scholarly journals CDKN2B-AS1 participates in high glucose-induced apoptosis and fibrosis via NOTCH2 through functioning as a miR-98-5p decoy in human podocytes and renal tubular cells

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Min Xiao ◽  
Shoujun Bai ◽  
Jing Chen ◽  
Yaxi Li ◽  
Shu Zhang ◽  
...  
Keyword(s):  
High Glucose ◽  
Kinase Inhibitor ◽  
Luciferase Reporter ◽  
Tubular Cells ◽  
Protein Levels ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Induced Apoptosis ◽  
Stage Renal Disease ◽  
End Stage

Abstract Background Diabetic nephropathy (DN) is the most common causes of end-stage renal disease. Long non-coding RNA cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) is connected with the development of DN, but the role of CDKN2B-AS1 in DN has not been entirely elucidated. Methods Quantitative real-time polymerase chain reaction (qRT-PCR) was carried out to measure CDKN2B-AS1 and miR-98-5p levels. Cell viability, proliferation, and apoptosis were analyzed with 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) or flow cytometry assays. Protein levels were measured by western blotting. The relationship between CDKN2B-AS1 or notch homolog 2 (NOTCH2) and miR-98-5p was verified via dual-luciferase reporter assay. Results CDKN2B-AS1 and NOTCH2 were upregulated in the serum of DN patients and high glucose-disposed human podocytes (HPCs) and human renal tubular cells (HK-2), whereas miR-98-5p was downregulated. High glucose repressed viability and accelerated apoptosis of HPCs and HK-2 cells. CDKN2B-AS1 knockdown impaired high glucose-induced apoptosis and fibrosis of HPCs and HK-2 cells. Mechanistically, CDKN2B-AS1 sponged miR-98-5p to regulate NOTCH2 expression. Also, CDKN2B-AS1 inhibition-mediated effects on apoptosis and fibrosis of high glucose-disposed HPCs and HK-2 cells were weakened by miR-98-5p inhibitor. Also, NOTCH2 knockdown partly reversed miR-98-5p inhibitor-mediated impacts on apoptosis and fibrosis of high glucose-disposed HPCs and HK-2 cells. Conclusion High glucose-induced CDKN2B-AS1 promoted apoptosis and fibrosis via the TGF-β1 signaling mediated by the miR-98-5p/NOTCH2 axis in HPCs and HK-2 cells.

scholarly journals Prostaglandin E1 attenuates high glucose-induced apoptosis in proximal renal tubular cells by inhibiting the JNK/Bim pathway

2019 ◽  
Vol 41 (4) ◽  
pp. 561-571 ◽  
Author(s):  
Yu-han Zhang ◽  
Ya-qin Zhang ◽  
Cong-cong Guo ◽  
Li-kang Wang ◽  
Yu-jiao Cui ◽  
...  
Keyword(s):  
High Glucose ◽  
Prostaglandin E1 ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Induced Apoptosis

SIRT1: Mechanism and Protective in Diabetic Nephropathy

2020 ◽  
Vol 20 ◽  
Author(s):  
Jing Ji ◽  
Pengyu Tao ◽  
Qian Wang ◽  
Lingxing Li ◽  
Yuzhen Xu
Keyword(s):  
Diabetic Nephropathy ◽  
Cellular Response ◽  
Symptomatic Relief ◽  
Kidney Injury ◽  
Protective Mechanism ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Stage Renal Disease ◽  
End Stage

: Diabetic nephropathy (DN) is referred to as the microvascular complication of the kidneys induced by insufficient production of insulin or an ineffective cellular response to insulin, and is the main cause of end-stage renal disease. Currently, available therapies provide only symptomatic relief and fail to improve the outcome of diabetic nephropathy. Studies on diabetic animals had shown overexpression of SIRT1 in both podocytes and renal tubular cells attenuated proteinuria and kidney injury in animal model of DN. Sirt1 exerts renoprotective effects in DKD in part through the deacetylation of transcription factors involved in the disease pathogenesis, such as NF-кB, Smad3, FOXO and p53. The purpose of this review is to highlight the protective mechanism of SIRT1 involved in the pathogenesis of diabetic nephropathy.

Transcriptome alterations in high glucose-induced renal tubular cells of bactrian camel

2020 ◽  
Vol 27 (3) ◽  
pp. 301-304
Author(s):  
Bin Yang ◽  
Lihui Chen ◽  
Xin Li ◽  
Zhuwei Guo ◽  
Shi Liu ◽  
...  
Keyword(s):  
High Glucose ◽  
Bactrian Camel ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular

Correction: Arg tyrosine kinase modulates TGF-β1 production in human renal tubular cells under high-glucose conditions (doi:10.1242/jcs.183640)

2019 ◽  
Vol 132 (19) ◽  
pp. jcs238832
Author(s):  
Barbara Torsello ◽  
Cristina Bianchi ◽  
Chiara Meregalli ◽  
Vitalba Di Stefano ◽  
Lara Invernizzi ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
High Glucose ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Arg Tyrosine Kinase ◽  
Renal Tubular ◽  
Tgf Β1

Naproxen-induced Ca2+ movement and death in MDCK canine renal tubular cells

2015 ◽  
Vol 34 (11) ◽  
pp. 1096-1105
Author(s):  
H-H Cheng ◽  
C-T Chou ◽  
T-K Sun ◽  
W-Z Liang ◽  
J-S Cheng ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Annexin V ◽  
Dependent Manner ◽  
Acetoxymethyl Ester ◽  
Concentration Dependent Manner ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Induced Apoptosis ◽  
Darby Canine Kidney

Naproxen is an anti-inflammatory drug that affects cellular calcium ion (Ca2+) homeostasis and viability in different cells. This study explored the effect of naproxen on [Ca2+]i and viability in Madin-Darby canine kidney cells (MDCK) canine renal tubular cells. At concentrations between 50 μM and 300 μM, naproxen induced [Ca2+]i rises in a concentration-dependent manner. This Ca2+ signal was reduced partly when extracellular Ca2+ was removed. The Ca2+ signal was inhibited by a Ca2+ channel blocker nifedipine but not by store-operated Ca2+ channel inhibitors (econazole and SKF96365), a protein kinase C (PKC) activator phorbol 12-myristate 13-acetate, and a PKC inhibitor GF109203X. In Ca2+-free medium, pretreatment with 2,5-di-tert-butylhydroquinone or thapsigargin, an inhibitor of endoplasmic reticulum Ca2+ pumps, partly inhibited naproxen-induced Ca2+ signal. Inhibition of phospholipase C with U73122 did not alter naproxen-evoked [Ca2+]i rises. At concentrations between 15 μM and 30 μM, naproxen killed cells in a concentration-dependent manner, which was not reversed by prechelating cytosolic Ca2+ with the acetoxymethyl ester of 1,2-bis(2-aminophenoxy)ethane- N, N, N′, N′-tetraacetic acid acetoxymethyl. Annexin V/propidium iodide staining data suggest that naproxen induced apoptosis. Together, in MDCK renal tubular cells, naproxen induced [Ca2+]i rises by inducing Ca2+ release from multiple stores that included the endoplasmic reticulum and Ca2+ entry via nifedipine-sensitive Ca2+ channels. Naproxen induced cell death that involved apoptosis.

The protective effect of prostacyclin on adriamycin-induced apoptosis in rat renal tubular cells

2006 ◽  
Vol 529 (1-3) ◽  
pp. 8-15 ◽  
Author(s):  
Cheng-Hsien Chen ◽  
Heng Lin ◽  
Yung-Ho Hsu ◽  
Yuh-Mou Sue ◽  
Tzu-Hurng Cheng ◽  
...  
Keyword(s):  
Protective Effect ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Induced Apoptosis
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