western blotting. (G) NFs were treated with IGF2 or IGF2 + 3-MA. Cell proliferation was examined by CCK-8 kit after 48 h. (H and I) NFs were treated with IGF2 or IGF2+3-MA. NFs migration was detected by trans-well assay after 24 h (scale bar, 100 μm). (J) NFs were treated with IGF2, CM, CM + IGF2 Ab, and CM + 3-MA. The AVOs formation was examined by AO staining (scale bar, 20 μm). (K) NFs were treated with CM, IGF2, and CM + IGF2 Ab. Protein expressions were detected by western blotting. (L) NFs were treated with IGF2, CM, CM + IGF2 Ab, and CM + 3-MA. Cell proliferation was examined by CCK-8 kit after 48 h. (M and N) NFs were treated with IGF2, CM, CM + IGF2 Ab, and CM + 3-MA. NFs migration was detected by trans-well assay after 24 h (scale bar, 100 μm). (O and P) NFs were treated with RAPA (100 nM); α-SMA and FAP expressions were detected by western blotting (scale bar, 20 μm). (Q and R) NFs were treated with RAPA; NFs migration was detected by trans-well assay after 24 h. Ab, neutralizing antibody (scale bar, 100 μm). Data represents the mean ± SD from three independent experiments. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 .

Journal: iScience

Article Title: Reprogramming of fibroblasts into cancer-associated fibroblasts via IGF2-mediated autophagy promotes metastasis of lung cancer cells

doi: 10.1016/j.isci.2024.111269

Figure Lengend Snippet: IGF2-induced autophagy mediated the effect of lung cancer cells on CAFs activation (A) NFs were treated with CM and then were stained with 0.5 μg/mL AO for 15 min. The acidic vesicular organelles (AVOs) formation was observed under a fluorescence microscope (scale bar, 20 μm). (B) NFs were treated with CM. The expression of LC-3II and ATG5 were detected by western blotting. (C) NFs were treated with IGF2 (50 or 100 mg/mL) for 24 h. The AVOs formation was examined by AO staining (scale bar, 20 μm). (D) NFs were treated with IGF2. The expression of LC-3II and ATG5 was detected by western blotting. (E) NFs were treated with IGF2 or IGF2 + 3-MA (5 mM). The AVOs formation was examined by AO staining (scale bar, 20 μm). (F) NFs were treated with IGF2 or IGF2 + 3-MA. Protein expressions were detected by western blotting. (G) NFs were treated with IGF2 or IGF2 + 3-MA. Cell proliferation was examined by CCK-8 kit after 48 h. (H and I) NFs were treated with IGF2 or IGF2+3-MA. NFs migration was detected by trans-well assay after 24 h (scale bar, 100 μm). (J) NFs were treated with IGF2, CM, CM + IGF2 Ab, and CM + 3-MA. The AVOs formation was examined by AO staining (scale bar, 20 μm). (K) NFs were treated with CM, IGF2, and CM + IGF2 Ab. Protein expressions were detected by western blotting. (L) NFs were treated with IGF2, CM, CM + IGF2 Ab, and CM + 3-MA. Cell proliferation was examined by CCK-8 kit after 48 h. (M and N) NFs were treated with IGF2, CM, CM + IGF2 Ab, and CM + 3-MA. NFs migration was detected by trans-well assay after 24 h (scale bar, 100 μm). (O and P) NFs were treated with RAPA (100 nM); α-SMA and FAP expressions were detected by western blotting (scale bar, 20 μm). (Q and R) NFs were treated with RAPA; NFs migration was detected by trans-well assay after 24 h. Ab, neutralizing antibody (scale bar, 100 μm). Data represents the mean ± SD from three independent experiments. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 .

Article Snippet: Recombinant human IGF2 , Sino Biological , Cat#13032-HNAY.

Techniques: Activation Assay, Staining, Fluorescence, Microscopy, Expressing, Western Blot, CCK-8 Assay, Migration

Journal: iScience

Article Title: Reprogramming of fibroblasts into cancer-associated fibroblasts via IGF2-mediated autophagy promotes metastasis of lung cancer cells

doi: 10.1016/j.isci.2024.111269

Figure Lengend Snippet:

Article Snippet: Recombinant human IGF2 , Sino Biological , Cat#13032-HNAY.

Techniques: Recombinant, Enzyme-linked Immunosorbent Assay

Journal: iScience

Article Title: Reprogramming of fibroblasts into cancer-associated fibroblasts via IGF2-mediated autophagy promotes metastasis of lung cancer cells

doi: 10.1016/j.isci.2024.111269

Figure Lengend Snippet: PCR primer sequences

Article Snippet: Recombinant human IGF2 , Sino Biological , Cat#13032-HNAY.

Techniques:

Journal: Frontiers in Immunology

Article Title: PTN/IGF-2 signaling modulates endometrial decidualization and immune cell trafficking to facilitate pregnancy maintenance

doi: 10.3389/fimmu.2026.1790942

Figure Lengend Snippet: PTN regulates endometrial stromal cell decidualization through the IGF-2 signaling axis. (A) PPI network of PTN, IGF-2, IGFBP1, LIF, PRL, and other decidualization-related genes. (B) The expression levels of PTN and its interacting partners (IGF-2, WNT4, PRL, IGFBP1, and LIF) in the RIF (left) and RPL (right) datasets. (C) Expressions of decidualization-related genes (including IGFBP1 , LIF , PRL , and WNT4 ) in NC or si PTN hESCs after treatment with control vehicle, cAMP, and IGF-2 via RT-qPCR (n = 9). (D) Immunoblotting for PTN, IGFBP1, and PRL expression levels with control vehicle, cAMP, and IGF-2. (E) ELISA for IGF-2 levels with control vehicle, cAMP, and IGF-2. (F) Schematic diagram of the experiments performed using the different treatments of hESCs. Data are presented as mean ± SEM and analyzed using t-test or one-way ANOVA test. * compared with NC treated with control vehicle, # compared with si PTN treated with control vehicle, $ compared with si PTN treated with control cAMP (NS, no significant difference; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ####p < 0.0001, $p < 0.05, $$p < 0.01, $$$p < 0.001, $$$$p< 0.0001). PPI, protein–protein interaction; RIF, recurrent implantation failure; RPL, recurrent pregnancy loss; hESCs, human endometrial stromal cells; cAMP, cyclic adenosine monophosphate.

Article Snippet: The remaining cells were digested with trypsin and inoculated into a new culture dish, and they were treated with control vehicle or IGF-2 (50 ng/mL, R&D Systems, Minneapolis, MN, USA, 292-G2) for 48 h and then collected for quantitative real-time polymerase chain reaction (qRT-PCR).

Techniques: Expressing, Control, Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay

Journal: Frontiers in Immunology

Article Title: PTN/IGF-2 signaling modulates endometrial decidualization and immune cell trafficking to facilitate pregnancy maintenance

doi: 10.3389/fimmu.2026.1790942

Figure Lengend Snippet: IGF-2 promotes decidualization and rescues decidualization defects caused by PTN deficiency. (A) Schematic diagram of the experiments performed using the different treatments of ESCs isolated from endometrium of RIF and RPL patients. (B, C) RT-qPCR analysis of levels of decidualization-related genes in ESCs isolated from endometrium of RIF (B) and RPL (C) patients after IGF-2 (50 ng/mL) treatment for 48 h (n = 9). (D) The flowchart depicts the steps involved in establishing a mouse model of intrauterine perfusion with siRNA-mediated knockdown of PTN and then supplemented with IGF-2 (50 ng/mL) through tail vein injection. (E) Expression of PTN after Ptn knockdown and supplemented with control vehicle or IGF-2 (50 ng/mL) in the mouse endometrium, measured by immunofluorescence, and quantitative analysis of immunofluorescence was performed (n = 6). (F) RT-qPCR analysis of levels of decidualization-related genes after Ptn knockdown and supplemented with control vehicle or IGF-2 (50 ng/mL) in the mouse endometrium (n = 6). Data are presented as mean ± SEM and analyzed using t-test or one-way ANOVA test. * compared with NC treated with control vehicle, # compared with si PTN treated with control vehicle (NS, no significant difference; *p < 0.05, **p < 0.01, ***p < 0.001, ****p< 0.0001, ## p < 0.01, ### p < 0.001, #### p < 0.0001). ESCs, endometrial stromal cells; PPI, protein–protein interaction; RIF, recurrent implantation failure.

Techniques: Isolation, Quantitative RT-PCR, Knockdown, Injection, Expressing, Control, Immunofluorescence

Journal: Frontiers in Immunology

Article Title: PTN/IGF-2 signaling modulates endometrial decidualization and immune cell trafficking to facilitate pregnancy maintenance

doi: 10.3389/fimmu.2026.1790942

Figure Lengend Snippet: PTN deficiency induces endometrial immune imbalance and leads to adverse pregnancy outcomes, which can be partially reversed by IGF-2. (A) PPI network of PTN, IGF-2, CXCR4, CD4, CD8, CD56, and other immunoregulators. (B, C) Flow cytometry analysis (B) and statistical quantification (C) of cell populations of NK cells and T cells, and the expression levels of CD16, CXCR4, and GZMB in NK cell form the endometrial tissues of NC and si PTN mice treated with control vehicle or IGF-2 (50 ng/mL) (n = 6). (D) The flowchart depicts the steps involved in establishing a mouse model of intrauterine perfusion with siRNA-mediated knockdown of Ptn and then supplemented with IGF-2 (50 ng/mL) through tail vein injection for 2 days; then, these female mice were mated with fertile male mice; analysis of fertility, including pregnancy rate, IF, and fluorescence-activated cell sorting (FACS). were performed at gestational day 13.5. (E) Representative images of uteri from pregnant mice in the NC and si PTN mice treated with control vehicle or IGF-2 (50 ng/mL) at gestational day 13.5 (n = 6) (arrow shows the absorption site). (F) Pregnancy rate (%) in NC and si PTN mice treated with control vehicle or IGF-2 (50 ng/mL) (n = 15). (G) Quantification of embryo numbers (left) and absorption rate (right) per mouse in NC (n = 13) and si PTN mice treated with control vehicle (n = 6) or IGF-2 (50 ng/mL) (n = 11) at gestational day 13.5. Data are presented as mean ± SEM and analyzed using one-way ANOVA test or χ 2 test. * Compared with NC treated with control vehicle, # compared with si PTN treated with control vehicle (NS, no significant difference; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ## p < 0.01, ### p < 0.001, #### p < 0.0001). IF, immunofluorescence.

Techniques: Flow Cytometry, Expressing, Control, Knockdown, Injection, Fluorescence, FACS, Immunofluorescence

Expression of miR-125b-5p and insulin-like growth factor 2 in vitro and in vivo . A: Quantitative real-time polymerase chain reaction (RT-qPCR) was used to detect the expression of miR-125b-5p in AR42J cell lines in activated and inactive state; B: RT-qPCR was used to detect the expression of insulin-like growth factor 2 (IGF2) in AR42J cell lines under activated and inactive state; C: Western blot was used to detect the expression level of IGF2, and β-actin was used as the internal reference; D: RT-qPCR was used to detect the expression of miR-125b-5p in normal pancreatic tissues and pancreatitis tissues; E: RT-qPCR was used to detect the expression of IGF2 in normal pancreatic tissues and pancreatitis tissues; F: The mRNA and protein expression of miR-125b-5p and IGF2 in 4 cases of pancreatitis tissues were detected by RT-qPCR and Western blot. Among them, sample 2 was used as the standard to calculate the fold change of miR-125b-5p expression in other samples by comparing the miR-125b-5p/U6 ratio in sample 2. Western blot was used to detect the expression level of IGF2, and β-actin was used as the internal reference. The experiment was repeated three times and is expressed as mean ± SD; G: miR-125b-5p was negatively correlated with IGF2 protein expression level, a P < 0.05, b P < 0.005. AP: Acute pancreatitis; IGF2: Insulin-like growth factor 2; N: Normal.

Journal: World Journal of Gastrointestinal Surgery

Article Title: Acinous cell AR42J-derived exosome miR125b-5p promotes acute pancreatitis exacerbation by inhibiting M2 macrophage polarization via PI3K/AKT signaling pathway

doi: 10.4240/wjgs.v15.i4.600

Figure Lengend Snippet: Expression of miR-125b-5p and insulin-like growth factor 2 in vitro and in vivo . A: Quantitative real-time polymerase chain reaction (RT-qPCR) was used to detect the expression of miR-125b-5p in AR42J cell lines in activated and inactive state; B: RT-qPCR was used to detect the expression of insulin-like growth factor 2 (IGF2) in AR42J cell lines under activated and inactive state; C: Western blot was used to detect the expression level of IGF2, and β-actin was used as the internal reference; D: RT-qPCR was used to detect the expression of miR-125b-5p in normal pancreatic tissues and pancreatitis tissues; E: RT-qPCR was used to detect the expression of IGF2 in normal pancreatic tissues and pancreatitis tissues; F: The mRNA and protein expression of miR-125b-5p and IGF2 in 4 cases of pancreatitis tissues were detected by RT-qPCR and Western blot. Among them, sample 2 was used as the standard to calculate the fold change of miR-125b-5p expression in other samples by comparing the miR-125b-5p/U6 ratio in sample 2. Western blot was used to detect the expression level of IGF2, and β-actin was used as the internal reference. The experiment was repeated three times and is expressed as mean ± SD; G: miR-125b-5p was negatively correlated with IGF2 protein expression level, a P < 0.05, b P < 0.005. AP: Acute pancreatitis; IGF2: Insulin-like growth factor 2; N: Normal.

Article Snippet: After adding primary antibodies against CD9 (Abcam, Cambridge, United Kingdom), CD81 (Abcam, Cambridge, United Kingdom), CD63 (Abcam, Cambridge, United Kingdom), TSG101 (Protein Tech Group, IL, United States), CD206 (Protein Tech Group, IL, United States), inducible nitric oxide synthase (iNOS) (Abcam, Cambridge, United Kingdom), insulin-like growth factor 2 (IGF2) (Protein Tech Group, IL, United States), Bax (Protein Tech Group, IL, United States), Bcl-2 (Protein Tech Group, IL, United States), HMGB1 (Protein Tech Group, IL, United States), PI3K (Protein Tech Group, IL, United States), p-PI3K (Protein Tech Group, IL, United States), AKT (Protein Tech Group, IL, United States), p-AKT (Protein Tech Group, IL, United States), β-tubulin (Protein Tech Group, IL, United States), β-actin (Protein Tech Group, IL, United States), and GAPDH (Abcam, ab8245, 1:1000), the membrane was incubated at 4 °C overnight.

Techniques: Expressing, In Vitro, In Vivo, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Western Blot

miR-125b-5p overexpression could promote necrosis and apoptosis of AR42J cells in the activated state. A: miR-125b-5p overexpression promoted the necrosis of AR42J cells in the activated state; B: Flow cytometry analysis confirmed that the percentage of cells in G0/G1 phase increased in AR42J cells in the activated state treated with the miR-125b-5p overexpression group; C: The percentage of apoptotic cells increased as confirmed by flow cytometry; D and E: The expression of insulin-like growth factor 2, BAX, Bcl-2 and HMGB-1 was confirmed by Western blot, a P < 0.05, c P < 0.0005. AP: Acute pancreatitis; IGF2: Insulin-like growth factor 2; N: Normal; NC: Negative control.

Journal: World Journal of Gastrointestinal Surgery

Article Title: Acinous cell AR42J-derived exosome miR125b-5p promotes acute pancreatitis exacerbation by inhibiting M2 macrophage polarization via PI3K/AKT signaling pathway

doi: 10.4240/wjgs.v15.i4.600

Figure Lengend Snippet: miR-125b-5p overexpression could promote necrosis and apoptosis of AR42J cells in the activated state. A: miR-125b-5p overexpression promoted the necrosis of AR42J cells in the activated state; B: Flow cytometry analysis confirmed that the percentage of cells in G0/G1 phase increased in AR42J cells in the activated state treated with the miR-125b-5p overexpression group; C: The percentage of apoptotic cells increased as confirmed by flow cytometry; D and E: The expression of insulin-like growth factor 2, BAX, Bcl-2 and HMGB-1 was confirmed by Western blot, a P < 0.05, c P < 0.0005. AP: Acute pancreatitis; IGF2: Insulin-like growth factor 2; N: Normal; NC: Negative control.

Techniques: Over Expression, Flow Cytometry, Expressing, Western Blot, Negative Control

miR-125b-5p promotes acute pancreatitis exacerbation by inhibiting insulin-like growth factor 2 protein expression in PI3K/AKT signaling pathway. A: The potential binding sites of miR-125b-5p in the 3¢-untranslated regions (UTR) of wild-type insulin-like growth factor 2 (IGF2) (red part). The blue section is the mutation site in mutant IGF2 3¢-UTR sequence; B: Luciferase activity in IGF2 3¢-UTR of wild-type and mutant was detected after transfection of miR-125b-5p mimics and negative control miRNAs. The normalized luciferase activity of the transfected control miRNA was set to a relative luciferase activity of 1; C: The protein expression of PI3K/AKT signaling pathway was confirmed by western blot. a P < 0.05, b P < 0.005. AP: Acute pancreatitis; IGF2: Insulin-like growth factor 2; N: Normal; NC: Negative control; WT: Wild-type; MUT: Mutant; UTR: Untranslated regions; CDS: Coding sequence.

Journal: World Journal of Gastrointestinal Surgery

Article Title: Acinous cell AR42J-derived exosome miR125b-5p promotes acute pancreatitis exacerbation by inhibiting M2 macrophage polarization via PI3K/AKT signaling pathway

doi: 10.4240/wjgs.v15.i4.600

Figure Lengend Snippet: miR-125b-5p promotes acute pancreatitis exacerbation by inhibiting insulin-like growth factor 2 protein expression in PI3K/AKT signaling pathway. A: The potential binding sites of miR-125b-5p in the 3¢-untranslated regions (UTR) of wild-type insulin-like growth factor 2 (IGF2) (red part). The blue section is the mutation site in mutant IGF2 3¢-UTR sequence; B: Luciferase activity in IGF2 3¢-UTR of wild-type and mutant was detected after transfection of miR-125b-5p mimics and negative control miRNAs. The normalized luciferase activity of the transfected control miRNA was set to a relative luciferase activity of 1; C: The protein expression of PI3K/AKT signaling pathway was confirmed by western blot. a P < 0.05, b P < 0.005. AP: Acute pancreatitis; IGF2: Insulin-like growth factor 2; N: Normal; NC: Negative control; WT: Wild-type; MUT: Mutant; UTR: Untranslated regions; CDS: Coding sequence.

Techniques: Expressing, Binding Assay, Mutagenesis, Sequencing, Luciferase, Activity Assay, Transfection, Negative Control, Control, Western Blot

miR125b-5p promotes the aggravation of inflammation in vivo . A: Intraperitoneal condition of rats in acute pancreatitis (AP) group and overexpression group; B: Ascites volume of rats in the three groups. The expression of miR-125b-5p in pancreatic tissues of sham group, AP group and overexpression group was detected by quantitative real-time polymerase chain reaction; C: The level of interleukin-6, tumor necrosis factor-alpha, C-reactive protein and reactive oxygen species was determined by enzyme linked immunosorbent assay; D: Histopathological image of rat pancreas in three groups; E: Pancreatic histopathology score and dry/wet ratio; F: Western blot showing the expression of BAX, Bcl-2, HMGB-1 and insulin-like growth factor 2 in the pancreatic tissues; G: Western blot showing the expression of p-PI3K, PI3K, p-AKT and AKT in the pancreatic tissues, a P < 0.05, b P < 0.005, c P < 0.0005. IGF2: Insulin-like growth factor 2; TNF-α: Tumor necrosis factor-alpha; AP: Acute pancreatitis; IL: Interleukin; TNF-α: Tumor necrosis factor-alpha; CRP: C-reactive protein; ROS: Reactive oxygen species; NC: Negative control.

Journal: World Journal of Gastrointestinal Surgery

Article Title: Acinous cell AR42J-derived exosome miR125b-5p promotes acute pancreatitis exacerbation by inhibiting M2 macrophage polarization via PI3K/AKT signaling pathway

doi: 10.4240/wjgs.v15.i4.600

Figure Lengend Snippet: miR125b-5p promotes the aggravation of inflammation in vivo . A: Intraperitoneal condition of rats in acute pancreatitis (AP) group and overexpression group; B: Ascites volume of rats in the three groups. The expression of miR-125b-5p in pancreatic tissues of sham group, AP group and overexpression group was detected by quantitative real-time polymerase chain reaction; C: The level of interleukin-6, tumor necrosis factor-alpha, C-reactive protein and reactive oxygen species was determined by enzyme linked immunosorbent assay; D: Histopathological image of rat pancreas in three groups; E: Pancreatic histopathology score and dry/wet ratio; F: Western blot showing the expression of BAX, Bcl-2, HMGB-1 and insulin-like growth factor 2 in the pancreatic tissues; G: Western blot showing the expression of p-PI3K, PI3K, p-AKT and AKT in the pancreatic tissues, a P < 0.05, b P < 0.005, c P < 0.0005. IGF2: Insulin-like growth factor 2; TNF-α: Tumor necrosis factor-alpha; AP: Acute pancreatitis; IL: Interleukin; TNF-α: Tumor necrosis factor-alpha; CRP: C-reactive protein; ROS: Reactive oxygen species; NC: Negative control.

Techniques: In Vivo, Over Expression, Expressing, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, Histopathology, Western Blot, Negative Control

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