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DsbA-L ameliorates high glucose induced tubular damage through maintaining MAM integrity.

Abstract：

BACKGROUND:The mitochondrial associated endoplasmic reticulum (ER) membrane (MAM) provides a platform for communication between the mitochondria and ER, and it plays a vital role in many biological functions. Disulphide-bond A oxidoreductase-like protein (DsbA-L), expressed in the MAM, serves as an antioxidant and reduces ER stress. However, the role of DsbA-L and MAM in kidney pathobiology remains unclear. METHODS:Molecular biology techniques, transmission electron microscopy (TEM), in situ proximity ligation assays (PLAs), confocal microscopy, TUNEL staining and flow cytometry were utilized to analyse apoptosis and status of MAM in DsbA-L mutant mice. FINDINGS:We showed that MAM was significantly reduced in the kidneys of streptozotocin-induced diabetic mice, which correlated with the extent of renal injury. We also observed a correlation between the loss of MAM integrity and increased apoptosis and renal injury in diabetic nephropathy (DN). These alterations were further exacerbated in diabetic DsbA-L gene-deficient mice (DsbA-L-/-). In vitro, overexpression of DsbA-L in HK-2 cells restored MAM integrity and reduced apoptosis induced by high-glucose ambience. These beneficial effects were partially blocked by overexpression of FATE-1, a MAM uncoupling protein. Finally, the expression of DsbA-L was positively correlated with MAM integrity in the kidneys of DN patients but negatively correlated with apoptosis and renal injury. INTERPRETATION:Our results indicate that DsbA-L exerts an antiapoptotic effect by maintaining MAM integrity, which is apparently disrupted in DN. FUND: This work was supported by the National Natural Science Foundation of China (81730018), the National Key R&D Program of China (2016YFC1305501) and NIH (DK60635).

journal_name

EBioMedicine

journal_title

EBioMedicine

authors

Yang M,Zhao L,Gao P,Zhu X,Han Y,Chen X,Li L,Xiao Y,Wei L,Li C,Xiao L,Yuan S,Liu F,Dong LQ,Kanwar YS,Sun L

doi

10.1016/j.ebiom.2019.04.044

subject

Has Abstract

pub_date

2019-05-01 00:00:00

pages

607-619

issn

2352-3964

pii

S2352-3964(19)30283-X

journal_volume

43

pub_type

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