Na+/H+ exchanger-1 reduces podocyte injury caused by endoplasmic reticulum stress via autophagy activation

Feng, Zhe; Tang, Li; Wu, Lingling; Cui, Shaoyuan; Hong, Quan; Cai, Guangyan; Wu, Di; Fu, Bo; Wei, Ri-bao; Chen, Xiangmei

doi:10.1038/labinvest.2014.4

Cited by 15 publications

(12 citation statements)

References 41 publications

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“…In our study, we detected the immunohistochemical expression of SSTR2A in meningiomas with a sensitivity of 89%. This is comparable with the findings detected by Bacchi et al [ 18 ], Agaimy et al [ 19 ] and Menke et al [ 20 ] in their studies that showed sensitivities of 100%, 87% and 100 % respectively. Lower sensitivities of 74% and 63% were stated by Barresi et al [ 21 ] and Durand et al [ 22 ] respectively.…”

Section: Discussionsupporting

confidence: 92%

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Value of SSTR2A and Claudin - 1 in Differentiating Meningioma from Schwannoma and Hemangiopericytoma

Anis¹,

Lotfalla²,

Zain³

et al. 2018

Open Access Maced J Med Sci

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BACKGROUND:The distinction between meningioma, schwannoma and solitary fibrous tumour/ hemangiopericytoma can be challenging in some cases. This study evaluates the expression of Somatostatin receptor 2A (SSTR2A) and Claudin-1 in these different tumours.MATERIAL AND METHODS:Thirty-five cases of meningioma, 10 cases of intracranial schwannoma and 10 cases of hemangiopericytoma were assessed. The immunohistochemical expression of SSTR2A and Claudin-1 was evaluated and scored according to the percentage of immunostained tumour cells (0: 1+, 2+ and 3). The intensity of staining was classified as weak, moderate and strong.RESULTS:Positivity for SSTR2A and Claudin-1 was encountered in 89% and 49% of meningiomas respectively. None of the schwannomas or hemangiopericytomas was positive for any of both markers. All grade I and II meningiomas were positive for SSTR2A, and only 20% of grade III showed positive staining (p < 0.05). Claudin-1 positivity was detected in 50%, 43% and 60% of grade I, II and III meningioma respectively, with significantly higher intensity in grade III (p < 0.05).CONCLUSION:SSTR2A is highly sensitive and specific for meningioma. Claudin-1 is highly specific for meningioma, with low sensitivity. The adjunctive use of both markers can be very helpful in the diagnosis of meningioma and its distinction from schwannoma and hemangiopericytoma.

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Section: Discussionsupporting

confidence: 92%

“…This was statistically highly significant. Bacchi et al [ 18 ] and Menke et al [ 20 ] reported slightly lower specificities of 90% and 88% respectively.…”

Section: Discussionmentioning

confidence: 99%

Value of SSTR2A and Claudin - 1 in Differentiating Meningioma from Schwannoma and Hemangiopericytoma

Anis¹,

Lotfalla²,

Zain³

et al. 2018

Open Access Maced J Med Sci

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“…Sdf4 is a member of the stromal cell derived factor (SDFs) family and functionally classified as a chemokine; SDF-2, SDF-4 and SDF-5 are expressed in mammary tumor tissues and cells and a reduced level of SDF-2, SDF2-L1 and SDF-4 are associated with a poor clinical outcome [ 71 ]. Sodium/hydrogen exchanger 1 (Slc9a1 or NHE-1) is regulator of membrane permeability, sodium ion transport, apoptosis, cell differentiation and growth; it is suppressed during ER stress that causes epithelial injury [ 72 ]. The down-regulation of NHE-1 during chlamydial infection would indicate the induction of ER stress.…”

Section: Resultsmentioning

confidence: 99%

Role of Epithelial-Mesenchyme Transition in Chlamydia Pathogenesis

et al. 2015

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Chlamydia trachomatis genital infection in women causes serious adverse reproductive complications, and is a strong co-factor for human papilloma virus (HPV)-associated cervical epithelial carcinoma. We tested the hypothesis that Chlamydia induces epithelial-mesenchyme transition (EMT) involving T cell-derived TNF-alpha signaling, caspase activation, cleavage inactivation of dicer and dysregulation of micro-RNA (miRNA) in the reproductive epithelium; the pathologic process of EMT causes fibrosis and fertility-related epithelial dysfunction, and also provides the co-factor function for HPV-related cervical epithelial carcinoma. Using a combination of microarrays, immunohistochemistry and proteomics, we showed that chlamydia altered the expression of crucial miRNAs that control EMT, fibrosis and tumorigenesis; specifically, miR-15a, miR-29b, miR-382 and MiR-429 that maintain epithelial integrity were down-regulated, while miR-9, mi-R-19a, miR-22 and miR-205 that promote EMT, fibrosis and tumorigenesis were up-regulated. Chlamydia induced EMT in vitro and in vivo, marked by the suppression of normal epithelial cell markers especially E-cadherin but up-regulation of mesenchymal markers of pathological EMT, including T-cadherin, MMP9, and fibronectin. Also, Chlamydia upregulated pro-EMT regulators, including the zinc finger E-box binding homeobox protein, ZEB1, Snail1/2, and thrombospondin1 (Thbs1), but down-regulated anti-EMT and fertility promoting proteins (i.e., the major gap junction protein connexin 43 (Cx43), Mets1, Add1Scarb1 and MARCKSL1). T cell-derived TNF-alpha signaling was required for chlamydial-induced infertility and caspase inhibitors prevented both infertility and EMT. Thus, chlamydial-induced T cell-derived TNF-alpha activated caspases that inactivated dicer, causing alteration in the expression of reproductive epithelial miRNAs and induction of EMT. EMT causes epithelial malfunction, fibrosis, infertility, and the enhancement of tumorigenesis of HPV oncogene-transformed epithelial cells. These findings provide a novel understanding of the molecular pathogenesis of chlamydia-associated diseases, which may guide a rational prevention strategy.

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“…It has been demonstrated that in rats with puromycin aminonucleoside (PAN) nephropathy, the activation of the PI3K/Akt signaling inhibits podocyte apoptosis (20). Furthermore, it has been reported that Na + /H+ exchanger-1 (NHE-1) attenuates podocyte injury via the PI3K/Akt pathway by inducing the activation of autophagy (21). It is thus possible that the PI3K/Akt pathway may be involved in both apoptosis and autophagy during the process of podocyte injury.…”

Section: Introductionmentioning

confidence: 99%

Notoginsenoside R1 attenuates glucose-induced podocyte injury via the inhibition of apoptosis and the activation of autophagy through the PI3K/Akt/mTOR signaling pathway

Huang

Zou

et al. 2017

International Journal of Molecular Medicine

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Injury to terminally differentiated podocytes contributes ignificantly to proteinuria and glomerulosclerosis. The aim of this study was to examine the protective effects of notoginsenoside R1 (NR1) on the maintenance of podocyte number and foot process architecture via the inhibition of apoptosis, the induction of autophagy and the maintenance pf podocyte biology in target cells. The effects of NR1 on conditionally immortalized human podocytes under high glucose conditions were evaluated by determining the percentage apoptosis, the percentage autophagy and the expression levels of slit diaphragm proteins. Our results revealed that NR1 protected the podocytes against high glucose-induced injury by decreasing apoptosis, increasing autophagy and by promoting cytoskeletal recovery. The phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling pathway was further investigated in order to elucidate the mechanisms responsible for the protective effects of NR1 on podocytes. Our data indicated that treatment with NR increased the phosphorylation levels of PI3K, Akt and mTOR, leading to the activation of the PI3K/Akt/mTOR signaling pathway in podocytes. To the best of our knowledge, this is the first in vitro study to demonstrate that NR1 protects podocytes by activating the PI3K/Akt/mTOR pathway.

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Na+/H+ exchanger-1 reduces podocyte injury caused by endoplasmic reticulum stress via autophagy activation

Cited by 15 publications

References 41 publications

Value of SSTR2A and Claudin - 1 in Differentiating Meningioma from Schwannoma and Hemangiopericytoma

Value of SSTR2A and Claudin - 1 in Differentiating Meningioma from Schwannoma and Hemangiopericytoma

Role of Epithelial-Mesenchyme Transition in Chlamydia Pathogenesis

Notoginsenoside R1 attenuates glucose-induced podocyte injury via the inhibition of apoptosis and the activation of autophagy through the PI3K/Akt/mTOR signaling pathway

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