Transgenic mice with neuron-specific overexpression of HtrA2/Omi suggest a neuroprotective role for HtrA2/Omi |
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Authors: | Liu Ming-Jie Liu Meng-Lu Shen Yan-Fei Kim Jin-Man Lee Byung-Ho Lee Youn-Sik Hong Seong-Tshool |
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Institution: | Laboratory of Genetics, Department of Microbiology and Immunology, Institute for Medical Science, Chonbuk National University Medical School, Chonju, Chonbuk 561-756, South Korea. |
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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. |
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Keywords: | Apoptosis HtrA2/Omi Neuroprotection Neuron-specific enolase promoter Overexpression Transgenic mice |
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