human hepatocyte carcinoma hepg2 cells  (ATCC)

Journal: Biotechnology Reports

Article Title: Insulin Resistance, Anti-inflammatory, and Antioxidant In vitro Activity of Heterologously Expressed Arenin from Dryophytes arenicolor

doi: 10.1016/j.btre.2026.e00947

Figure Lengend Snippet: In vitro modulation of hepatic insulin resistance by arenin in hepatic insulin-resistant (HepG2) cells . Arenin concentrations (3.90–1000 µg/mL) were incubated for 5 h in hepatic insulin-resistant cells. Negative control (N) cells were cultured in the absence of insulin, whereas insulin-resistant (IR) control cells were cultured in the presence of insulin. Rosiglitazone (ROSI) at 10 μM (3.57 µg/mL) was used as the positive reference control. Different letters abc indicate statistical differences between concentrations analyzed using Tukey test ( p < 0.05).

Article Snippet: Human hepatocyte carcinoma (HepG2) cells, human primary dermal fibroblasts (HDFa) cells, and murine macrophage (RAW 264.7) cells were obtained from the American Type Culture Collection (ATCC, VA, USA).

Techniques: In Vitro, Incubation, Negative Control, Cell Culture, Control

Journal: bioRxiv

Article Title: On the role of cell chaining in the attenuation of a Listeria monocytogenes divIVA mutant

doi: 10.64898/2026.01.05.697648

Figure Lengend Snippet: (A) Contribution of divIVA , mreB and ezrA to hepatocyte invasion. Invasion of L. monocytogenes strains EGD-e (wt), BUG2214 (Δ prfA ), LMS2 (Δ divIVA ), LMSW49 (i mreB ) and LMJR183 (i ezrA ) pre-grown in the absence or presence of 1 mM IPTG into HepG2 hepatocytes. Values are expressed relative to wild type. Average values and standard deviations are shown. Asterisks mark statistically significant differences compared to wild type ( P <0.01, t -test with Bonferroni Holm correction). (B) Contribution of divIVA , mreB and ezrA to intracellular growth in macrophages. J774 mouse macrophages were infected with L. monocytogenes strains EGD-e (wt), LMS250 (Δ hly ), LMS2 (Δ divIVA ), LMSW49 (i mreB ) and LMJR183 (i ezrA ) and then cultivated in the absence or presence of IPTG, where appropriate. Average values and standard deviations were calculated from experiments performed in triplicates. Statistically significant differences (compared to wild type or between depleted and induced conditions) are marked by asterisks ( P <0.01, t -test with Bonferroni-Holm correction, n. s. – not significant). (C) Effect of DivIVA, MreB or EzrA depletion on cell-to-cell spread. Plaque formation assay using 3T3 mouse fibroblasts with L. monocyctogenes strains EGD-e (wt), LMS30 (i divIVA ), LMSW49 (i mreB ) and LMJR183 (i ezrA ) ± IPTG. (D) Necessity of DivIVA, MreB and EzrA for actin coating and actin tail formation. J774 mouse macrophages were infected with DsRed producing L. monocytogenes strains LMJD20 (wt), LMSF2 (Δ actA ), LMSW205 (Δ divIVA ), LMSW202 (EzrA depletion) and LMSW203 (MreB depletion). Infections were carried out in the absence of IPTG and analyzed by fluorescence microscopy 4 hours post infection after DAPI and phalloidin staining. Composite images are shown.

Article Snippet: Invasion of L. monocytogenes into HepG2 human hepatocytes (ATCC® HB-8065 TM ) was quantified as described earlier [ ].

Techniques: Infection, Plaque Formation Assay, Fluorescence, Microscopy, Staining

Journal: bioRxiv

Article Title: On the role of cell chaining in the attenuation of a Listeria monocytogenes divIVA mutant

doi: 10.64898/2026.01.05.697648

Figure Lengend Snippet: (A) The prfA* mutation suppresses the invasion defect of the Δ divIVA mutant. Invasion of L. monocytogenes strains EGD-e (wt), BUG2214 (Δ prfA ), BUG3057 ( prfA* ), LMS2 (Δ divIVA ) and LMSW251 (Δ divIVA prfA* ) into HepG2 hepatocytes. Values are expressed relative to wild type. Average values and standard deviations are shown. The asterisks mark statistically significant differences compared to wild type ( P <0.01, t -test with Bonferroni-Holm correction) or to the Δ divIVA prfA* mutant ( P <0.01, t -test, n. s. – not significant). (B) No suppression of the intracellular replication defect of the Δ divIVA mutant by the prfA* mutation. J774 mouse macrophages were infected with the same strains as in panel A. Average values and standard deviations were calculated from experiments performed in triplicates. No statistically significant difference in the number of intracellular bacteria was detected between Δ divIVA and Δ divIVA prfA* cells six hours post infection ( P <0.01, t -test, n. s. – not significant). (C) Dominance of the Δ divIVA deletion over the prfA* mutation in a plaque forming assay. The same strains as above were used to infect 3T3 mouse fibroblasts to analyze cell-to-cell spread.

Article Snippet: Invasion of L. monocytogenes into HepG2 human hepatocytes (ATCC® HB-8065 TM ) was quantified as described earlier [ ].

Techniques: Mutagenesis, Infection, Bacteria

Journal: bioRxiv

Article Title: On the role of cell chaining in the attenuation of a Listeria monocytogenes divIVA mutant

doi: 10.64898/2026.01.05.697648

Figure Lengend Snippet: (A) Localisation of Δ divIVA suppressor mutations M95I and T123A in the SecA2 protein. SecA2 domains (colored) and walker A and B motifs (black) are indicated. Abbreviations: NBD –nucleotide binding domain, PPXD – preprotein crosslinking domain, IRA 1/2 – intramolecular regulator of ATPase domains 1 and 2, SD – scaffold domain. (B) Micrographs showing the cellular morphology of L. monocytogenes strains EGD-e (wt), LMS2 (Δ divIVA ), LMSW222 (Δ divIVA secA2 M95I ) and LMSW223 (Δ divIVA secA2 T123A ) during growth in BHI broth at 37°C. Membranes were stained with nile red. Scale bar is 2 µm. (C) Separation of secretome samples of the same set of strains by SDS-PAGE. The position of p60 (CwhA) is indicated. (D) Flagellar motility of the same set of strains on swarming agar after two days of incubation at 30°C. (E) Cell-to-cell spread of the same strains in 3T3 mouse fibroblast. (F) Full suppression of the Δ divIVA invasion defect by secA2 mutations. The same set of strains as in panel A was used to infect HepG2 hepatocytes. Values are expressed relative to wild type. Average values and standard deviations are shown. The asterisk marks a statistically significant difference ( P <0.01, t -test with Bonferroni-Holm correction, n. s. – not significant). (G) Partial suppression of the intracellular replication defect of the Δ divIVA mutant by secA2 mutations. J774 mouse macrophages were infected with the same strains as above and intracellular bacteria were enumerated right after infection (0 h p. i.) and six hours later (6 h p. i.). Average values and standard deviations were calculated from experiments performed in triplicates. Statistically significant differences are indicated by asterisks ( P <0.01, t -test with Bonferroni-Holm correction).

Article Snippet: Invasion of L. monocytogenes into HepG2 human hepatocytes (ATCC® HB-8065 TM ) was quantified as described earlier [ ].

Techniques: Binding Assay, Staining, SDS Page, Incubation, Mutagenesis, Infection, Bacteria