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Overstimulation can create health problems due to increases in PI3K/Akt/GSK3 insensitivity and GSK3 activity.

Liu X - Springerplus (2014)

Bottom Line: This study shows high GSK3 activity can result from PI3K/Akt overstimulation.Type II Diabetes shows insulin resistance that the body cells decrease insulin use.These results suggest an alternative explanation of the body cells declining hormone use since various kinds of cell signaling-induced overstimulation events almost always linked to PI3K/Akt, increase with age.

View Article: PubMed Central - PubMed

Affiliation: Intramural Research Program, National Center for Complementary and Alternative Medicine, US Department of Health and Human Services, National Institutes of Health, Bethesda, MD 20892 USA.

ABSTRACT
Aging is linked to decrease of the body cell use of growth hormone (GH) and thyroxine, whereas the decrease is via "death hormones" inhibition? This study proposes different viewpoints. Since interleukin 17 receptor C (IL17RC) is highly expressed in tissues from age-related macular degeneration (AMD) patients, IL17RC signaling pathways are explored to evaluate Wnts/vascular endothelial growth factor (VEGF) expression and complement activity, which are pathological factors in AMD. IL17RC overexpression or VEGF treatment was performed in two cell lines for up to two-day. Real-time Quantitative PCR, confocal microscopy, immune-blot, MTT assay, etc. measured downstream effects. IL17RC overexpression increases Wnts and VEGF that forms complexes with Wnt-signaling components. VEGF or the Wnt-signaling components interacting with C3 suggests alternative complement pathway activation. Moreover, IL17RC-overexpressed cells or VEGF-treated cells for two-day, which is overstimulation, increase PI3K/Akt/GSK3 insensitivity and GSK3 activity, and decrease growth/survival. High GSK3 activity associates with many chronic diseases including type II Diabetes. This study shows high GSK3 activity can result from PI3K/Akt overstimulation. Type II Diabetes shows insulin resistance that the body cells decrease insulin use. Possessing little sensitive PI3K/Akt for receptor activation, cells after overstimulation, although live, hardly respond to PI3K/Akt activators including GH, thyroxine and insulin. These results suggest an alternative explanation of the body cells declining hormone use since various kinds of cell signaling-induced overstimulation events almost always linked to PI3K/Akt, increase with age. Playing pathological roles in senescence and diseases, overstimulation eventually generates health problems.

No MeSH data available.


Related in: MedlinePlus

IL17RC overexpression increases colocalization of VEGF/β-catenin and VEGF/GSK3β. Confocal microscopy procedures were applied to EV-transfected ARPE or IL17RC-transfected ARPE treated without or with sFRP2. Images were indicated in the figures. DAPI is the intensity control. Data represent three separate experiments.
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Fig2: IL17RC overexpression increases colocalization of VEGF/β-catenin and VEGF/GSK3β. Confocal microscopy procedures were applied to EV-transfected ARPE or IL17RC-transfected ARPE treated without or with sFRP2. Images were indicated in the figures. DAPI is the intensity control. Data represent three separate experiments.

Mentions: EV- or IL17RC-transfected ARPE cells were plated onto sterile cover slips. Cells were left untreated or treated with sFRP2 for two-day. The fixing, blocking and staining procedures have been described (Liu et al. 2011), but the buffers did not contain any detergent. Samples were stained with primary rabbit antibodies 1:50 (α-IL17RC for Figure 1A, α-β-catenin for Figures 2 and 3A, α-VEGF for Figure 2, the bottom panel and Figure 3C, α-GSK3β for Figure 3B) and primary mouse antibodies (α-VEGF for Figure 2, the top panel, α-GSK3β for Figure 2, α-C3 for Figures 3A-C), as well as secondary antibodies goat anti-rabbit conjugated FITC 1:100 for Figure 1A or donkey/goat anti-rabbit conjugated rhodamine 1:100 combining with goat anti-mouse IgG1 conjugated FITC at 1:100 for Figures 2 and 3. The secondary antibodies were purchased from Santa Cruz. VECTA-SHIELD HardSet Mounted Medium with DAPI (Vector Labs) was employed for mounting cover slips. Cells were viewed with a confocal laser microscope (Lenses: 63 W;LSM510; Carl Zeiss MicroImaging, Inc.) in the Lab of Cellular and Developmental Biology, NIDDK, NIH.Figure 1


Overstimulation can create health problems due to increases in PI3K/Akt/GSK3 insensitivity and GSK3 activity.

Liu X - Springerplus (2014)

IL17RC overexpression increases colocalization of VEGF/β-catenin and VEGF/GSK3β. Confocal microscopy procedures were applied to EV-transfected ARPE or IL17RC-transfected ARPE treated without or with sFRP2. Images were indicated in the figures. DAPI is the intensity control. Data represent three separate experiments.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4117863&req=5

Fig2: IL17RC overexpression increases colocalization of VEGF/β-catenin and VEGF/GSK3β. Confocal microscopy procedures were applied to EV-transfected ARPE or IL17RC-transfected ARPE treated without or with sFRP2. Images were indicated in the figures. DAPI is the intensity control. Data represent three separate experiments.
Mentions: EV- or IL17RC-transfected ARPE cells were plated onto sterile cover slips. Cells were left untreated or treated with sFRP2 for two-day. The fixing, blocking and staining procedures have been described (Liu et al. 2011), but the buffers did not contain any detergent. Samples were stained with primary rabbit antibodies 1:50 (α-IL17RC for Figure 1A, α-β-catenin for Figures 2 and 3A, α-VEGF for Figure 2, the bottom panel and Figure 3C, α-GSK3β for Figure 3B) and primary mouse antibodies (α-VEGF for Figure 2, the top panel, α-GSK3β for Figure 2, α-C3 for Figures 3A-C), as well as secondary antibodies goat anti-rabbit conjugated FITC 1:100 for Figure 1A or donkey/goat anti-rabbit conjugated rhodamine 1:100 combining with goat anti-mouse IgG1 conjugated FITC at 1:100 for Figures 2 and 3. The secondary antibodies were purchased from Santa Cruz. VECTA-SHIELD HardSet Mounted Medium with DAPI (Vector Labs) was employed for mounting cover slips. Cells were viewed with a confocal laser microscope (Lenses: 63 W;LSM510; Carl Zeiss MicroImaging, Inc.) in the Lab of Cellular and Developmental Biology, NIDDK, NIH.Figure 1

Bottom Line: This study shows high GSK3 activity can result from PI3K/Akt overstimulation.Type II Diabetes shows insulin resistance that the body cells decrease insulin use.These results suggest an alternative explanation of the body cells declining hormone use since various kinds of cell signaling-induced overstimulation events almost always linked to PI3K/Akt, increase with age.

View Article: PubMed Central - PubMed

Affiliation: Intramural Research Program, National Center for Complementary and Alternative Medicine, US Department of Health and Human Services, National Institutes of Health, Bethesda, MD 20892 USA.

ABSTRACT
Aging is linked to decrease of the body cell use of growth hormone (GH) and thyroxine, whereas the decrease is via "death hormones" inhibition? This study proposes different viewpoints. Since interleukin 17 receptor C (IL17RC) is highly expressed in tissues from age-related macular degeneration (AMD) patients, IL17RC signaling pathways are explored to evaluate Wnts/vascular endothelial growth factor (VEGF) expression and complement activity, which are pathological factors in AMD. IL17RC overexpression or VEGF treatment was performed in two cell lines for up to two-day. Real-time Quantitative PCR, confocal microscopy, immune-blot, MTT assay, etc. measured downstream effects. IL17RC overexpression increases Wnts and VEGF that forms complexes with Wnt-signaling components. VEGF or the Wnt-signaling components interacting with C3 suggests alternative complement pathway activation. Moreover, IL17RC-overexpressed cells or VEGF-treated cells for two-day, which is overstimulation, increase PI3K/Akt/GSK3 insensitivity and GSK3 activity, and decrease growth/survival. High GSK3 activity associates with many chronic diseases including type II Diabetes. This study shows high GSK3 activity can result from PI3K/Akt overstimulation. Type II Diabetes shows insulin resistance that the body cells decrease insulin use. Possessing little sensitive PI3K/Akt for receptor activation, cells after overstimulation, although live, hardly respond to PI3K/Akt activators including GH, thyroxine and insulin. These results suggest an alternative explanation of the body cells declining hormone use since various kinds of cell signaling-induced overstimulation events almost always linked to PI3K/Akt, increase with age. Playing pathological roles in senescence and diseases, overstimulation eventually generates health problems.

No MeSH data available.


Related in: MedlinePlus