Transgenic mice with neuron-specific overexpression of HtrA2/Omi suggest a neuroprotective role for HtrA2/Omi

Ming Jie Liu, Meng Lu Liu, Yan Fei Shen, Jin Man Kim, Byung Ho Lee, Youn Sik Lee, Seong Tshool Hong

Research output: Contribution to journalArticle

26 Scopus citations

Abstract

Mammalian serine protease HtrA2/Omi has been known as an apoptosis inducer involved inactivation of caspase-dependent as well as caspase-independent cell death. Recent studies with the HtrA2/Omi mutant and knockout mouse models, however, suggested that HtrA2/Omi might play a protective role in neurons. It is important to establish a transgenic mouse model with neuron-specific overexpression of HtrA2/Omi to clarify the physiological function of mammalian HtrA2/Omi in neurons. In the present study, a transgene containing HtrA2/Omi cDNA downstream of a rat neuron-specific enolase promoter was constructed and microinjected into the pronuclei of fertilized zygotes to establish transgenic mice. Transgenic mice successfully overexpressed HtrA2/Omi in brain tissue. As expected, HtrA2/Omi-overexpressing transgenic mice showed normal development without any sign of apoptotic cell death. Our results suggest that the primary function of neuronal HtrA2/Omi might be to protect neurons against stress in contrast to its role in the somatic system.

Original languageEnglish (US)
Pages (from-to)295-300
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume362
Issue number2
DOIs
StatePublished - Oct 19 2007

Keywords

  • Apoptosis
  • HtrA2/Omi
  • Neuron-specific enolase promoter
  • Neuroprotection
  • Overexpression
  • Transgenic mice

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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