Tubule-specific deletion of LincRNA-p21 ameliorates lipotoxic kidney injury

Li, Bin; Leung, Joseph C.K.; Chan, Loretta Y.Y.; Li, Hongyu; Yiu, Wai Han; Lok, Sarah W Y; Xue, Rui; Zou, Yixin; Chen, Wei; Lai, Kar‐Neng; Tang, Sydney C. W.

doi:10.1016/j.omtn.2021.10.029

Cited by 5 publications

(3 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To confirm the action of EUP on renal tubular injury, we stained kidneys with an anti-NGAL antibody. NGAL is widely used as renal tubular injury marker because it is produced in renal tubular epithelial cells and increases rapidly after tubular injury [ 30 , 31 ]. The percentage of NGAL-stained area increased after LPS injection, whereas EUP decreased renal NGAL expression in LPS-treated mice ( Figure 3 A,B).…”

Section: Resultsmentioning

confidence: 99%

“…EUP also decreased the renal expression of NGAL and KIM-1. NGAL is a member of the lipocalin protein family and its expression is robustly increased in renal tubular epithelial cells following kidney injury [ 30 , 31 ]. KIM-1 is a type 1 transmembrane protein, whose expression is also strongly increased on injured renal tubular epithelial cells [ 45 ].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Eupatilin Ameliorates Lipopolysaccharide-Induced Acute Kidney Injury by Inhibiting Inflammation, Oxidative Stress, and Apoptosis in Mice

Kim,

Hong,

Kim

et al. 2023

CIMB

View full text Add to dashboard Cite

Acute kidney injury (AKI) is a common complication of sepsis. Eupatilin (EUP) is a natural flavone with multiple biological activities and has beneficial effects against various inflammatory disorders. However, whether EUP has a favorable effect on septic AKI remains unknown. Here, we examined the effect of EUP on lipopolysaccharide (LPS)-evoked AKI in mice. LPS-evoked renal dysfunction was attenuated by EUP, as reflected by reductions in serum creatinine and blood urea nitrogen levels. LPS injection also induced structural damage such as tubular cell detachment, tubular dilatation, brush border loss of proximal tubules, and upregulation of tubular injury markers. However, EUP significantly ameliorated this structural damage. EUP decreased serum and renal cytokine levels, prevented macrophage infiltration, and inhibited mitogen-activated protein kinase and NF-κB signaling cascades. Lipid peroxidation and DNA oxidation were increased after LPS treatment. However, EUP mitigated LPS-evoked oxidative stress through downregulation of NPDPH oxidase 4 and upregulation of antioxidant enzymes. EUP also inhibited p53-mediated apoptosis in LPS-treated mice. Therefore, these results suggest that EUP ameliorates LPS-evoked AKI through inhibiting inflammation, oxidative stress, and apoptosis.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Eupatilin Ameliorates Lipopolysaccharide-Induced Acute Kidney Injury by Inhibiting Inflammation, Oxidative Stress, and Apoptosis in Mice

Kim,

Hong,

Kim

et al. 2023

CIMB

View full text Add to dashboard Cite

show abstract

“…Down-regulation of lincRNA-p21 has been shown to alleviate extracellular matrix induced by high glucose and plays an important role in diabetic nephropathy [12]. Deletion of lincRNA-p21 in renal tubular epithelial cells has been found to attenuate kidney injury caused by persistent obesity and hyperlipidemia through in ammation, apoptosis, and endoplasmic reticulum stress [13]. Spurlock et al have con rmed that administration of methotrexate upregulates the expression of lincRNA-p21 and inhibits the activity of NF-κB [14].…”

Section: Introductionmentioning

confidence: 99%

Exosomal lincRNA-p21/AIF-1 promoted inflammation of human tubular epithelial cell via CMPK2/NLRP3 pathway in urate nephropathy

Hao,

Guo,

Wang

et al. 2024

Preprint

View full text Add to dashboard Cite

Background and hypothesis Urate nephropathy, a common complication of hyperuricemia, has garnered increasing attention worldwide. However, the exact pathogenesis of this condition remains unclear. Currently, inflammation is widely accepted as the key factor in urate nephropathy. Therefore, the aim of this study was to elucidate the mechanism of exosomal lincRNA-p21/AIF-1 in urate nephropathy. Methods This study evaluated the effects of exosomes using clinical data collected from patients with urate nephropathy and human renal tubular epithelial cells (HK2) cultured with different concentrations of urate. Results In the clinical research section, the level of exosomal lincRNA-p21/AIF-1 in the urine of patients with hyperuricemia or urate nephropathy was found to be increased, particularly in patients with urate nephropathy. In vitro study section, the levels of exosomes, inflammation, autophagy, and apoptosis were increased in HK2 cells induced by urate. Additionally, the expressions of lincRNA-p21, AIF-1, CMPK2, and NLRP3 were upregulated in exosomes and HK2 cells. Furthermore, manipulating the activity of lincRNA-p21, AIF-1, CMPK2, and NLRP3 through overexpression or interference vectors promoted inflammation, autophagy, and apoptosis in HK2 cells induced by urate. Conclusions: In conclusion, the aforementioned results suggested that exosomal lincRNA-p21/AIF-1 induces inflammation via the CMPK2/NLRP3 pathway, thereby promoting autophagy and apoptosis in renal tubular epithelial cells induced by urate.

show abstract

PGC1-α in diabetic kidney disease: unraveling renoprotection and molecular mechanisms

Ye,

Zhang,

Tang

et al. 2024

Mol Biol Rep

View full text Add to dashboard Cite

Tubule-specific deletion of LincRNA-p21 ameliorates lipotoxic kidney injury

Cited by 5 publications

References 39 publications

Eupatilin Ameliorates Lipopolysaccharide-Induced Acute Kidney Injury by Inhibiting Inflammation, Oxidative Stress, and Apoptosis in Mice

Eupatilin Ameliorates Lipopolysaccharide-Induced Acute Kidney Injury by Inhibiting Inflammation, Oxidative Stress, and Apoptosis in Mice

Exosomal lincRNA-p21/AIF-1 promoted inflammation of human tubular epithelial cell via CMPK2/NLRP3 pathway in urate nephropathy

PGC1-α in diabetic kidney disease: unraveling renoprotection and molecular mechanisms

Contact Info

Product

Resources

About