Agmatine ameliorates high glucose-induced neuronal cell senescence by regulating the p21 and p53 signaling

Juhyun Song, Byeori Lee, Somang Kang, Yumi Oh, Eosu Kim, Chul Hoon Kim, Ho Taek Song, Jong Eun Lee

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Neuronal senescence caused by diabetic neuropathy is considered a common complication of diabetes mellitus. Neuronal senescence leads to the secretion of pro-inflammatory cytokines, the production of reactive oxygen species, and the alteration of cellular homeostasis. Agmatine, which is biosynthesized by arginine decarboxylation, has been reported in previous in vitro to exert a protective effect against various stresses. In present study, agmatine attenuated the cell death and the expression of pro-inflammatory cytokines such as IL-6, TNF-alpha and CCL2 in high glucose in vitro conditions. Moreover, the senescence associated-β-galatosidase's activity in high glucose exposed neuronal cells was reduced by agmatine. Increased p21 and reduced p53 in high glucose conditioned cells were changed by agmatine. Ultimately, agmatine inhibits the neuronal cell senescence through the activation of p53 and the inhibition of p21. Here, we propose that agmatine may ameliorate neuronal cell senescence in hyperglycemia.

Original languageEnglish
Pages (from-to)24-32
Number of pages9
JournalExperimental Neurobiology
Volume25
Issue number1
DOIs
Publication statusPublished - 2016 Feb 1

Fingerprint

Agmatine
Cell Aging
Glucose
Cytokines
Decarboxylation
Diabetic Neuropathies
Diabetes Complications
Hyperglycemia
Arginine
Interleukin-6
Reactive Oxygen Species
Homeostasis
Cell Death
Tumor Necrosis Factor-alpha

All Science Journal Classification (ASJC) codes

  • Clinical Neurology
  • Cellular and Molecular Neuroscience

Cite this

Song, Juhyun ; Lee, Byeori ; Kang, Somang ; Oh, Yumi ; Kim, Eosu ; Kim, Chul Hoon ; Song, Ho Taek ; Lee, Jong Eun. / Agmatine ameliorates high glucose-induced neuronal cell senescence by regulating the p21 and p53 signaling. In: Experimental Neurobiology. 2016 ; Vol. 25, No. 1. pp. 24-32.
@article{1f633a1d22d04bb2bfdaf099b451f6f4,
title = "Agmatine ameliorates high glucose-induced neuronal cell senescence by regulating the p21 and p53 signaling",
abstract = "Neuronal senescence caused by diabetic neuropathy is considered a common complication of diabetes mellitus. Neuronal senescence leads to the secretion of pro-inflammatory cytokines, the production of reactive oxygen species, and the alteration of cellular homeostasis. Agmatine, which is biosynthesized by arginine decarboxylation, has been reported in previous in vitro to exert a protective effect against various stresses. In present study, agmatine attenuated the cell death and the expression of pro-inflammatory cytokines such as IL-6, TNF-alpha and CCL2 in high glucose in vitro conditions. Moreover, the senescence associated-β-galatosidase's activity in high glucose exposed neuronal cells was reduced by agmatine. Increased p21 and reduced p53 in high glucose conditioned cells were changed by agmatine. Ultimately, agmatine inhibits the neuronal cell senescence through the activation of p53 and the inhibition of p21. Here, we propose that agmatine may ameliorate neuronal cell senescence in hyperglycemia.",
author = "Juhyun Song and Byeori Lee and Somang Kang and Yumi Oh and Eosu Kim and Kim, {Chul Hoon} and Song, {Ho Taek} and Lee, {Jong Eun}",
year = "2016",
month = "2",
day = "1",
doi = "10.5607/en.2016.25.1.24",
language = "English",
volume = "25",
pages = "24--32",
journal = "Experimental Neurobiology",
issn = "1226-2560",
publisher = "Korean Society for Brain and Neural Science",
number = "1",

}

Agmatine ameliorates high glucose-induced neuronal cell senescence by regulating the p21 and p53 signaling. / Song, Juhyun; Lee, Byeori; Kang, Somang; Oh, Yumi; Kim, Eosu; Kim, Chul Hoon; Song, Ho Taek; Lee, Jong Eun.

In: Experimental Neurobiology, Vol. 25, No. 1, 01.02.2016, p. 24-32.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Agmatine ameliorates high glucose-induced neuronal cell senescence by regulating the p21 and p53 signaling

AU - Song, Juhyun

AU - Lee, Byeori

AU - Kang, Somang

AU - Oh, Yumi

AU - Kim, Eosu

AU - Kim, Chul Hoon

AU - Song, Ho Taek

AU - Lee, Jong Eun

PY - 2016/2/1

Y1 - 2016/2/1

N2 - Neuronal senescence caused by diabetic neuropathy is considered a common complication of diabetes mellitus. Neuronal senescence leads to the secretion of pro-inflammatory cytokines, the production of reactive oxygen species, and the alteration of cellular homeostasis. Agmatine, which is biosynthesized by arginine decarboxylation, has been reported in previous in vitro to exert a protective effect against various stresses. In present study, agmatine attenuated the cell death and the expression of pro-inflammatory cytokines such as IL-6, TNF-alpha and CCL2 in high glucose in vitro conditions. Moreover, the senescence associated-β-galatosidase's activity in high glucose exposed neuronal cells was reduced by agmatine. Increased p21 and reduced p53 in high glucose conditioned cells were changed by agmatine. Ultimately, agmatine inhibits the neuronal cell senescence through the activation of p53 and the inhibition of p21. Here, we propose that agmatine may ameliorate neuronal cell senescence in hyperglycemia.

AB - Neuronal senescence caused by diabetic neuropathy is considered a common complication of diabetes mellitus. Neuronal senescence leads to the secretion of pro-inflammatory cytokines, the production of reactive oxygen species, and the alteration of cellular homeostasis. Agmatine, which is biosynthesized by arginine decarboxylation, has been reported in previous in vitro to exert a protective effect against various stresses. In present study, agmatine attenuated the cell death and the expression of pro-inflammatory cytokines such as IL-6, TNF-alpha and CCL2 in high glucose in vitro conditions. Moreover, the senescence associated-β-galatosidase's activity in high glucose exposed neuronal cells was reduced by agmatine. Increased p21 and reduced p53 in high glucose conditioned cells were changed by agmatine. Ultimately, agmatine inhibits the neuronal cell senescence through the activation of p53 and the inhibition of p21. Here, we propose that agmatine may ameliorate neuronal cell senescence in hyperglycemia.

UR - http://www.scopus.com/inward/record.url?scp=84995571187&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84995571187&partnerID=8YFLogxK

U2 - 10.5607/en.2016.25.1.24

DO - 10.5607/en.2016.25.1.24

M3 - Article

AN - SCOPUS:84995571187

VL - 25

SP - 24

EP - 32

JO - Experimental Neurobiology

JF - Experimental Neurobiology

SN - 1226-2560

IS - 1

ER -