SERCA2 deficiency on tubular epithelial cell promotes acute kidney injury by regulating ER-mitochondria crosstalk via VDAC

 

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SERCA2 deficiency on tubular epithelial cell promotes acute kidney injury by regulating ER-mitochondria crosstalk via VDAC

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Zhangzhe
Peng
Xin He xin_he0101@163.com Central South University Department of Nephrology, Xiangya Hospital Changsha China -
Yanyun Xie xieyanyun@csu.edu.cn Central South University Department of Nephrology, Xiangya Hospital Changsha China -
Lijian Tao taolj@csu.edu.cn Central South University Department of Nephrology, Xiangya Hospital Changsha China -
Zhangzhe Peng pengzhangzhe@csu.edu.cn Central South University Department of Nephrology, Xiangya Hospital Changsha China *
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Acute renal injury (AKI) is a serious medical condition characterized by a rapid loss of renal function. Sarcoplasmic/endoplasmic reticulum calcium ATPase 2 (SERCA2) is a critical enzyme located in the sarcoplasmic reticulum (SR) and endoplasmic reticulum (ER) to maintain calcium homeostasis by transporting Ca2+ from the cytoplasm to the SR and ER. While the relationship between SERCA2 and the occurrence and development of AKI and its regulatory mechanism remain unclear. 

Renal proximal tubule-specific ATP2a2 gene-knockdown mice (ATP2a2tKD) and control mice (ATP2a2fl/wt) were used to determine its function and potential mechanisms in AKI. AKI models were established by ischemia/reperfusion injury (IRI) and lipopolysaccharide (LPS) injection. Endoplasmic reticulum (ER) and mitochondria function were assessed by Transmission electron microscopy (TEM), Western blot and RT‒PCR. Intracellular and mitochondrial Calcium Ion were detected by Fluo-4 AM and Rhod-2 AM, separately. 

Compared with minimal change disease (MCD) patients, SERCA2 was significantly decreased in proximal tubules of kidneys from AKI patients. Similar observations were also obtained from kidneys of AKI models induced by IRI and LPS. Conditional knockdown of SERCA2 in tubular epithelial cells worsened renal function and caused more tubular injury in AKI induced by IRI and LPS. TEM images and Western blot showed that SERCA2 deficiency aggravated ER stress, mitochondria dysfunction and calcium overloading in primary renal tubular epithelial cells. Mechanically, SERCA2 directly binds to voltage-Dependent Anion Channel (VDAC), thereby regulating calcium homeostasis and ER-mitochondria crosstalk in renal tubule epithelial cells.(a) Immunofluorescence of SERCA2 (green) in proximal tubules (LTL, red) of kidney sections from AKI patients and minimal change disease (MCD) patients. (b) Immunofluorescence of SERCA2 (green) in proximal tubules (LTL, red) of kidney sections from control (Ctrl) and AKI mouse models (200×, scale bar = 100 μm). (c) Relative mRNA expression of ATP2a2 in control (Ctrl) and AKI mouse kidney samples. (d) Western blot analysis of SERCA2 and neutrophil gelatinase-associated lipocalin (NGAL) expression in kidney from Sham and IRI-induced AKI mice. (e) Western blot analysis of SERCA2 and NGAL expression in kidney from Ctrl and lipopolysaccharide (LPS)-induced AKI mice.(a) Representative images of hematoxylin and eosin (HE) staining of kidney sections from control mice (ATP2a2fl/wt) and SERCA2 conditional knockdown mice (ATP2a2tKD) induced by IRI. (b) Tubular injury scores of kidney tissues. (c, d) Serum creatinine (SCr) and blood urea nitrogen (BUN) levels of ATP2a2fl/wt and ATP2a2tKD mice induced by IRI. (e) Western blot analysis and of SERCA2 and NGAL expression in kidney from kidney samples from ATP2a2fl/wt and ATP2a2tKD mice induced by IRI. (f) Representative images of HE staining of kidney sections from ATP2a2fl/wt and ATP2a2tKD mice induced by LPS. (g) Tubular injury scores of kidney tissues. (h, i) SCr and BUN levels of ATP2a2fl/wt and ATP2a2tKD mice induced by LPS. (j) Western blot analysis of SERCA2 and NGAL expression in kidney from TP2a2fl/wt and ATP2a2tKD mice induced by LPS.

Our results revealed that SERCA2 may play a protective role in AKI by regulating ER-mitochondria crosstalk and calcium homeostasis, thereby identifying a novel and important therapeutic target for AKI.

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