Renovascular hypertension leads to DNA damage and apoptosis in bone marrow cells

DNA Cell Biol. 2013 Aug;32(8):458-66. doi: 10.1089/dna.2013.2065. Epub 2013 Jun 20.

Abstract

Angiotensin II (Ang II), which plays a pivotal role in the pathophysiology of the two-kidney, one-clip (2K1C) Goldblatt hypertension, has been associated with augmented generation of reactive oxygen species (ROS) in some cells and tissues. In the present study, we evaluated the influence of 2K1C hypertension on oxidative stress, DNA fragmentation, and apoptosis of bone marrow (BM) cells. Two weeks after the renal artery clipping or Sham operation, flow cytometry analysis showed a higher production of superoxide anions (approximately sixfold) and hydrogen peroxide (approximately twofold) in 2K1C hypertensive than in Sham normotensive mice. 2K1C mice also showed an augmented DNA fragmentation (54%) and apoptotic cells (21%). Our data show that the 2K1C renovascular hypertension is characterized by an increased production of ROS, DNA damage, and apoptosis of BM, which is a fundamental source of the cells involved in tissue repair.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis* / genetics
  • Apoptosis* / physiology
  • Blood Pressure / physiology
  • Bone Marrow Cells / metabolism
  • Bone Marrow Cells / pathology*
  • Bone Marrow Cells / physiology
  • Bone Marrow Diseases / etiology
  • Bone Marrow Diseases / genetics
  • Bone Marrow Diseases / pathology
  • Cells, Cultured
  • DNA Damage* / physiology
  • Hypertension, Renovascular / complications*
  • Hypertension, Renovascular / genetics
  • Hypertension, Renovascular / pathology*
  • Hypertension, Renovascular / physiopathology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Oxidative Stress / physiology
  • Reactive Oxygen Species / metabolism
  • Reactive Oxygen Species / pharmacology

Substances

  • Reactive Oxygen Species