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| Author(s): |
Wilson Mitsuo Tatagiba Kuwabara
Total Authors: 1
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| Document type: | Master's Dissertation |
| Press: | São Paulo. |
| Institution: | Universidade de São Paulo (USP). Instituto de Ciências Biomédicas (ICB/SDI) |
| Defense date: | 2013-09-18 |
| Examining board members: |
Tatiana Carolina Alba Loureiro;
Ana Campa;
Silvana Auxiliadora Bordin da Silva
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| Advisor: | Tatiana Carolina Alba Loureiro |
| Abstract | |
Endoplasmic reticulum (ER) has been gaining evidence when it comes to cell death. The accumulation of unfolded proteins initiates the activation of the Unfolded Protein Response (UPR). The UPR may resolve the ER stress by upregulating genes responsible to maintain the ER homeostasis; or it can activate genes that lead to the cell death when the ER disbalance is not solved. Hyperglycemia, one of many symptoms observed is Diabetes, may cause ER stress in various types of cells. Thus, this study aims to investigate the possible involvement of the ER stress in the process of cell death in neutrophils from diabetic rats. In summary, our study found that neutrophils from diabetic rats when stimulated with PMA exhibit greater susceptibility to death due to activation of IRE1a and subsequent phosphorylation of JNK, reduced safety in mitochondria-ER interaction in the MAM compartment and increased caspase-3 activation. Control group seems to be protect against the ER stress by ROS production by higher expression of GRP78 and MAM proteins. (AU) | |
| FAPESP's process: | 10/12818-0 - The role of ER stress in cell death of neutrophils from diabetic rats |
| Grantee: | Wilson Mitsuo Tatagiba Kuwabara |
| Support Opportunities: | Scholarships in Brazil - Master |