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 journalArticlepeer-review

62 Citations (Scopus)


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
Issue number1
Publication statusPublished - 2005 Apr 1
Externally publishedYes


  • Hypertrophy
  • Leptin
  • SB203580
  • Vascular smooth muscle cells
  • p38 MAP kinase

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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