| Project/Area Number |
16H06639
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Tohoku University |
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Principal Investigator |
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| Project Period (FY) |
2016-08-26 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | sickle cell disease / Nrf2 / Keap1 knockout / Myeloid cells / endothelial cells / Sickle cell disease / Nrf2 activation / Oxidative stress / Specific activation / oxidative stress |
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| Outline of Final Research Achievements |
Our research project was aimed to understand the mechanisms of specific-cell response to the activation of Nrf2 and how they contribute to the amelioration of the sickle cell disease (SCD) phenotype. We studied the function of Nrf2 in myeloid and endothelial cells and it influence to the surrounding organs by using mutant mice harboring the globin mutation, Keap1 deletion in either myeloid cells (SCD::Keap1F/F::LysM-Cre mice) or endothelial cells (SCD::Keap1F/F::Tie1-Cre mice). We collected peritoneal macrophages and cultured primary pulmonary endothelial cells for the cell specificity experiments; and some tissues we collected and to perform histological and hematological analysis; biochemistry; IMS and LC-mass; and genes expression (using PCR and RNA- sequencing). All the results are summarized in the manuscript that we submitted to Blood Advances journal for publication which is currently under revision.
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