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Neuron-specific <t>Igfbp2</t> deficiency in the PFC induces cognitive dysfunction (A) Schematic of the experimental design. (B) Diagram of viral injection into the PFC (top) and representative image of viral expression (bottom); scale bars, 500 μm. (C) Representative western blot bands (top) and quantification of Igfbp2 protein levels in the PFC (bottom); n = 4 mice per group. (D) Schematic of the novel object recognition test, depicting the training phase (top) and the test phase (bottom). (E) Representative trajectory plots from the novel object recognition test. (F) Quantification of time spent investigating the novel object during the test phase; n = 8 mice per group. (G) Quantification of the number of investigations of the novel object during the test phase; n = 8 mice per group. (H) Schematic of the Y-maze test, depicting the training phase (top) and the test phase (bottom). (I) Representative trajectory plots from the Y-maze test. (J) Quantification of time spent in the novel arm during the test phase; n = 8 mice per group. (K) Quantification of the number of entries into the novel arm during the test phase; n = 8 mice per group. Analyzed by unpaired t test; ∗∗ p < 0.01. Data are presented as means ± SEM.
Recombinant Igfbp2 Protein, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Neuron-specific <t>Igfbp2</t> deficiency in the PFC induces cognitive dysfunction (A) Schematic of the experimental design. (B) Diagram of viral injection into the PFC (top) and representative image of viral expression (bottom); scale bars, 500 μm. (C) Representative western blot bands (top) and quantification of Igfbp2 protein levels in the PFC (bottom); n = 4 mice per group. (D) Schematic of the novel object recognition test, depicting the training phase (top) and the test phase (bottom). (E) Representative trajectory plots from the novel object recognition test. (F) Quantification of time spent investigating the novel object during the test phase; n = 8 mice per group. (G) Quantification of the number of investigations of the novel object during the test phase; n = 8 mice per group. (H) Schematic of the Y-maze test, depicting the training phase (top) and the test phase (bottom). (I) Representative trajectory plots from the Y-maze test. (J) Quantification of time spent in the novel arm during the test phase; n = 8 mice per group. (K) Quantification of the number of entries into the novel arm during the test phase; n = 8 mice per group. Analyzed by unpaired t test; ∗∗ p < 0.01. Data are presented as means ± SEM.
Anti Igfbp2, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Neuron-specific <t>Igfbp2</t> deficiency in the PFC induces cognitive dysfunction (A) Schematic of the experimental design. (B) Diagram of viral injection into the PFC (top) and representative image of viral expression (bottom); scale bars, 500 μm. (C) Representative western blot bands (top) and quantification of Igfbp2 protein levels in the PFC (bottom); n = 4 mice per group. (D) Schematic of the novel object recognition test, depicting the training phase (top) and the test phase (bottom). (E) Representative trajectory plots from the novel object recognition test. (F) Quantification of time spent investigating the novel object during the test phase; n = 8 mice per group. (G) Quantification of the number of investigations of the novel object during the test phase; n = 8 mice per group. (H) Schematic of the Y-maze test, depicting the training phase (top) and the test phase (bottom). (I) Representative trajectory plots from the Y-maze test. (J) Quantification of time spent in the novel arm during the test phase; n = 8 mice per group. (K) Quantification of the number of entries into the novel arm during the test phase; n = 8 mice per group. Analyzed by unpaired t test; ∗∗ p < 0.01. Data are presented as means ± SEM.
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Neuron-specific <t>Igfbp2</t> deficiency in the PFC induces cognitive dysfunction (A) Schematic of the experimental design. (B) Diagram of viral injection into the PFC (top) and representative image of viral expression (bottom); scale bars, 500 μm. (C) Representative western blot bands (top) and quantification of Igfbp2 protein levels in the PFC (bottom); n = 4 mice per group. (D) Schematic of the novel object recognition test, depicting the training phase (top) and the test phase (bottom). (E) Representative trajectory plots from the novel object recognition test. (F) Quantification of time spent investigating the novel object during the test phase; n = 8 mice per group. (G) Quantification of the number of investigations of the novel object during the test phase; n = 8 mice per group. (H) Schematic of the Y-maze test, depicting the training phase (top) and the test phase (bottom). (I) Representative trajectory plots from the Y-maze test. (J) Quantification of time spent in the novel arm during the test phase; n = 8 mice per group. (K) Quantification of the number of entries into the novel arm during the test phase; n = 8 mice per group. Analyzed by unpaired t test; ∗∗ p < 0.01. Data are presented as means ± SEM.
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Neuron-specific <t>Igfbp2</t> deficiency in the PFC induces cognitive dysfunction (A) Schematic of the experimental design. (B) Diagram of viral injection into the PFC (top) and representative image of viral expression (bottom); scale bars, 500 μm. (C) Representative western blot bands (top) and quantification of Igfbp2 protein levels in the PFC (bottom); n = 4 mice per group. (D) Schematic of the novel object recognition test, depicting the training phase (top) and the test phase (bottom). (E) Representative trajectory plots from the novel object recognition test. (F) Quantification of time spent investigating the novel object during the test phase; n = 8 mice per group. (G) Quantification of the number of investigations of the novel object during the test phase; n = 8 mice per group. (H) Schematic of the Y-maze test, depicting the training phase (top) and the test phase (bottom). (I) Representative trajectory plots from the Y-maze test. (J) Quantification of time spent in the novel arm during the test phase; n = 8 mice per group. (K) Quantification of the number of entries into the novel arm during the test phase; n = 8 mice per group. Analyzed by unpaired t test; ∗∗ p < 0.01. Data are presented as means ± SEM.
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Neuron-specific <t>Igfbp2</t> deficiency in the PFC induces cognitive dysfunction (A) Schematic of the experimental design. (B) Diagram of viral injection into the PFC (top) and representative image of viral expression (bottom); scale bars, 500 μm. (C) Representative western blot bands (top) and quantification of Igfbp2 protein levels in the PFC (bottom); n = 4 mice per group. (D) Schematic of the novel object recognition test, depicting the training phase (top) and the test phase (bottom). (E) Representative trajectory plots from the novel object recognition test. (F) Quantification of time spent investigating the novel object during the test phase; n = 8 mice per group. (G) Quantification of the number of investigations of the novel object during the test phase; n = 8 mice per group. (H) Schematic of the Y-maze test, depicting the training phase (top) and the test phase (bottom). (I) Representative trajectory plots from the Y-maze test. (J) Quantification of time spent in the novel arm during the test phase; n = 8 mice per group. (K) Quantification of the number of entries into the novel arm during the test phase; n = 8 mice per group. Analyzed by unpaired t test; ∗∗ p < 0.01. Data are presented as means ± SEM.
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Fetal testosterone supplementation rescues the adult kidney size by normalizing gene expression in the fetal kidney. (A) Anogenital distance of 3‐month‐old Hsd17b3 −/− (KO) and WT males without and with testosterone supplementation (res) at E14.5–17.5. The lines indicate means. * = p ≤ 0.05 ** = p ≤ 0.01. (B) kidney weights of 3‐month‐old Hsd17b3 −/− (KO) and WT males without and with testosterone supplementation (res) at E14.5–17.5. The lines indicate means. * = p ≤ 0.05 ** = p ≤ 0.01. (C) <t>Igfbp5</t> expression (RNA‐seq) in E16.5 kidneys of WT, Hsd17b3 −/− (KO) and treated KO (res) groups (RPKM = Reads Per Kilobase Million). The lines indicate means. * = p ≤ 0.05. (D) Igfbp5 mRNA expression (qPCR) at different age points in WT kidneys. Points indicate means and whiskers SD. d = day, wk. = week. (E) Representative western blot images in E18.5 and quantification of IGFBP5 and loading control β‐actin in E15.5 and E18.5 WT and Hsd17b3 −/− (KO) kidney homogenates. The lines indicate means. * = p ≤ 0.05. (F) Immunofluorescent staining of IGFBP5 (red) and LRP2 (green) in E18.5 and 2‐week‐old WT and Hsd17b3 −/− (KO) kidneys. Scale bar: 50 μm.
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Neuron-specific Igfbp2 deficiency in the PFC induces cognitive dysfunction (A) Schematic of the experimental design. (B) Diagram of viral injection into the PFC (top) and representative image of viral expression (bottom); scale bars, 500 μm. (C) Representative western blot bands (top) and quantification of Igfbp2 protein levels in the PFC (bottom); n = 4 mice per group. (D) Schematic of the novel object recognition test, depicting the training phase (top) and the test phase (bottom). (E) Representative trajectory plots from the novel object recognition test. (F) Quantification of time spent investigating the novel object during the test phase; n = 8 mice per group. (G) Quantification of the number of investigations of the novel object during the test phase; n = 8 mice per group. (H) Schematic of the Y-maze test, depicting the training phase (top) and the test phase (bottom). (I) Representative trajectory plots from the Y-maze test. (J) Quantification of time spent in the novel arm during the test phase; n = 8 mice per group. (K) Quantification of the number of entries into the novel arm during the test phase; n = 8 mice per group. Analyzed by unpaired t test; ∗∗ p < 0.01. Data are presented as means ± SEM.

Journal: iScience

Article Title: Neuronal Igfbp2 deficiency in the prefrontal cortex impairs cognition through synaptic dysfunction in male mice

doi: 10.1016/j.isci.2026.115629

Figure Lengend Snippet: Neuron-specific Igfbp2 deficiency in the PFC induces cognitive dysfunction (A) Schematic of the experimental design. (B) Diagram of viral injection into the PFC (top) and representative image of viral expression (bottom); scale bars, 500 μm. (C) Representative western blot bands (top) and quantification of Igfbp2 protein levels in the PFC (bottom); n = 4 mice per group. (D) Schematic of the novel object recognition test, depicting the training phase (top) and the test phase (bottom). (E) Representative trajectory plots from the novel object recognition test. (F) Quantification of time spent investigating the novel object during the test phase; n = 8 mice per group. (G) Quantification of the number of investigations of the novel object during the test phase; n = 8 mice per group. (H) Schematic of the Y-maze test, depicting the training phase (top) and the test phase (bottom). (I) Representative trajectory plots from the Y-maze test. (J) Quantification of time spent in the novel arm during the test phase; n = 8 mice per group. (K) Quantification of the number of entries into the novel arm during the test phase; n = 8 mice per group. Analyzed by unpaired t test; ∗∗ p < 0.01. Data are presented as means ± SEM.

Article Snippet: Recombinant Igfbp2 protein (MCE; Cat# HY- P74846 ) was dissolved in sterile saline at 10 μg/μL.

Techniques: Injection, Expressing, Western Blot

Neuron-specific Igfbp2 deficiency in the PFC reduces excitatory synaptic transmission and neuronal excitability (A) Representative traces of sEPSC recorded from PFC neurons in AAV-scramble (top) and AAV-shRNA (bottom) groups. (B) Cumulative probability plots (main panel) and quantification (insert panel) of sEPSC frequency in AAV-Scramble and AAV-shRNA groups. (C) Cumulative probability plots (main panel) and quantification (insert panel) of sEPSC amplitude in AAV-Scramble and AAV-shRNA groups. (D) Representative traces of sIPSC recorded from PFC neurons in AAV-Scramble (top) and AAV-shRNA (bottom) groups. (E) Cumulative probability plots (main panel) and quantification (insert panel) of sIPSC frequency in AAV-Scramble and AAV-shRNA groups. (F) Cumulative probability plots (main panel) and quantification (insert panel) of sIPSC amplitude in AAV-Scramble and AAV-shRNA groups. (G) Representative traces of AP elicited by 200 pA current injections in PFC neurons from AAV-Scramble (left) and AAV-shRNA (right) groups. (H) Quantification of AP firing frequency in response to a range of current injections in PFC neurons from AAV-Scramble and AAV-shRNA groups. Analyzed by unpaired t test in B, C, E, and F, and two-way repeated-measure ANOVA in H; n = 8 neurons from 4 mice per group; ns: not significant, ∗∗ p < 0.01. Data are presented as means ± SEM.

Journal: iScience

Article Title: Neuronal Igfbp2 deficiency in the prefrontal cortex impairs cognition through synaptic dysfunction in male mice

doi: 10.1016/j.isci.2026.115629

Figure Lengend Snippet: Neuron-specific Igfbp2 deficiency in the PFC reduces excitatory synaptic transmission and neuronal excitability (A) Representative traces of sEPSC recorded from PFC neurons in AAV-scramble (top) and AAV-shRNA (bottom) groups. (B) Cumulative probability plots (main panel) and quantification (insert panel) of sEPSC frequency in AAV-Scramble and AAV-shRNA groups. (C) Cumulative probability plots (main panel) and quantification (insert panel) of sEPSC amplitude in AAV-Scramble and AAV-shRNA groups. (D) Representative traces of sIPSC recorded from PFC neurons in AAV-Scramble (top) and AAV-shRNA (bottom) groups. (E) Cumulative probability plots (main panel) and quantification (insert panel) of sIPSC frequency in AAV-Scramble and AAV-shRNA groups. (F) Cumulative probability plots (main panel) and quantification (insert panel) of sIPSC amplitude in AAV-Scramble and AAV-shRNA groups. (G) Representative traces of AP elicited by 200 pA current injections in PFC neurons from AAV-Scramble (left) and AAV-shRNA (right) groups. (H) Quantification of AP firing frequency in response to a range of current injections in PFC neurons from AAV-Scramble and AAV-shRNA groups. Analyzed by unpaired t test in B, C, E, and F, and two-way repeated-measure ANOVA in H; n = 8 neurons from 4 mice per group; ns: not significant, ∗∗ p < 0.01. Data are presented as means ± SEM.

Article Snippet: Recombinant Igfbp2 protein (MCE; Cat# HY- P74846 ) was dissolved in sterile saline at 10 μg/μL.

Techniques: Transmission Assay, shRNA

Neuron-specific Igfbp2 deficiency in the PFC disrupts synaptic integrity (A) Representative images of dendritic spines in the PFC from AAV-Scramble (left) and AAV-shRNA (right) groups; scale bars, 10 μm. (B) Quantification of dendritic spine density (number per 10 μm) in the PFC from AAV-Scramble and AAV-shRNA groups; n = 9 brain sections from 3 mice per group. (C) Representative western blot bands (top) and quantification of synapsin-1 protein levels (bottom) in the PFC from AAV-scramble and AAV-shRNA groups; n = 4 mice per group. (D) Representative western blot bands (top) and quantification of PSD-95 protein levels (bottom) in the PFC from AAV-Scramble and AAV-shRNA groups; n = 4 mice per group. Analyzed by unpaired t test; ∗ p < 0.05 and ∗∗∗ p < 0.001. Data are presented as means ± SEM.

Journal: iScience

Article Title: Neuronal Igfbp2 deficiency in the prefrontal cortex impairs cognition through synaptic dysfunction in male mice

doi: 10.1016/j.isci.2026.115629

Figure Lengend Snippet: Neuron-specific Igfbp2 deficiency in the PFC disrupts synaptic integrity (A) Representative images of dendritic spines in the PFC from AAV-Scramble (left) and AAV-shRNA (right) groups; scale bars, 10 μm. (B) Quantification of dendritic spine density (number per 10 μm) in the PFC from AAV-Scramble and AAV-shRNA groups; n = 9 brain sections from 3 mice per group. (C) Representative western blot bands (top) and quantification of synapsin-1 protein levels (bottom) in the PFC from AAV-scramble and AAV-shRNA groups; n = 4 mice per group. (D) Representative western blot bands (top) and quantification of PSD-95 protein levels (bottom) in the PFC from AAV-Scramble and AAV-shRNA groups; n = 4 mice per group. Analyzed by unpaired t test; ∗ p < 0.05 and ∗∗∗ p < 0.001. Data are presented as means ± SEM.

Article Snippet: Recombinant Igfbp2 protein (MCE; Cat# HY- P74846 ) was dissolved in sterile saline at 10 μg/μL.

Techniques: shRNA, Western Blot

Exogenous supplementation of Igfbp2 in the PFC rescues cognitive deficits induced by neuron-specific Igfbp2 deficiency (A) Schematic of the experimental design. (B) Diagram shows virus injection and cannula placement into the PFC (top), and a representative image of cannula position and viral expression in the PFC (bottom); scale bars, 500 μm. (C) Representative western blot bands (top) and quantification of Igfbp2 protein levels in the PFC (bottom); n = 4 mice per group. (D) Schematic of the novel object recognition test, depicting the training phase (top) and the test phase (bottom). (E) Representative trajectory plots from the novel object recognition test. (F) Quantification of time spent investigating the novel object during the test phase; n = 8 mice per group. (G) Quantification of the number of investigations of the novel object during the test phase; n = 8 mice per group. (H) Schematic of the Y-maze test, depicting the training phase (top) and the test phase (bottom). (I) Representative trajectory plots from the Y-maze test. (J) Quantification of time spent in the novel arm during the test phase; n = 8 mice per group. (K) Quantification of the number of entries into the novel arm during the test phase; n = 8 mice per group. Analyzed by unpaired t test; ∗∗ p < 0.01. Data are presented as means ± SEM.

Journal: iScience

Article Title: Neuronal Igfbp2 deficiency in the prefrontal cortex impairs cognition through synaptic dysfunction in male mice

doi: 10.1016/j.isci.2026.115629

Figure Lengend Snippet: Exogenous supplementation of Igfbp2 in the PFC rescues cognitive deficits induced by neuron-specific Igfbp2 deficiency (A) Schematic of the experimental design. (B) Diagram shows virus injection and cannula placement into the PFC (top), and a representative image of cannula position and viral expression in the PFC (bottom); scale bars, 500 μm. (C) Representative western blot bands (top) and quantification of Igfbp2 protein levels in the PFC (bottom); n = 4 mice per group. (D) Schematic of the novel object recognition test, depicting the training phase (top) and the test phase (bottom). (E) Representative trajectory plots from the novel object recognition test. (F) Quantification of time spent investigating the novel object during the test phase; n = 8 mice per group. (G) Quantification of the number of investigations of the novel object during the test phase; n = 8 mice per group. (H) Schematic of the Y-maze test, depicting the training phase (top) and the test phase (bottom). (I) Representative trajectory plots from the Y-maze test. (J) Quantification of time spent in the novel arm during the test phase; n = 8 mice per group. (K) Quantification of the number of entries into the novel arm during the test phase; n = 8 mice per group. Analyzed by unpaired t test; ∗∗ p < 0.01. Data are presented as means ± SEM.

Article Snippet: Recombinant Igfbp2 protein (MCE; Cat# HY- P74846 ) was dissolved in sterile saline at 10 μg/μL.

Techniques: Virus, Injection, Expressing, Western Blot

Exogenous supplementation of Igfbp2 in the PFC restores excitatory synaptic transmission and neuronal excitability impaired by neuron-specific Igfbp2 deficiency (A) Representative traces of sEPSC recorded from PFC neurons in saline (top) and Igfbp2 (bottom) groups. (B) Cumulative probability plots (main panel) and quantification (insert panel) of sEPSC frequency in saline (top) and Igfbp2 (bottom) groups. (C) Cumulative probability plots (main panel) and quantification (insert panel) of sEPSC amplitude in saline and Igfbp2 groups. (D) Representative traces of sIPSC recorded from PFC neurons in saline (top) and Igfbp2 (bottom) groups. (E) Cumulative probability plots (main panel) and quantification (insert panel) of sIPSC frequency in saline and Igfbp2 groups. (F) Cumulative probability plots (main panel) and quantification (insert panel) of sIPSC amplitude in saline and Igfbp2 groups. (G) Representative traces of AP elicited by 200 pA current injections in PFC neurons from saline (left) and Igfbp2 (right) groups. (H) Quantification of AP firing frequency in response to a range of current injections in PFC neurons from Saline (left) and Igfbp2 (right) groups. Analyzed by unpaired t test in B, C, E, and F, and two-way repeated-measure ANOVA in H; n = 8 neurons from 4 mice per group; ns: not significant, ∗∗ p < 0.01. Data are presented as means ± SEM.

Journal: iScience

Article Title: Neuronal Igfbp2 deficiency in the prefrontal cortex impairs cognition through synaptic dysfunction in male mice

doi: 10.1016/j.isci.2026.115629

Figure Lengend Snippet: Exogenous supplementation of Igfbp2 in the PFC restores excitatory synaptic transmission and neuronal excitability impaired by neuron-specific Igfbp2 deficiency (A) Representative traces of sEPSC recorded from PFC neurons in saline (top) and Igfbp2 (bottom) groups. (B) Cumulative probability plots (main panel) and quantification (insert panel) of sEPSC frequency in saline (top) and Igfbp2 (bottom) groups. (C) Cumulative probability plots (main panel) and quantification (insert panel) of sEPSC amplitude in saline and Igfbp2 groups. (D) Representative traces of sIPSC recorded from PFC neurons in saline (top) and Igfbp2 (bottom) groups. (E) Cumulative probability plots (main panel) and quantification (insert panel) of sIPSC frequency in saline and Igfbp2 groups. (F) Cumulative probability plots (main panel) and quantification (insert panel) of sIPSC amplitude in saline and Igfbp2 groups. (G) Representative traces of AP elicited by 200 pA current injections in PFC neurons from saline (left) and Igfbp2 (right) groups. (H) Quantification of AP firing frequency in response to a range of current injections in PFC neurons from Saline (left) and Igfbp2 (right) groups. Analyzed by unpaired t test in B, C, E, and F, and two-way repeated-measure ANOVA in H; n = 8 neurons from 4 mice per group; ns: not significant, ∗∗ p < 0.01. Data are presented as means ± SEM.

Article Snippet: Recombinant Igfbp2 protein (MCE; Cat# HY- P74846 ) was dissolved in sterile saline at 10 μg/μL.

Techniques: Transmission Assay, Saline

Exogenous supplementation of Igfbp2 in the PFC restores synaptic integrity disrupted by neuron-specific Igfbp2 deficiency (A) Representative images of dendritic spines in the PFC from saline (left) and Igfbp2 (right) groups; scale bars, 10 μm. (B) Quantification of dendritic spine density (number per 10 μm) in the PFC from saline and Igfbp2 groups; n = 9 brain sections from 3 mice per group. (C) Representative western blot bands (top) and quantification of synapsin-1 protein levels (bottom) in the PFC from AAV-Scramble and AAV-shRNA groups; n = 4 mice per group. (D) Representative western blot bands (top) and quantification of PSD-95 protein levels (bottom) in the PFC from AAV-Scramble and AAV-shRNA groups; n = 4 mice per group. Analyzed by unpaired t test; ∗ p < 0.05 and ∗∗∗ p < 0.001. Data are presented as means ± SEM.

Journal: iScience

Article Title: Neuronal Igfbp2 deficiency in the prefrontal cortex impairs cognition through synaptic dysfunction in male mice

doi: 10.1016/j.isci.2026.115629

Figure Lengend Snippet: Exogenous supplementation of Igfbp2 in the PFC restores synaptic integrity disrupted by neuron-specific Igfbp2 deficiency (A) Representative images of dendritic spines in the PFC from saline (left) and Igfbp2 (right) groups; scale bars, 10 μm. (B) Quantification of dendritic spine density (number per 10 μm) in the PFC from saline and Igfbp2 groups; n = 9 brain sections from 3 mice per group. (C) Representative western blot bands (top) and quantification of synapsin-1 protein levels (bottom) in the PFC from AAV-Scramble and AAV-shRNA groups; n = 4 mice per group. (D) Representative western blot bands (top) and quantification of PSD-95 protein levels (bottom) in the PFC from AAV-Scramble and AAV-shRNA groups; n = 4 mice per group. Analyzed by unpaired t test; ∗ p < 0.05 and ∗∗∗ p < 0.001. Data are presented as means ± SEM.

Article Snippet: Recombinant Igfbp2 protein (MCE; Cat# HY- P74846 ) was dissolved in sterile saline at 10 μg/μL.

Techniques: Saline, Western Blot, shRNA

Schematic summary of this study Neuron-specific Igfbp2 deficiency in the PFC impairs cognitive function by disrupting synaptic integrity, excitatory transmission, and neuronal activity, whereas exogenous Igfbp2 supplementation mitigates cognitive deficits by restoring synaptic integrity, excitatory transmission, and neuronal activity. PFC prefrontal cortex, sEPSC spontaneous excitatory postsynaptic currents, Igfbp2 insulin-like growth factor-binding protein 2.

Journal: iScience

Article Title: Neuronal Igfbp2 deficiency in the prefrontal cortex impairs cognition through synaptic dysfunction in male mice

doi: 10.1016/j.isci.2026.115629

Figure Lengend Snippet: Schematic summary of this study Neuron-specific Igfbp2 deficiency in the PFC impairs cognitive function by disrupting synaptic integrity, excitatory transmission, and neuronal activity, whereas exogenous Igfbp2 supplementation mitigates cognitive deficits by restoring synaptic integrity, excitatory transmission, and neuronal activity. PFC prefrontal cortex, sEPSC spontaneous excitatory postsynaptic currents, Igfbp2 insulin-like growth factor-binding protein 2.

Article Snippet: Recombinant Igfbp2 protein (MCE; Cat# HY- P74846 ) was dissolved in sterile saline at 10 μg/μL.

Techniques: Transmission Assay, Activity Assay, Binding Assay

Fetal testosterone supplementation rescues the adult kidney size by normalizing gene expression in the fetal kidney. (A) Anogenital distance of 3‐month‐old Hsd17b3 −/− (KO) and WT males without and with testosterone supplementation (res) at E14.5–17.5. The lines indicate means. * = p ≤ 0.05 ** = p ≤ 0.01. (B) kidney weights of 3‐month‐old Hsd17b3 −/− (KO) and WT males without and with testosterone supplementation (res) at E14.5–17.5. The lines indicate means. * = p ≤ 0.05 ** = p ≤ 0.01. (C) Igfbp5 expression (RNA‐seq) in E16.5 kidneys of WT, Hsd17b3 −/− (KO) and treated KO (res) groups (RPKM = Reads Per Kilobase Million). The lines indicate means. * = p ≤ 0.05. (D) Igfbp5 mRNA expression (qPCR) at different age points in WT kidneys. Points indicate means and whiskers SD. d = day, wk. = week. (E) Representative western blot images in E18.5 and quantification of IGFBP5 and loading control β‐actin in E15.5 and E18.5 WT and Hsd17b3 −/− (KO) kidney homogenates. The lines indicate means. * = p ≤ 0.05. (F) Immunofluorescent staining of IGFBP5 (red) and LRP2 (green) in E18.5 and 2‐week‐old WT and Hsd17b3 −/− (KO) kidneys. Scale bar: 50 μm.

Journal: The FASEB Journal

Article Title: Testosterone Exposure During Fetal Masculinization Programming Window Determines the Kidney Size in Adult Mice

doi: 10.1096/fj.202500761RR

Figure Lengend Snippet: Fetal testosterone supplementation rescues the adult kidney size by normalizing gene expression in the fetal kidney. (A) Anogenital distance of 3‐month‐old Hsd17b3 −/− (KO) and WT males without and with testosterone supplementation (res) at E14.5–17.5. The lines indicate means. * = p ≤ 0.05 ** = p ≤ 0.01. (B) kidney weights of 3‐month‐old Hsd17b3 −/− (KO) and WT males without and with testosterone supplementation (res) at E14.5–17.5. The lines indicate means. * = p ≤ 0.05 ** = p ≤ 0.01. (C) Igfbp5 expression (RNA‐seq) in E16.5 kidneys of WT, Hsd17b3 −/− (KO) and treated KO (res) groups (RPKM = Reads Per Kilobase Million). The lines indicate means. * = p ≤ 0.05. (D) Igfbp5 mRNA expression (qPCR) at different age points in WT kidneys. Points indicate means and whiskers SD. d = day, wk. = week. (E) Representative western blot images in E18.5 and quantification of IGFBP5 and loading control β‐actin in E15.5 and E18.5 WT and Hsd17b3 −/− (KO) kidney homogenates. The lines indicate means. * = p ≤ 0.05. (F) Immunofluorescent staining of IGFBP5 (red) and LRP2 (green) in E18.5 and 2‐week‐old WT and Hsd17b3 −/− (KO) kidneys. Scale bar: 50 μm.

Article Snippet: Cells were cultured on poly‐L‐lysine–coated plates (#P4832, Sigma‐Aldrich) and switched to serum‐free medium (DMEM/F12, #D2906, Sigma; 1% Penicillin/streptomycin, #A5256701, Gibco; 1% L‐Glutamine, #25030–024, Gibco; 20 nM DHT) for 3 h before changing to fresh serum‐free medium with 25, 50, or 100 nM recombinant IGFBP5 (#578‐B5, R&D Systems).

Techniques: Gene Expression, Expressing, RNA Sequencing, Western Blot, Control, Staining

IGFBP5 is likely regulated by AR and HNF4A, and in turn can affect cell proliferation. (A) Visualization of AR and HNF4A binding peaks and H3K4m1 and H3K27ac histone marks near Igfbp5 in ChIP‐seq data from Pihlajamaa et al., 2014. T = testosterone treatment. (B) Proliferation analysis of HEK 239 cells cultured with 0 (Ctrl), 25, 50, or 100 nM recombinant human IGFBP5. The lines indicate means. * = p ≤ 0.05. (C) Representative western blot images in E15.5 and quantification of phosphorylated AKT (pAKT), AKT, and loading control β‐actin in E15.5 and E18.5 WT and Hsd17b3 −/− (KO) kidney homogenates. The lines indicate means. (D) Representative western blot images in E15.5 and quantification of phosphorylated S6 ribosomal protein (pS6) and loading control β‐actin in E15.5 and E18.5 WT and Hsd17b3 −/− (KO) kidney homogenates. The lines indicate means. ** = p ≤ 0.01.

Journal: The FASEB Journal

Article Title: Testosterone Exposure During Fetal Masculinization Programming Window Determines the Kidney Size in Adult Mice

doi: 10.1096/fj.202500761RR

Figure Lengend Snippet: IGFBP5 is likely regulated by AR and HNF4A, and in turn can affect cell proliferation. (A) Visualization of AR and HNF4A binding peaks and H3K4m1 and H3K27ac histone marks near Igfbp5 in ChIP‐seq data from Pihlajamaa et al., 2014. T = testosterone treatment. (B) Proliferation analysis of HEK 239 cells cultured with 0 (Ctrl), 25, 50, or 100 nM recombinant human IGFBP5. The lines indicate means. * = p ≤ 0.05. (C) Representative western blot images in E15.5 and quantification of phosphorylated AKT (pAKT), AKT, and loading control β‐actin in E15.5 and E18.5 WT and Hsd17b3 −/− (KO) kidney homogenates. The lines indicate means. (D) Representative western blot images in E15.5 and quantification of phosphorylated S6 ribosomal protein (pS6) and loading control β‐actin in E15.5 and E18.5 WT and Hsd17b3 −/− (KO) kidney homogenates. The lines indicate means. ** = p ≤ 0.01.

Article Snippet: Cells were cultured on poly‐L‐lysine–coated plates (#P4832, Sigma‐Aldrich) and switched to serum‐free medium (DMEM/F12, #D2906, Sigma; 1% Penicillin/streptomycin, #A5256701, Gibco; 1% L‐Glutamine, #25030–024, Gibco; 20 nM DHT) for 3 h before changing to fresh serum‐free medium with 25, 50, or 100 nM recombinant IGFBP5 (#578‐B5, R&D Systems).

Techniques: Binding Assay, ChIP-sequencing, Cell Culture, Recombinant, Western Blot, Control