PDIA6 ja beetasolusaareke. PubMed haku

 

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1

Exploration of shared gene signatures and molecular mechanisms between type 2 diabetes and osteoporosis.

Du A, Xu R, Yang Q, Lu Y, Luo X. J Cell Mol Med. 2024 May;28(9):e18141. doi: 10.1111/jcmm.18141. PMID: 38742851 Free PMC article.

The miRNA-mRNA network analysis revealed co-expression of PDIA6 and SLC16A1; their expression was upregulated in patients with T2D and islet beta-cell lines. Remarkably, PDIA6 and SLC16A1 were observed to inhibit the proliferation of pancreatic beta cells and promot …

2

A point mutation in the Pdia6 gene results in loss of pancreatic beta-cell identity causing overt diabetes.

Chhabra NF, Amend AL, Bastidas-Ponce A, Sabrautzki S, Tarquis-Medina M, Sachs S, Rubey M, Lorenz-Depiereux B, Feuchtinger A, Bakhti M, Lickert H, Przemeck GKH, Hrabě de Angelis M. Mol Metab. 2021 Dec;54:101334. doi: 10.1016/j.molmet.2021.101334. Epub 2021 Sep 4. PMID: 34487921 Free PMC article.

This study aimed to describe the consequences of a point mutation in Pdia6 on beta-cell development and function. METHODS: We generated an ENU mouse model carrying a missense mutation (Phe175Ser) in the second thioredoxin domain of the Pdia6 gene. ...CONCLUSIONS: Th …

3

Thapsigargin down-regulates protein levels of GRP78/BiP in INS-1E cells.

Rosengren V, Johansson H, Lehtiö J, Fransson L, Sjöholm A, Ortsäter H. J Cell Biochem. 2012 May;113(5):1635-44. doi: 10.1002/jcb.24032. PMID: 22189689

 

 We have observed an unexpected decrease in chaperone protein level in the β-cell model INS-1E after exposure to the ER stress inducing agent thapsigargin. As these cells are a commonly used model for primary β-cells and has been shown to be vulnerable to ER stress, we hypothesize these cells are incapable of mounting a chaperone defense upon activation of ER stress. To investigate the chaperone expression during an ER stress response, induced by thapsigargin in INS-1E cells, we used quantitative mass spectrometry based proteomics. 

The results displayed a decrease of GRP78/BiP, PDIA3 and PDIA6. Decrease of GRP78/BiP was verified by Western blot and occurred in parallel with enhanced levels of p-eIF2α and CHOP. 

In contrast to INS-1E cells, GRP78/BiP was not decreased in MIN6 cell or rat and mouse islets after thapsigargin exposure. Investigation of the decreased protein levels of GRP78/BiP indicates that this is not a consequence of reduced mRNA expression. Rather the reduction results from the combined effect of reduced protein synthesis and enhanced proteosomal degradation and possibly also degradation via autophagy. Induction of ER stress with thapsigargin leads to lower protein levels of GRP78/BiP, PDIA3 and PDIA6 in INS-1E cells which may contribute to the susceptibility of ER stress in this β-cell model.