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Ginsenoside Rg1 drives lymphangiogenesis by activating the <t>VEGFC/D‐VEGFR3‐ERK‐Prox‐1</t> axis, co‐activates the AKT pathway to maintain lymphatic endothelial cell homeostasis, and upregulates lymphatic function‐related genes. (A) Representative western blot bands showing the expression of phosphorylated (p)‐ERK, total ERK, p‐AKT, total AKT, LYVE‐1, and Prox‐1 proteins in lung tissues. (B) Relative quantitative analysis of the p‐ERK/ERK protein ratio. (C) Relative quantitative analysis of the p‐AKT/AKT protein ratio. (D) Relative quantitative analysis of Prox‐1 protein expression normalized to β‐actin expression. (E) Relative quantitative analysis of LYVE‐1 protein expression normalized to β‐actin expression. (F) Relative mRNA expression levels of Prox‐1 in lung tissues measured by qRT‐PCR and normalized to GAPDH . (G) Relative mRNA expression levels of LYVE‐1 in lung tissues measured by qRT‐PCR and normalized to GAPDH . (H) Relative mRNA expression levels of CCL21a in lung tissues measured by qRT‐PCR. (I) Relative mRNA expression levels of ACKR2 in lung tissues measured by qRT‐PCR.
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Variant allele fractions (VAFs) from amplicon sequencing were compared across brain regions and cell types (A) . In four of six cases with findings, the causal somatic variant was identified in both cortex and hippocampus tissue (B) . One case with a PTPN11 A461T variant exhibited extensive neuronal loss in the CA1 region, as seen in H&E and NeuN stains (C) . Fluorescence-activated nuclei sorting was used to isolate hippocampal cell types from this tissue for amplicon sequencing (D) . The PTPN11 A461T variant was present in all cell types but highly enriched among <t>Prox1-neurons</t> (E) .
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Ginsenoside Rg1 drives lymphangiogenesis by activating the VEGFC/D‐VEGFR3‐ERK‐Prox‐1 axis, co‐activates the AKT pathway to maintain lymphatic endothelial cell homeostasis, and upregulates lymphatic function‐related genes. (A) Representative western blot bands showing the expression of phosphorylated (p)‐ERK, total ERK, p‐AKT, total AKT, LYVE‐1, and Prox‐1 proteins in lung tissues. (B) Relative quantitative analysis of the p‐ERK/ERK protein ratio. (C) Relative quantitative analysis of the p‐AKT/AKT protein ratio. (D) Relative quantitative analysis of Prox‐1 protein expression normalized to β‐actin expression. (E) Relative quantitative analysis of LYVE‐1 protein expression normalized to β‐actin expression. (F) Relative mRNA expression levels of Prox‐1 in lung tissues measured by qRT‐PCR and normalized to GAPDH . (G) Relative mRNA expression levels of LYVE‐1 in lung tissues measured by qRT‐PCR and normalized to GAPDH . (H) Relative mRNA expression levels of CCL21a in lung tissues measured by qRT‐PCR. (I) Relative mRNA expression levels of ACKR2 in lung tissues measured by qRT‐PCR.

Journal: The Kaohsiung Journal of Medical Sciences

Article Title: Ginsenoside Rg1 Ameliorates LPS ‐Induced Sepsis‐Associated Lung Injury in Mice via VEGFC /D‐ VEGFR3 Signaling‐Mediated Lymphangiogenesis and Lymphatic Remodeling

doi: 10.1002/kjm2.70229

Figure Lengend Snippet: Ginsenoside Rg1 drives lymphangiogenesis by activating the VEGFC/D‐VEGFR3‐ERK‐Prox‐1 axis, co‐activates the AKT pathway to maintain lymphatic endothelial cell homeostasis, and upregulates lymphatic function‐related genes. (A) Representative western blot bands showing the expression of phosphorylated (p)‐ERK, total ERK, p‐AKT, total AKT, LYVE‐1, and Prox‐1 proteins in lung tissues. (B) Relative quantitative analysis of the p‐ERK/ERK protein ratio. (C) Relative quantitative analysis of the p‐AKT/AKT protein ratio. (D) Relative quantitative analysis of Prox‐1 protein expression normalized to β‐actin expression. (E) Relative quantitative analysis of LYVE‐1 protein expression normalized to β‐actin expression. (F) Relative mRNA expression levels of Prox‐1 in lung tissues measured by qRT‐PCR and normalized to GAPDH . (G) Relative mRNA expression levels of LYVE‐1 in lung tissues measured by qRT‐PCR and normalized to GAPDH . (H) Relative mRNA expression levels of CCL21a in lung tissues measured by qRT‐PCR. (I) Relative mRNA expression levels of ACKR2 in lung tissues measured by qRT‐PCR.

Article Snippet: Membranes were blocked with Rapid Blocking Buffer (Catalog No.: P30500 ; NCM Biotech, Suzhou, China) for 1 h at room temperature, followed by overnight incubation at 4°C with primary antibodies targeting β‐actin (1:1000; Catalog No.: ab8227; Abcam), β‐tubulin (1:1000; Catalog No.: 10094‐1‐AP; Proteintech, USA), VEGFR3 (1:1000; Catalog No.: ab300403; Abcam), VEGFC (1:1000; Catalog No.: A12530; Abclonal, Wuhan, China), VEGFD (1:1000; Catalog No.: A19242; Abclonal), ERK (1:1000; Catalog No.: ab184699; Abcam), phosphorylated ERK (pERK) (1:1000; Catalog No.: ab278538; Abcam), AKT (1:1000; Catalog No.: 4685; CST, MA, USA), phosphorylated AKT (pAKT) (1:1000; Catalog No.: ab81283; Abcam), Prox‐1 (1:1000; Catalog No.: A9047; Abclonal), and LYVE‐1 (1:1000; Catalog No.: ab218535; Abcam).

Techniques: Western Blot, Expressing, Quantitative RT-PCR

Variant allele fractions (VAFs) from amplicon sequencing were compared across brain regions and cell types (A) . In four of six cases with findings, the causal somatic variant was identified in both cortex and hippocampus tissue (B) . One case with a PTPN11 A461T variant exhibited extensive neuronal loss in the CA1 region, as seen in H&E and NeuN stains (C) . Fluorescence-activated nuclei sorting was used to isolate hippocampal cell types from this tissue for amplicon sequencing (D) . The PTPN11 A461T variant was present in all cell types but highly enriched among Prox1-neurons (E) .

Journal: bioRxiv

Article Title: Somatic variants activating the RAS-MAPK pathway confer susceptibility to hippocampal sclerosis in drug-resistant epilepsy

doi: 10.64898/2026.04.06.716727

Figure Lengend Snippet: Variant allele fractions (VAFs) from amplicon sequencing were compared across brain regions and cell types (A) . In four of six cases with findings, the causal somatic variant was identified in both cortex and hippocampus tissue (B) . One case with a PTPN11 A461T variant exhibited extensive neuronal loss in the CA1 region, as seen in H&E and NeuN stains (C) . Fluorescence-activated nuclei sorting was used to isolate hippocampal cell types from this tissue for amplicon sequencing (D) . The PTPN11 A461T variant was present in all cell types but highly enriched among Prox1-neurons (E) .

Article Snippet: Nuclei were labeled using the following antibodies: NeuN (Millipore, #MAB377X), PROX1 (Novus Biologicals, #NBP1-30045AF647), OLIG2 (Novus Biologicals, # NBP2-89201AF594), and PAX6 (Novus Biologicals, #NBP2-34705AF647) at 1:100 followed by incubation for 1 hour at 4°C with agitation.

Techniques: Variant Assay, Amplification, Sequencing, Fluorescence

Sorting scheme to enrich astrocytes, oligodendrocytes, Prox1-negative neurons and Prox1-positive neurons for amplicon sequencing.

Journal: bioRxiv

Article Title: Somatic variants activating the RAS-MAPK pathway confer susceptibility to hippocampal sclerosis in drug-resistant epilepsy

doi: 10.64898/2026.04.06.716727

Figure Lengend Snippet: Sorting scheme to enrich astrocytes, oligodendrocytes, Prox1-negative neurons and Prox1-positive neurons for amplicon sequencing.

Article Snippet: Nuclei were labeled using the following antibodies: NeuN (Millipore, #MAB377X), PROX1 (Novus Biologicals, #NBP1-30045AF647), OLIG2 (Novus Biologicals, # NBP2-89201AF594), and PAX6 (Novus Biologicals, #NBP2-34705AF647) at 1:100 followed by incubation for 1 hour at 4°C with agitation.

Techniques: Amplification, Sequencing