Far-infrared protects vascular endothelial cells from advanced glycation end products-induced injury via PLZF-mediated autophagy in diabetic mice

Cheng Hsien Chen, Tso Hsiao Chen, Mei Yi Wu, Tz Chong Chou, Jia Rung Chen, Meng Jun Wei, San Liang Lee, Li Yu Hong, Cai Mei Zheng, I. Jen Chiu, Yuh Feng Lin, Ching Min Hsu, Yung Ho Hsu

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Abstract

The accumulation of advanced glycation end products (AGEs) in diabetic patients induces vascular endothelial injury. Promyelocytic leukemia zinc finger protein (PLZF) is a transcription factor that can be activated by low-temperature far-infrared (FIR) irradiation to exert beneficial effects on the vascular endothelium. In the present study, we investigated the influence of FIR-induced PLZF activation on AGE-induced endothelial injury both in vitro and in vivo. FIR irradiation inhibited AGE-induced apoptosis in human umbilical vein endothelial cells (HUVECs). PLZF activation increased the expression of phosphatidylinositol-3 kinases (PI3K), which are important kinases in the autophagic signaling pathway. FIR-induced PLZF activation led to autophagy in HUVEC, which was mediated through the upregulation of PI3K. Immunofluorescence staining showed that AGEs were engulfed by HUVECs and localized to lysosomes. FIR-induced autophagy promoted AGEs degradation in HUVECs. In nicotinamide/streptozotocin-induced diabetic mice, FIR therapy reduced serum AGEs and AGEs deposition at the vascular endothelium. FIR therapy also reduced diabetes-induced inflammatory markers in the vascular endothelium and improved vascular endothelial function. These protective effects of FIR therapy were not found in PLZF-knockout mice. Our data suggest that FIR-induced PLZF activation in vascular endothelial cells protects the vascular endothelium in diabetic mice from AGE-induced injury.

Original languageEnglish
Article number40442
JournalScientific Reports
Volume7
DOIs
Publication statusPublished - Jan 10 2017

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Advanced Glycosylation End Products
Zinc Fingers
Autophagy
Leukemia
Endothelial Cells
Human Umbilical Vein Endothelial Cells
Vascular Endothelium
Wounds and Injuries
Proteins
Phosphatidylinositol 3-Kinases
Niacinamide
Vascular System Injuries
Streptozocin
Lysosomes
Knockout Mice
Fluorescent Antibody Technique
Blood Vessels
Transcription Factors
Phosphotransferases
Up-Regulation

ASJC Scopus subject areas

  • General

Cite this

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title = "Far-infrared protects vascular endothelial cells from advanced glycation end products-induced injury via PLZF-mediated autophagy in diabetic mice",
abstract = "The accumulation of advanced glycation end products (AGEs) in diabetic patients induces vascular endothelial injury. Promyelocytic leukemia zinc finger protein (PLZF) is a transcription factor that can be activated by low-temperature far-infrared (FIR) irradiation to exert beneficial effects on the vascular endothelium. In the present study, we investigated the influence of FIR-induced PLZF activation on AGE-induced endothelial injury both in vitro and in vivo. FIR irradiation inhibited AGE-induced apoptosis in human umbilical vein endothelial cells (HUVECs). PLZF activation increased the expression of phosphatidylinositol-3 kinases (PI3K), which are important kinases in the autophagic signaling pathway. FIR-induced PLZF activation led to autophagy in HUVEC, which was mediated through the upregulation of PI3K. Immunofluorescence staining showed that AGEs were engulfed by HUVECs and localized to lysosomes. FIR-induced autophagy promoted AGEs degradation in HUVECs. In nicotinamide/streptozotocin-induced diabetic mice, FIR therapy reduced serum AGEs and AGEs deposition at the vascular endothelium. FIR therapy also reduced diabetes-induced inflammatory markers in the vascular endothelium and improved vascular endothelial function. These protective effects of FIR therapy were not found in PLZF-knockout mice. Our data suggest that FIR-induced PLZF activation in vascular endothelial cells protects the vascular endothelium in diabetic mice from AGE-induced injury.",
author = "Chen, {Cheng Hsien} and Chen, {Tso Hsiao} and Wu, {Mei Yi} and Chou, {Tz Chong} and Chen, {Jia Rung} and Wei, {Meng Jun} and Lee, {San Liang} and Hong, {Li Yu} and Zheng, {Cai Mei} and Chiu, {I. Jen} and Lin, {Yuh Feng} and Hsu, {Ching Min} and Hsu, {Yung Ho}",
year = "2017",
month = "1",
day = "10",
doi = "10.1038/srep40442",
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T1 - Far-infrared protects vascular endothelial cells from advanced glycation end products-induced injury via PLZF-mediated autophagy in diabetic mice

AU - Chen, Cheng Hsien

AU - Chen, Tso Hsiao

AU - Wu, Mei Yi

AU - Chou, Tz Chong

AU - Chen, Jia Rung

AU - Wei, Meng Jun

AU - Lee, San Liang

AU - Hong, Li Yu

AU - Zheng, Cai Mei

AU - Chiu, I. Jen

AU - Lin, Yuh Feng

AU - Hsu, Ching Min

AU - Hsu, Yung Ho

PY - 2017/1/10

Y1 - 2017/1/10

N2 - The accumulation of advanced glycation end products (AGEs) in diabetic patients induces vascular endothelial injury. Promyelocytic leukemia zinc finger protein (PLZF) is a transcription factor that can be activated by low-temperature far-infrared (FIR) irradiation to exert beneficial effects on the vascular endothelium. In the present study, we investigated the influence of FIR-induced PLZF activation on AGE-induced endothelial injury both in vitro and in vivo. FIR irradiation inhibited AGE-induced apoptosis in human umbilical vein endothelial cells (HUVECs). PLZF activation increased the expression of phosphatidylinositol-3 kinases (PI3K), which are important kinases in the autophagic signaling pathway. FIR-induced PLZF activation led to autophagy in HUVEC, which was mediated through the upregulation of PI3K. Immunofluorescence staining showed that AGEs were engulfed by HUVECs and localized to lysosomes. FIR-induced autophagy promoted AGEs degradation in HUVECs. In nicotinamide/streptozotocin-induced diabetic mice, FIR therapy reduced serum AGEs and AGEs deposition at the vascular endothelium. FIR therapy also reduced diabetes-induced inflammatory markers in the vascular endothelium and improved vascular endothelial function. These protective effects of FIR therapy were not found in PLZF-knockout mice. Our data suggest that FIR-induced PLZF activation in vascular endothelial cells protects the vascular endothelium in diabetic mice from AGE-induced injury.

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