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

Ming Yang1, Li Zhao2, Peng Gao1

  • 1Department of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.

Ebiomedicine
|May 8, 2019
PubMed
Abstract

Insights

Disulphide-bond A oxidoreductase-like protein (DsbA-L) maintains mitochondrial-ER membrane (MAM) integrity, preventing kidney injury in diabetic nephropathy. Loss of DsbA-L exacerbates apoptosis and renal damage in this condition.

Area of Science:

  • Cell Biology
  • Mitochondrial-ER interactions
  • Kidney Pathobiology

Background:

  • The mitochondrial-associated endoplasmic reticulum (ER) membrane (MAM) is crucial for cell communication and function.
  • Disulphide-bond A oxidoreductase-like protein (DsbA-L) acts as an antioxidant within the MAM, mitigating ER stress.
  • The specific roles of DsbA-L and MAM in kidney disease, particularly diabetic nephropathy, are not fully understood.

Purpose of the Study:

  • To investigate the role of DsbA-L and MAM integrity in the context of diabetic nephropathy (DN).
  • To determine if DsbA-L influences apoptosis and renal injury in DN.
  • To elucidate the therapeutic potential of DsbA-L in preserving kidney function.

Main Methods:

  • Utilized DsbA-L mutant mice and streptozotocin-induced diabetes model.
  • Employed molecular biology techniques, transmission electron microscopy (TEM), and confocal microscopy.
  • Assessed apoptosis using TUNEL staining and flow cytometry; evaluated MAM integrity via in situ proximity ligation assays (PLAs).

Main Results:

  • MAM integrity was significantly reduced in diabetic mouse kidneys, correlating with renal injury.
  • Loss of MAM integrity was linked to increased apoptosis and renal damage in diabetic nephropathy (DN).
  • DsbA-L deficiency exacerbated these detrimental effects; DsbA-L overexpression in HK-2 cells restored MAM integrity and reduced high-glucose-induced apoptosis.

Conclusions:

  • DsbA-L plays a protective role by maintaining MAM integrity, thereby exerting an antiapoptotic effect.
  • Disruption of MAM integrity is a key feature of DN, and DsbA-L is a critical factor in its preservation.
  • Targeting DsbA-L may offer a therapeutic strategy for managing diabetic nephropathy.
Keywords:
ApoptosisDiabetic nephropathyDsbA-LMitochondrial associated endoplasmic reticulum membrane (MAM)Tubulointerstitial injury

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