Leptin induces hypertrophy via p38 mitogen-activated protein kinase in rat vascular smooth muscle cells

Hye Jin Shin, Jaewon Oh, Seok Min Kang, Jong Ho Lee, Min Jeong Shin, Ki Chul Hwang, Yangsoo Jang, Ji Hyung Chung

Research output: Contribution to journalArticle

58 Citations (Scopus)

Abstract

The hypertrophy of vascular smooth muscle cells (VSMCs) is critical in vascular remodeling associated with hypertension, atherosclerosis, and restenosis. Recently, leptin has appeared to play a pivotal role in vascular remodeling. However, the mechanism by which leptin induces hypertrophy in vascular smooth muscle cells is still unknown. We studied the role of leptin as a potential hypertrophic factor in rat VSMCs. In the present study, leptin significantly increased [3H]leucine incorporation and the total protein/DNA ratio in VSMCs. The maximal hypertrophic effect was at 100 ng/ml of leptin. Leptin induced phosphorylation and activation of p38 mitogen-activated protein (p38 MAP) kinase and of signal transducers and activators of transcription 3 in a concentration- and time-dependent manner. A p38 MAP kinase inhibitor SB203580 significantly inhibited leptin-induced hypertrophy, AG490 (a JAK2 inhibitor) partially inhibited it, and other MAP kinase inhibitors, PD98059 (an ERK inhibitor) and SP600125 (a JNK inhibitor), had no effect. These results indicate that leptin directly stimulates cellular hypertrophy via p38 MAP kinase in rat VSMCs.

Original languageEnglish
Pages (from-to)18-24
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume329
Issue number1
DOIs
Publication statusPublished - 2005 Apr 1

Fingerprint

p38 Mitogen-Activated Protein Kinases
Leptin
Vascular Smooth Muscle
Hypertrophy
Smooth Muscle Myocytes
Muscle
Rats
Cells
STAT3 Transcription Factor
Phosphorylation
Protein Kinase Inhibitors
Leucine
Atherosclerosis
Phosphotransferases
Chemical activation
Hypertension
DNA

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

@article{0ba16d76aba14ca4bf914b9da0c6e7e3,
title = "Leptin induces hypertrophy via p38 mitogen-activated protein kinase in rat vascular smooth muscle cells",
abstract = "The hypertrophy of vascular smooth muscle cells (VSMCs) is critical in vascular remodeling associated with hypertension, atherosclerosis, and restenosis. Recently, leptin has appeared to play a pivotal role in vascular remodeling. However, the mechanism by which leptin induces hypertrophy in vascular smooth muscle cells is still unknown. We studied the role of leptin as a potential hypertrophic factor in rat VSMCs. In the present study, leptin significantly increased [3H]leucine incorporation and the total protein/DNA ratio in VSMCs. The maximal hypertrophic effect was at 100 ng/ml of leptin. Leptin induced phosphorylation and activation of p38 mitogen-activated protein (p38 MAP) kinase and of signal transducers and activators of transcription 3 in a concentration- and time-dependent manner. A p38 MAP kinase inhibitor SB203580 significantly inhibited leptin-induced hypertrophy, AG490 (a JAK2 inhibitor) partially inhibited it, and other MAP kinase inhibitors, PD98059 (an ERK inhibitor) and SP600125 (a JNK inhibitor), had no effect. These results indicate that leptin directly stimulates cellular hypertrophy via p38 MAP kinase in rat VSMCs.",
author = "Shin, {Hye Jin} and Jaewon Oh and Kang, {Seok Min} and Lee, {Jong Ho} and Shin, {Min Jeong} and Hwang, {Ki Chul} and Yangsoo Jang and Chung, {Ji Hyung}",
year = "2005",
month = "4",
day = "1",
doi = "10.1016/j.bbrc.2004.12.195",
language = "English",
volume = "329",
pages = "18--24",
journal = "Biochemical and Biophysical Research Communications",
issn = "0006-291X",
publisher = "Academic Press Inc.",
number = "1",

}

Leptin induces hypertrophy via p38 mitogen-activated protein kinase in rat vascular smooth muscle cells. / Shin, Hye Jin; Oh, Jaewon; Kang, Seok Min; Lee, Jong Ho; Shin, Min Jeong; Hwang, Ki Chul; Jang, Yangsoo; Chung, Ji Hyung.

In: Biochemical and Biophysical Research Communications, Vol. 329, No. 1, 01.04.2005, p. 18-24.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Leptin induces hypertrophy via p38 mitogen-activated protein kinase in rat vascular smooth muscle cells

AU - Shin, Hye Jin

AU - Oh, Jaewon

AU - Kang, Seok Min

AU - Lee, Jong Ho

AU - Shin, Min Jeong

AU - Hwang, Ki Chul

AU - Jang, Yangsoo

AU - Chung, Ji Hyung

PY - 2005/4/1

Y1 - 2005/4/1

N2 - The hypertrophy of vascular smooth muscle cells (VSMCs) is critical in vascular remodeling associated with hypertension, atherosclerosis, and restenosis. Recently, leptin has appeared to play a pivotal role in vascular remodeling. However, the mechanism by which leptin induces hypertrophy in vascular smooth muscle cells is still unknown. We studied the role of leptin as a potential hypertrophic factor in rat VSMCs. In the present study, leptin significantly increased [3H]leucine incorporation and the total protein/DNA ratio in VSMCs. The maximal hypertrophic effect was at 100 ng/ml of leptin. Leptin induced phosphorylation and activation of p38 mitogen-activated protein (p38 MAP) kinase and of signal transducers and activators of transcription 3 in a concentration- and time-dependent manner. A p38 MAP kinase inhibitor SB203580 significantly inhibited leptin-induced hypertrophy, AG490 (a JAK2 inhibitor) partially inhibited it, and other MAP kinase inhibitors, PD98059 (an ERK inhibitor) and SP600125 (a JNK inhibitor), had no effect. These results indicate that leptin directly stimulates cellular hypertrophy via p38 MAP kinase in rat VSMCs.

AB - The hypertrophy of vascular smooth muscle cells (VSMCs) is critical in vascular remodeling associated with hypertension, atherosclerosis, and restenosis. Recently, leptin has appeared to play a pivotal role in vascular remodeling. However, the mechanism by which leptin induces hypertrophy in vascular smooth muscle cells is still unknown. We studied the role of leptin as a potential hypertrophic factor in rat VSMCs. In the present study, leptin significantly increased [3H]leucine incorporation and the total protein/DNA ratio in VSMCs. The maximal hypertrophic effect was at 100 ng/ml of leptin. Leptin induced phosphorylation and activation of p38 mitogen-activated protein (p38 MAP) kinase and of signal transducers and activators of transcription 3 in a concentration- and time-dependent manner. A p38 MAP kinase inhibitor SB203580 significantly inhibited leptin-induced hypertrophy, AG490 (a JAK2 inhibitor) partially inhibited it, and other MAP kinase inhibitors, PD98059 (an ERK inhibitor) and SP600125 (a JNK inhibitor), had no effect. These results indicate that leptin directly stimulates cellular hypertrophy via p38 MAP kinase in rat VSMCs.

UR - http://www.scopus.com/inward/record.url?scp=13844280463&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=13844280463&partnerID=8YFLogxK

U2 - 10.1016/j.bbrc.2004.12.195

DO - 10.1016/j.bbrc.2004.12.195

M3 - Article

C2 - 15721267

AN - SCOPUS:13844280463

VL - 329

SP - 18

EP - 24

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

IS - 1

ER -