The Effect of Hydrogen Peroxide on Sarco/Endoplasmic and Plasma Membrane Calcium ATPase Gene Expression in Cultured Human Lens Epithelial Cells

نویسندگان

  • M.J Marian
  • P Mukhopadhyay
  • D Borchman
  • D Tang
  • C.A Paterson
چکیده

The loss of calcium homeostasis in the lens of the eye appears to be a factor contributing to lens opacity. In the human lens, calcium homeostasis depends on the Ca²⁺-ATPase pumps found only in the epithelium. A plasma membrane calcium pump, PMCA2 is upregulated in human cataractous lenses. To determine if oxidation caused the plasma membrane Ca²⁺-ATPases (PMCA) or sarcoplasmic/endoplasmic Ca²⁺-ATPases (SERCA) to become upregulated, we cultured a human lens epithelial cell line, in the presence of hydrogen peroxide. We observed an increase in PMCA1, PMCA2 SERCA2b and SERCA3 mRNA levels and protein expression with increasing hydrogen peroxide concentrations and treatment times. Hydrogen peroxide caused a rise in the intracellular calcium which could be an initiating factor in the concerted upregulation of PMCA1 and SERCA3. Our data support the idea that oxidative stress could contribute to a selective rise in PMCA/SERCA expression in human cataractous lenses.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

EXPRESSION OF INDUCIBLE NITRIC OXIDE SYNTHASE GENE (iNOS) STIMULATED BY HYDROGEN PEROXIDE IN HUMAN ENDOTHELIAL CELLS

Inducible nitric oxide synthase (iNOS) gene expresses a calcium calmudolin-independent enzyme which can catalyse NO production from L-arginine. The induction of iNOS activity has been demonstrated in a wide variety of cell types under stimulation with cytokines and lipopoly saccharide (LPS). Previous studies indicated that all nitric oxide synthases (NOS) activated in human umbilical vein endot...

متن کامل

Oxidant-impaired intracellular Ca2+ signaling in pancreatic acinar cells: role of the plasma membrane Ca2+-ATPase.

Pancreatitis is an inflammatory disease of pancreatic acinar cells whereby intracellular calcium concentration ([Ca(2+)](i)) signaling and enzyme secretion are impaired. Increased oxidative stress has been suggested to mediate the associated cell injury. The present study tested the effects of the oxidant, hydrogen peroxide, on [Ca(2+)](i) signaling in rat pancreatic acinar cells by simultaneou...

متن کامل

Up-regulation of plasma membrane H+-ATPase under salt stress may enable Aeluropus littoralis to cope with stress

Plasma membrane H+-ATPase is a major integral membrane protein with a role in various physiological processes including abiotic stress response. To study the effect of NaCl on the expression pattern of a gene encoding the plasma membrane H+-ATPase, an experiment was carried out in a completely random design with three replications. A pair of specific primers was designed based on the sequence o...

متن کامل

Heavy metal regulation of plasma membrane H+-ATPase gene expression in halophyte Aeluropus littoralis

The present study was conducted to find the effect of three heavy metals, Ag, Hg and Pb on the expression level of a gene encoding plasma membrane H+-ATPase in Aeluropus littoralis. The experiment was laid out in a completely random design with three replications. The expression of the main gene was normalized to the expression of the housekeeping gene actin. Two 259 and 187 bp fragments were a...

متن کامل

Calcium regulation in tissue-cultured human and bovine lens epithelial cells.

PURPOSE To study calcium regulatory mechanisms in lens cells with particular reference to the relative contributions from the calcium adenosine triphosphatase of plasma and endoplasmic reticulum membranes, respectively. METHODS The calcium-sensitive fluorescent dye, Fura 2, was incorporated into tissue-cultured human and bovine epithelial cells and internal calcium was calibrated using the io...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:

دوره 2  شماره 

صفحات  -

تاریخ انتشار 2008