Journal: Cancers

Article Title: A Double-Negative Feedback Interaction between miR-21 and PPAR-α in Clear Renal Cell Carcinoma

doi: 10.3390/cancers14030795

Figure Lengend Snippet: miR-21 and PPAR-α expressions in HK-2 and renal cancer cell lines before confluence (BC) and two days after confluence (C + 2). ( A ) Using RT-qPCR, miR-21 expression was determined in the 786-O, ACHN, RCC10, and RCC4 renal cancer cells as compared to normal HK-2 renal epithelial cells. RNU48 was used as an internal control. The values are means ± SEM and represent at least three separate experiments (* p < 0.05, ** p < 0.01, and *** p < 0.001). ( B ) Western blotting was performed on whole cell extracts. Antibodies against PPAR-α and β-actin were used.

Article Snippet: The HK-2 human proximal tubule epithelial cell line, ACHN, and 786-O human renal cancer cell lines were purchased from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Quantitative RT-PCR, Expressing, Control, Western Blot

Journal: Methods in cell biology

Article Title: Analysis of primary cilia in renal tissue and cells

doi: 10.1016/bs.mcb.2019.04.008

Figure Lengend Snippet: Immortalized and primary renal epithelial cells.

Article Snippet: The balance between cilia assembly and disassembly regulates cilia length ( Mirvis, Stearns, & James Nelson, 2018 ; Spalluto, Wilson, & Hearn, 2013 ). table ft1 table-wrap mode="anchored" t5 caption a7 Cell line Description Source References M-1 Murine cortical collecting duct epithelial cells ATCC Stoos et al. (1991) IMCD-3 Murine inner medullary collecting duct epithelial cells ATCC Rauchman et al. (1993) LLC-PK1 Porcine proximal tubule epithelial cells ATCC Nielsen et al. (1998) MDCK Madin-Darby canine kidney epithelial cells ATCC Gaush et al. (1966) NHK/ADPKD Primary cortical epithelial cells from normal human kidney (NHK) or Autosomal Dominant PKD (ADPKD) KUMC Graham et al. (1977) and Reif et al. (2011) Open in a separate window Immortalized and primary renal epithelial cells. table ft1 table-wrap mode="anchored" t5 caption a7 Antibody Company Cilia structure References Acetylated-α-tubulin Sigma-Aldrich Axoneme Ishikawa et al. (2012) , Seixas et al. (2015) , Silva et al. (2018) , and Yu, Sharma, Skowronek, and Erdmann (2016) γ-tubulin Sigma-Aldrich Centrioles Breslow et al. (2013) Pericentrin Covance Centrioles Ishikawa et al. (2012) ARL13B Proteintech Ciliary membrane Seixas et al. (2015) INPP5E Proteintech Ciliary membrane Plotnikova et al. (2015) IFT52 Proteintech Axoneme Silva et al. (2018) IFT81 Proteintech Axoneme Silva et al. (2018) IFT88 Proteintech Axoneme Silva et al. (2018) IFT140 Proteintech Axoneme Silva et al. (2018) BBS2 Proteintech Axoneme Silva et al. (2018) BBS5 Proteintech Axoneme Silva et al. (2018) Open in a separate window Markers of primary cilia.

Techniques:

Journal: bioRxiv

Article Title: Development of high-affinity, single-domain protein binders for neutralizing household allergens

doi: 10.1101/2025.08.03.668213

Figure Lengend Snippet: (a) Thermostability profile of AVA-1-1-C3 as a representative protein, as determined by differential scanning fluorimetry. (b-g) Cytotoxicity of primary human cells following 48-hour exposure to AVA-1-1-C3 or an equivalent concentration of bovine serum albumin (BSA), evaluated using the CellTiter-Glo® (CTG) luminescent cell viability assay. Cell types included human epithelial keratinocytes (HEK, b), human dermal fibroblasts (HDF, c), human follicle dermal papilla cells (HFDPC, d), human renal cortical epithelial cells (HRCEPC, e), human skeletal muscle cells (HSKMC, f), and human dermal microvascular endothelial cells (HDMEC, g). No significant differences in cell viability were observed. Data in (b-g) represents mean ± s.d. and are representative of two experimental replicates.

Article Snippet: For in vitro toxicity studies, primary cells including human dermal fibroblasts (HDF, Cell Applications, Cat# 106K-05a, lot 1632), human epidermal keratinocytes (HEK, Cell Applications, Cat# 102-05a, lot 2146), human dermal microvascular endothelial cells (HDMEC, PromoCell, Cat# C-12210, lot 483Z001.3), human skeletal muscle cells (HSKMC, Cell Applications, Cat# 150K-05a, lot 3507), and human renal cortical epithelial cells (HRCEpC, Promocell, Cat# C-12660, lot 501Z019.23).

Techniques: Concentration Assay, Cell Viability Assay

Journal: Experimental and Therapeutic Medicine

Article Title: High lncRNA MEG3 expression is associated with high mortality rates in patients with sepsis and increased lipopolysaccharide-induced renal epithelial cell and cardiomyocyte apoptosis

doi: 10.3892/etm.2019.8049

Figure Lengend Snippet: LncRNA MEG3 regulates renal epithelial cell and cardiomyocyte apoptosis following LPS treatment. LncRNA MEG3 overexpression and knockdown were confirmed. Following LPS treatment, LncRNA MEG3 overexpression resulted in significantly increased apoptosis, whereas lncRNA MEG3 knockdown by siRNA significantly inhibited apoptosis in (A) renal epithelial cells and (B) AC12 cardiomyocytes. *P<0.05. LncRNA, long non-coding RNA; MEG3, maternally expressed 3; LPS, lipopolysaccharide.

Article Snippet: Human primary renal mixed epithelial cells (ATCC ® PCS-400-012TM) were purchased from American Type Culture Collection.

Techniques: Over Expression, Knockdown

Journal: PLoS Pathogens

Article Title: NK Cell Activation in Human Hantavirus Infection Explained by Virus-Induced IL-15/IL15Rα Expression

doi: 10.1371/journal.ppat.1004521

Figure Lengend Snippet: (A) Representative FACS analysis of CD69 expression on CD56 dim NK cells after 24 h incubation with HTNV particles (black), IL-15 (grey) or medium (white). (B) Expression level (MFI) of CD69 on CD56 dim NK cells (n = 6) treated as indicated. (C–F) CD69 and CD38 expression on CD56 dim NK cells after contact with uninfected and HTNV-infected endothelial (C and D) or epithelial (E and F) cells. (C and E) Expression of CD69 and CD38 on CD56 dim NK cells incubated with medium (grey), uninfected endothelial or epithelial cells (white) and HTNV-infected endothelial or epithelial cells (black). Representative FACS plots are depicted. (D and F) Summary of CD69 and CD38 expression (MFI) on CD56 dim NK cells incubated in the indicated conditions. CD69 (n = 17) and CD38 (n = 5). TW (transwell). (*** p≤0.001, ** p≤0.01, paired t -test).

Article Snippet: Primary human endothelial cells (HUVEC) and renal epithelial cells (Lonza) were grown according to the manufacturer's instructions using EGM-2 BulletKit and REGM BulletKit, respectively.

Techniques: Expressing, Incubation, Infection

Journal: PLoS Pathogens

Article Title: NK Cell Activation in Human Hantavirus Infection Explained by Virus-Induced IL-15/IL15Rα Expression

doi: 10.1371/journal.ppat.1004521

Figure Lengend Snippet: (A and B) Kinetics of IL-15 and IL-15Rα mRNA-expression in HTNV-infected endothelial (A) and epithelial (B) cells analyzed with RT-qPCR. Fold change compared to the expression level in the respective uninfected cell is depicted. Results of one experiment run in triplicates are shown. (C and D) Expression of IL-15 and IL-15Rα protein in uninfected and HTNV-infected endothelial cells analyzed with flow cytometry after cell permeabilization. (C) One representative FACS analysis is shown. Uninfected cells (white), HTNV-infected cells (black) and isotype control (grey). (D) The expression levels (MFI) of IL-15 and IL-15Rα protein in uninfected (white) or HTNV-infected (black) endothelial cells (n = 3). (E–H) Surface expression of IL-15 and IL-15Rα on uninfected and HTNV-infected endothelial (E and F) and epithelial (G and H). (E and G) Representative FACS analysis of the surface expression of IL-15 and IL-15Rα on uninfected and HTNV-infected endothelial cells and epithelial cells. Uninfected cells (white), HTNV-infected cells (black) and isotype (grey). (F and H) The expression levels (MFI) of IL-15 and IL-15Rα on uninfected (white) or HTNV-infected (black) endothelial (n = 4) and epithelial cells (n = 4) are shown. (I–L) CD69 expression on CD56 dim NK cells after co-incubation with HTNV-infected endothelial cells (I and J) and epithelial cells (K and L) in the presence of anti-IL-15 or isotype control antibody. (I and K) Representative FACS analysis of CD69 expression on CD56 dim NK cells incubated with endothelial cells (I) and epithelial cells (K) in the presence of isotype control (black) or anti-IL-15 antibody (grey). (J and L) Expression levels (MFI) of CD69 on CD56 dim NK cells after co-incubation with endothelial cells (n = 8) (J) and epithelial cells (n = 6) (L). The dashed lines represent upper and lower SEM intervals for means of CD69 expression on CD56 dim NK cells after incubation with the respective uninfected cells.

Article Snippet: Primary human endothelial cells (HUVEC) and renal epithelial cells (Lonza) were grown according to the manufacturer's instructions using EGM-2 BulletKit and REGM BulletKit, respectively.

Techniques: Expressing, Infection, Quantitative RT-PCR, Flow Cytometry, Control, Incubation

Journal: PLoS Pathogens

Article Title: NK Cell Activation in Human Hantavirus Infection Explained by Virus-Induced IL-15/IL15Rα Expression

doi: 10.1371/journal.ppat.1004521

Figure Lengend Snippet: (A–C) Degranulation (CD107a) and intracellular cytokine production of CD56 dim NK cells reacting to K562 cells after pre-stimulation with uninfected or HTNV-infected endothelial and epithelial cells. (A) Representative FACS analysis of CD107a, IFN-γ and TNF expression in one NK cell donor is shown. (B and C) Summary of the CD56 dim NK cell responses against K562 cells (n = 9) after pre-stimulation with uninfected (white) or HTNV-infected (black) endothelial (B) and epithelial cells (C). (*** p≤0.001, ** p≤0.01; paired t -test). (D) NK cell-mediated specific lysis of K562 cells after pre-stimulation of NK cells with uninfected (white) and HTNV-infected (black) endothelial cells. Depicted are mean values (+/− SD) from 5 donors and 2 independent experiments (** p≤0.01, *p≤0.05; paired t -test).

Article Snippet: Primary human endothelial cells (HUVEC) and renal epithelial cells (Lonza) were grown according to the manufacturer's instructions using EGM-2 BulletKit and REGM BulletKit, respectively.

Techniques: Infection, Expressing, Lysis

Journal: BMC Nephrology

Article Title: A low-dose pemetrexed-cisplatin combination regimen induces significant nephrotoxicity in mice

doi: 10.1186/s12882-024-03822-5

Figure Lengend Snippet: Pemetrexed-cisplatin combination induced renal epithelial cell apoptosis. A : Live-cell images of fluorogenic caspase 3/7 DNA dye and B-D : mean data showing apoptotic cell counts at different concentrations in primary mouse renal epithelial cells treated with pemetrexed or cisplatin alone and pemetrexed-cisplatin combination. Control, captisol; PEME, pemetrexed, CIS, cisplatin. n = 6 wells each; * P < 0.05 vs. Control; # P < 0.05 vs. PEME and CIS

Article Snippet: Mouse primary renal epithelial cells were purchased from Cell Biologics Inc (C57-6034; Chicago, IL).

Techniques: Control