Parthenolide (PTL) is a natural product from the shoots of Tanacetum parthenium, which has immunomodulatory effects in multiply type of diseases. This study aimed to explore the effect and the underlying mechanism of PTL on the anti-apoptotic and anti- inflammatory ability of tweak-induced podocytes. Conditionally immortalized mouse podocytes were incubated with Tumor necrosis factor-like weak inducer of apoptosis (Tweak, 100 ng/ml), PTL(10 µM) or Tweak + PTL for 12 h, 24 and 48 h, respectively. Podocytes viability was detected by CCK-8 assay. Tweak and Cxcl16 expression were evaluated by western blot and immunofluorescence assay. Dil-oxLDL stain was detected by immunofluorescence analysis. Intracellular Total Cholesterol (TC) content was measured through TC detection Kit. These results demonstrated that the podocytes cells viability was gradually decreased after treatment with different concentrations of Tweak (0, 50, 100, 150). Tweak and Cxcl16 protein expression in mouse podocytes treated with tweak were remarkably elevated and were found to have higher intracellular lipid accumulation compared with the control group, whereas co-administration with PTL, tweak and Cxcl16 expression as well as the intracellular lipid accumulation were notablely decreased in tweak-induced podocytes. Therefore, our conclusion was that tweak and Cxcl16 were involved in the regulation of tweak-induced podocytes injury. Meanwhile, the anti-apoptotic and anti-inflammatory effect of PTL may be correlated with the tweak and Cxcl16 expression decreased.
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http://dx.doi.org/10.1007/s11033-020-05591-4 | DOI Listing |
J Autoimmun
February 2024
Department of Biomedical Engineering, University of Houston, Houston, TX, USA. Electronic address:
Objective: To identify urinary biomarkers that can distinguish active renal involvement in Lupus Nephritis (LN), a severe manifestation of systemic lupus erythematosus (SLE).
Methods: Urine from 117 subjects, comprised of inactive SLE, active non-renal lupus, active LN, and healthy controls, were subjected to Proximity Extension Assay (PEA) based comprehensive proteomics followed by ELISA validation in an independent, ethnically diverse cohort. Proteomic data is also cross-referenced to renal transcriptomic data to elucidate cellular origins of biomarkers.
Int J Mol Sci
January 2022
Taipei Heart Institute, Taipei Medical University, Taipei 11031, Taiwan.
Myocardial infarction (MI) is a multifactorial global disease, recognized as one of the leading causes of cardiovascular morbidity and mortality. Timely and correct diagnoses and effective treatments could significantly reduce incidence of complications and improve patient prognoses. In this study, seven unconventional differentially expressed genes (DEGs) (MAN2A2, TNFRSF12A, SPP1, CSNK1D, PLAUR, PFKFB3, and CXCL16, collectively termed the MTSCPPC signature) were identified through integrating DEGs from six MI microarray datasets.
View Article and Find Full Text PDFMol Biol Rep
July 2020
Department of Pediatric Nephrology and Rheumatism and Immunology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, People's Republic of China.
Parthenolide (PTL) is a natural product from the shoots of Tanacetum parthenium, which has immunomodulatory effects in multiply type of diseases. This study aimed to explore the effect and the underlying mechanism of PTL on the anti-apoptotic and anti- inflammatory ability of tweak-induced podocytes. Conditionally immortalized mouse podocytes were incubated with Tumor necrosis factor-like weak inducer of apoptosis (Tweak, 100 ng/ml), PTL(10 µM) or Tweak + PTL for 12 h, 24 and 48 h, respectively.
View Article and Find Full Text PDFCurr Opin Nephrol Hypertens
January 2014
aIIS-Fundación Jiménez Díaz bREDinREN cUniversidad Autonoma de Madrid dIRSIN, Madrid, Spain.
Purpose Of Review: The tumor necrosis factor-like weak inducer of apoptosis (TWEAK) cytokine has been linked to kidney injury by functional studies in experimental animals, and has biomarker potential in kidney disease.
Recent Findings: TWEAK was known to promote tubular cell injury and kidney inflammation. Recent studies have expanded these observations, identifying additional targets of TWEAK relevant to kidney injury.
Nefrologia
December 2013
IIS-Fundación Jiménez Díaz, Universidad Autónoma de Madrid and Fundación Renal Iñigo Álvarez de Toledo. Madrid, Spain.
There are no pathophysiolgical therapeutic approaches to acute kidney injury (AKI) and the mortality remains high. In addition chronic kidney disease (CKD) predisposes to AKI and AKI contributes to progression of CKD. Recently a transcriptomics approach unveiled a relationship between AKI, inflammation and the regulation of ageing.
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