Abstract |
The role of two heat shock proteins, Hsp70 and Hsp90α, on stress response in mice with severe diabetes mellitus induced by a high dose of alloxan (500 mg/kg body weight), as well as in RIN-m5F β cells cultured in the presence of cytokines (IL-1 and TNF-α) was studied. Our results showed that severe type 1 diabetes mellitus (T1D) caused a higher expression of Hsp90α, but not Hsp70. Moreover, injections of the peroxiredoxin 6 antioxidant enzyme (PRDX6) did not affect the expression of these chaperones. Conversely, pro-inflammatory cytokines added to β-cells caused a significant increase in the expression of Hsp90α and, substantially, Hsp70. Moreover, cells cultivated in the presence of PRDX6 were more susceptible to the cytokine effect. Thus, in the course of severe alloxan-induced T1D, no protective role of the heat shock proteins, was revealed, and their expression level was not increased by PRDX6. At the same time the protective potential of these proteins was shown in vitro with the use of RIN-m5F β cells. Thus, the system of heat shock proteins was unable to prevent the devastating effects of severe T1D accompanied by high animal mortality.
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Authors | E G Novoselova, O V Glushkova, M O Khrenov, S B Parfenyuk, S M Lunin, T V Novoselova, E E Fesenko |
Journal | Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections
(Dokl Biol Sci)
Vol. 493
Issue 1
Pg. 124-127
(Jul 2020)
ISSN: 1608-3105 [Electronic] United States |
PMID | 32894426
(Publication Type: Journal Article)
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Chemical References |
- HSP70 Heat-Shock Proteins
- HSP90 Heat-Shock Proteins
- Hspca protein, mouse
- Peroxiredoxin VI
- Prdx6 protein, mouse
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Topics |
- Animals
- Diabetes Mellitus, Experimental
(metabolism)
- Diabetes Mellitus, Type 1
(metabolism, pathology)
- HSP70 Heat-Shock Proteins
(metabolism)
- HSP90 Heat-Shock Proteins
(metabolism)
- Insulin-Secreting Cells
(metabolism)
- Mice, Inbred BALB C
- Peroxiredoxin VI
(metabolism)
- Rats
- Spleen
(metabolism, pathology)
- Stress, Physiological
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