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hei oc1 cells (Dojindo Labs)

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Dojindo Labs hei oc1 cells
Hei Oc1 Cells, supplied by Dojindo Labs, used in various techniques. Bioz Stars score: 99/100, based on 59887 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/hei+oc1+cells/Cell+Counting+Kit-8/10__1097_slash_cm9__0000000000003633-101-5-14
Average 99 stars, based on 59887 article reviews

hei oc1 cells - by Bioz Stars, 2026-09

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CCK-8 Assay:

Article Title: New application of ombuoside in protecting auditory cells from cisplatin-induced ototoxicity via the apoptosis pathway
Article Snippet: .. The viability of HEI-OC1 cells after drug treatment was measured using the cell counting kit-8 (CCK-8) assay according to the manufacturer's instructions (CK04, Dojindo Laboratories). ..

Article Title: Profiles of oxidative stress-related microRNA and mRNA expression in auditory cells.
Article Snippet: Article history: Accepted 20 May 2010 Available online 26 May 2010 Oxidative stress and high levels of reactive oxygen species (ROS) are risk factors of auditory cell injury and hearing impairment.. MicroRNAs (miRNAs) are critical for the posttranscriptional regulation of gene expression and cell proliferation and survival.. However, little is known about the impact of oxidative stress on the expression of miRNAs and their targetedmRNAs in auditory cells.We employed a cell model of oxidative stress by treatment of House Ear Institute-Organ of Corti 1 (HEI-OC1) cells with different concentrations of tertbutyl hydroperoxide (t-BHP) to examine the t-BHP-induced production of ROS and to determine the impact of t-BHP treatment on the relative levels of miRNA and mRNA transcripts in HEI-OC1 cells.

Article Title: MLL1 downregulation drives hair cell ferroptosis via mitochondrial and endoplasmic reticulum stress mechanisms through PERK–eIF2α–Atf4–Chop and PI3K/Akt–Lrp1 signaling pathway
Article Snippet: .. To assess the viability of HEI-OC1 cells, a cell counting kit-8 (CCK-8) kit (CK04; Dojindo Molecular Technologies, Inc.) was used. ..

Incubation:

Article Title: Epac1 Signaling Pathway Mediates the Damage and Apoptosis of Inner Ear Hair Cells after Noise Exposure in a Rat Model.
Article Snippet: To investigate the role of the exchange protein directly activated by cAMP (Epac) signaling pathway in inner ear hair cell damage and apoptosis after noise exposure, we analyzed the expression level of Epac1 in a rat model of noise-induced hearing loss (NIHL), based on rat exposure to a 4-kHz and 106-dB sound pressure level (SPL) for 8 h. Loss of outer hair cells (OHCs), mitochondrial lesions, and hearing loss were examined after treatment with the Epac agonist, 8-CPT, or the Epac inhibitor, ESI-09.. The effects of 8-CPT and ESI-09 on cell proliferation and apoptosis were examined by CCK-8 assays, holographic microscopy imaging, and Annexin-V FITC/PI staining in HEI-OC1 cells.. The effects of 8-CPT and ESI-09 on Ca entry were evaluated by confocal Ca fluorescence measurement.

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Construction of mimetic aging mouse and cell models with D-gal. (A) Experimental protocol for D-gal-induced mimetic aging mice. (B) Statistical analysis of the click ABR between the control group and the D-gal group ( n = 5). (C) Statistical analysis of tone burst ABR in different frequencies between the control group and the D-gal group ( n = 5). (D) Immunofluorescence staining of the cochlear from the control mice and the D-gal mice with Myosin7a (green), Phalloidin (red) and DAPI (blue). (E) Quantification of OHCs in the control group and the D-gal group ( n = 4). (F) Experimental protocol for D-gal-induced mimetic aging cells. (G) CCK-8 assay results for HEI-OC1 cells after 72-h treatment with different concentrations of D-gal ( n = 3). (H) Quantification of the mtDNA CD levels in the control group and the D-gal group ( n = 4). (I) Flow cytometric analysis of apoptosis in the control group and the D-gal group. (J) Quantification of apoptotic cells in the control group and the D-gal group ( n = 3). (K) Quantification of dead cells in the control group and the D-gal group ( n = 3). (L) Flow cytometric analysis of ROS in the control group and the D-gal group. (M) Quantification of ROS levels in the control group and the D-gal group ( n = 4). (N) TEM results of structural changes in cells from the control group and the D-gal group (Red arrows: mitochondrial pathology, Blue arrows: chromatin condensation, Yellow arrows: cytoplasmic accumulation). Control cells received an equal volume of saline. NS, not significant, * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Frontiers in Molecular Neuroscience

Article Title: The H3K9me2-FOXG1-microRNA axis reduces cochlear hair cells damage by modulating autophagy in age-related hearing loss

doi: 10.3389/fnmol.2026.1834102

Figure Lengend Snippet: Construction of mimetic aging mouse and cell models with D-gal. (A) Experimental protocol for D-gal-induced mimetic aging mice. (B) Statistical analysis of the click ABR between the control group and the D-gal group ( n = 5). (C) Statistical analysis of tone burst ABR in different frequencies between the control group and the D-gal group ( n = 5). (D) Immunofluorescence staining of the cochlear from the control mice and the D-gal mice with Myosin7a (green), Phalloidin (red) and DAPI (blue). (E) Quantification of OHCs in the control group and the D-gal group ( n = 4). (F) Experimental protocol for D-gal-induced mimetic aging cells. (G) CCK-8 assay results for HEI-OC1 cells after 72-h treatment with different concentrations of D-gal ( n = 3). (H) Quantification of the mtDNA CD levels in the control group and the D-gal group ( n = 4). (I) Flow cytometric analysis of apoptosis in the control group and the D-gal group. (J) Quantification of apoptotic cells in the control group and the D-gal group ( n = 3). (K) Quantification of dead cells in the control group and the D-gal group ( n = 3). (L) Flow cytometric analysis of ROS in the control group and the D-gal group. (M) Quantification of ROS levels in the control group and the D-gal group ( n = 4). (N) TEM results of structural changes in cells from the control group and the D-gal group (Red arrows: mitochondrial pathology, Blue arrows: chromatin condensation, Yellow arrows: cytoplasmic accumulation). Control cells received an equal volume of saline. NS, not significant, * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: HEI-OC1 cells from the control, D-gal, and D-gal combined with si-FOXG1 groups were collected for untargeted metabolomic profiling (Novogene, Beijing, China), with three independent replicates per group.

Techniques: Control, Immunofluorescence, Staining, CCK-8 Assay, Saline

Changes in FOXG1, H3K9me2, and autophagy levels following D-gal treatment. (A) Western blot of FOXG1 and LC3 expression levels in the cochlear of the control mice and the D-gal mice. D-gal (200 mg/kg/day) was administered via subcutaneous injection for 8 weeks. (B) Quantitative analysis of the FOXG1 levels in (A) ( n = 3). (C) Quantitative analysis of the LC3-II levels in (A) ( n = 3). (D) Immunofluorescence staining of the cochlear from the control mice and the D-gal mice with anti-FOXG1 (red), Phalloidin (green) and DAPI (blue). (E) Quantification of FOXG1 expression in (D) ( n = 3). (F) Immunofluorescence staining of the cochlear from the control mice and the D-gal mice with anti-H3K9me2 (green), Phalloidin (red) and DAPI (blue). (G) Immunofluorescence staining of the cochlear from the control mice and the D-gal mice with anti-LC3B (green), Phalloidin (red) and DAPI (blue). (H) Quantification of H3K9me2 expression in (F) ( n = 3). (I) Quantification of LC3B expression in (G) ( n = 3). (J) Western blot of FOXG1 and H3K9me2 expression levels in the HEI-OC1 cells after 72-h treatment with different concentrations of D-gal. (K) Quantitative analysis of the FOXG1 levels in (J) ( n = 3). (L) Quantitative analysis of the H3K9me2 levels in (J) ( n = 3). (M) Western blot of LC3 expression levels in the HEI-OC1 cells after 72-h treatment with different concentrations of D-gal. (N) Quantitative analysis of the LC3-II levels in (M) ( n = 3). NS, not significant, * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Frontiers in Molecular Neuroscience

Article Title: The H3K9me2-FOXG1-microRNA axis reduces cochlear hair cells damage by modulating autophagy in age-related hearing loss

doi: 10.3389/fnmol.2026.1834102

Figure Lengend Snippet: Changes in FOXG1, H3K9me2, and autophagy levels following D-gal treatment. (A) Western blot of FOXG1 and LC3 expression levels in the cochlear of the control mice and the D-gal mice. D-gal (200 mg/kg/day) was administered via subcutaneous injection for 8 weeks. (B) Quantitative analysis of the FOXG1 levels in (A) ( n = 3). (C) Quantitative analysis of the LC3-II levels in (A) ( n = 3). (D) Immunofluorescence staining of the cochlear from the control mice and the D-gal mice with anti-FOXG1 (red), Phalloidin (green) and DAPI (blue). (E) Quantification of FOXG1 expression in (D) ( n = 3). (F) Immunofluorescence staining of the cochlear from the control mice and the D-gal mice with anti-H3K9me2 (green), Phalloidin (red) and DAPI (blue). (G) Immunofluorescence staining of the cochlear from the control mice and the D-gal mice with anti-LC3B (green), Phalloidin (red) and DAPI (blue). (H) Quantification of H3K9me2 expression in (F) ( n = 3). (I) Quantification of LC3B expression in (G) ( n = 3). (J) Western blot of FOXG1 and H3K9me2 expression levels in the HEI-OC1 cells after 72-h treatment with different concentrations of D-gal. (K) Quantitative analysis of the FOXG1 levels in (J) ( n = 3). (L) Quantitative analysis of the H3K9me2 levels in (J) ( n = 3). (M) Western blot of LC3 expression levels in the HEI-OC1 cells after 72-h treatment with different concentrations of D-gal. (N) Quantitative analysis of the LC3-II levels in (M) ( n = 3). NS, not significant, * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques: Western Blot, Expressing, Control, Injection, Immunofluorescence, Staining

H3K9me2 may regulate autophagy through FOXG1. (A) Western blot of G9a and H3K9me2 expression levels in the HEI-OC1 cells after 24-h treatment with different concentrations of BIX01294. (B) Quantitative analysis of the G9a levels in (A) ( n = 3). (C) Quantitative analysis of the H3K9me2 levels in (A) ( n = 3). (D) Western blot of FOXG1 and LC3 expression levels in the HEI-OC1 cells after 24-h treatment with different concentrations of BIX01294. (E) Quantitative analysis of the FOXG1 levels in (D) ( n = 3). (F) Quantitative analysis of the LC3-II levels in (D) ( n = 3). (G) Western blot of H3K9me2, FOXG1 and LC3 expression levels in the HEI-OC1 cells following D-gal and BIX01294 treatment. (H) Quantitative analysis of the H3K9me2 levels in G ( n = 4). (I) Quantitative analysis of the FOXG1 levels in (G) ( n = 4). (J) Quantitative analysis of the LC3-II levels in (G) ( n = 4). (K) Western blot of FOXG1 and LC3 expression levels in the HEI-OC1 cells following D-gal treatment and FOXG1 overexpression. (L) Quantitative analysis of the FOXG1 levels in (K) ( n = 3). (M) Quantitative analysis of the LC3-II levels in (K) ( n = 3). (N) Western blot of FOXG1 and LC3 expression levels in the HEI-OC1 cells following BIX01294 treatment and FOXG1 knockdown. (O) Quantitative analysis of the FOXG1 levels in (N) ( n = 3). (P) Quantitative analysis of the LC3-II levels in (N) ( n = 3). NS, not significant, * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Frontiers in Molecular Neuroscience

Article Title: The H3K9me2-FOXG1-microRNA axis reduces cochlear hair cells damage by modulating autophagy in age-related hearing loss

doi: 10.3389/fnmol.2026.1834102

Figure Lengend Snippet: H3K9me2 may regulate autophagy through FOXG1. (A) Western blot of G9a and H3K9me2 expression levels in the HEI-OC1 cells after 24-h treatment with different concentrations of BIX01294. (B) Quantitative analysis of the G9a levels in (A) ( n = 3). (C) Quantitative analysis of the H3K9me2 levels in (A) ( n = 3). (D) Western blot of FOXG1 and LC3 expression levels in the HEI-OC1 cells after 24-h treatment with different concentrations of BIX01294. (E) Quantitative analysis of the FOXG1 levels in (D) ( n = 3). (F) Quantitative analysis of the LC3-II levels in (D) ( n = 3). (G) Western blot of H3K9me2, FOXG1 and LC3 expression levels in the HEI-OC1 cells following D-gal and BIX01294 treatment. (H) Quantitative analysis of the H3K9me2 levels in G ( n = 4). (I) Quantitative analysis of the FOXG1 levels in (G) ( n = 4). (J) Quantitative analysis of the LC3-II levels in (G) ( n = 4). (K) Western blot of FOXG1 and LC3 expression levels in the HEI-OC1 cells following D-gal treatment and FOXG1 overexpression. (L) Quantitative analysis of the FOXG1 levels in (K) ( n = 3). (M) Quantitative analysis of the LC3-II levels in (K) ( n = 3). (N) Western blot of FOXG1 and LC3 expression levels in the HEI-OC1 cells following BIX01294 treatment and FOXG1 knockdown. (O) Quantitative analysis of the FOXG1 levels in (N) ( n = 3). (P) Quantitative analysis of the LC3-II levels in (N) ( n = 3). NS, not significant, * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques: Western Blot, Expressing, Over Expression, Knockdown

FOXG1-induced autophagy activation may be mediated by autophagy-related miRNAs. (A) Expression levels of miR-34a, miR-96, miR-182, and miR-183 in the cochlea of the control mice and the D-gal mice ( n = 3). (B) Expression levels of miR-34a, miR-96, miR-182, and miR-183 in the hippocampus of the control mice and the D-gal mice ( n = 3). (C) Expression levels of miR-34a, miR-96, miR-182, and miR-183 in the cortex of the control mice and the D-gal mice ( n = 3). (D) Expression levels of miR-34a, miR-96, miR-182, and miR-183 in the HEI-OC1 cells after knocking down FOXG1 ( n = 3). (E) Expression levels of miR-34a, miR-96, miR-182, and miR-183 in HEI-OC1 cells treated with D-gal after BIX01294 pretreatment or FOXG1 overexpression ( n = 3). (F) Western blot of LC3 expression levels in the HEI-OC1 cells following inhibition of miR-34a, miR-96, miR-182, and miR-183. (G) Quantitative analysis of the LC3-II levels in (F) ( n = 3). (H) Western blot of FOXG1 and LC3 expression levels in the HEI-OC1 cells treated with BIX01294 combined with miR-34a, miR-96, miR-182, and miR-183 inhibitors, respectively. (I) Quantitative analysis of the FOXG1 levels in (H) ( n = 3). (J) Quantitative analysis of the LC3-II levels in (H) ( n = 3). (K) Western blot of FOXG1 and LC3 expression levels in the HEI-OC1 cells treated with D-gal combined with miR-34a, miR-96, miR-182, and miR-183 mimics, respectively. (L) Quantitative analysis of the FOXG1 levels in (K) ( n = 4). (M) Quantitative analysis of the LC3-II levels in K ( n = 4). NS, not significant, * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Frontiers in Molecular Neuroscience

Article Title: The H3K9me2-FOXG1-microRNA axis reduces cochlear hair cells damage by modulating autophagy in age-related hearing loss

doi: 10.3389/fnmol.2026.1834102

Figure Lengend Snippet: FOXG1-induced autophagy activation may be mediated by autophagy-related miRNAs. (A) Expression levels of miR-34a, miR-96, miR-182, and miR-183 in the cochlea of the control mice and the D-gal mice ( n = 3). (B) Expression levels of miR-34a, miR-96, miR-182, and miR-183 in the hippocampus of the control mice and the D-gal mice ( n = 3). (C) Expression levels of miR-34a, miR-96, miR-182, and miR-183 in the cortex of the control mice and the D-gal mice ( n = 3). (D) Expression levels of miR-34a, miR-96, miR-182, and miR-183 in the HEI-OC1 cells after knocking down FOXG1 ( n = 3). (E) Expression levels of miR-34a, miR-96, miR-182, and miR-183 in HEI-OC1 cells treated with D-gal after BIX01294 pretreatment or FOXG1 overexpression ( n = 3). (F) Western blot of LC3 expression levels in the HEI-OC1 cells following inhibition of miR-34a, miR-96, miR-182, and miR-183. (G) Quantitative analysis of the LC3-II levels in (F) ( n = 3). (H) Western blot of FOXG1 and LC3 expression levels in the HEI-OC1 cells treated with BIX01294 combined with miR-34a, miR-96, miR-182, and miR-183 inhibitors, respectively. (I) Quantitative analysis of the FOXG1 levels in (H) ( n = 3). (J) Quantitative analysis of the LC3-II levels in (H) ( n = 3). (K) Western blot of FOXG1 and LC3 expression levels in the HEI-OC1 cells treated with D-gal combined with miR-34a, miR-96, miR-182, and miR-183 mimics, respectively. (L) Quantitative analysis of the FOXG1 levels in (K) ( n = 4). (M) Quantitative analysis of the LC3-II levels in K ( n = 4). NS, not significant, * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques: Activation Assay, Expressing, Control, Over Expression, Western Blot, Inhibition

Flow cytometric analysis of apoptosis and ROS levels in the HEI-OC1 cells following inhibition of miRNAs and D-gal treatment. (A) Flow cytometric analysis of apoptosis in the HEI-OC1 cells following inhibition of miR-34a, miR-96, miR-182, and miR-183, and combined with D-gal treatment. (B) Quantification of apoptotic cells in (A) ( n = 3). (C) Quantification of dead cells in (A) ( n = 3). (D) Flow cytometric analysis of ROS levels in the HEI-OC1 cells following inhibition of miR-34a, miR-96, miR-182, and miR-183, and combined with D-gal treatment. (E) Quantification of ROS levels in (D) ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Frontiers in Molecular Neuroscience

Article Title: The H3K9me2-FOXG1-microRNA axis reduces cochlear hair cells damage by modulating autophagy in age-related hearing loss

doi: 10.3389/fnmol.2026.1834102

Figure Lengend Snippet: Flow cytometric analysis of apoptosis and ROS levels in the HEI-OC1 cells following inhibition of miRNAs and D-gal treatment. (A) Flow cytometric analysis of apoptosis in the HEI-OC1 cells following inhibition of miR-34a, miR-96, miR-182, and miR-183, and combined with D-gal treatment. (B) Quantification of apoptotic cells in (A) ( n = 3). (C) Quantification of dead cells in (A) ( n = 3). (D) Flow cytometric analysis of ROS levels in the HEI-OC1 cells following inhibition of miR-34a, miR-96, miR-182, and miR-183, and combined with D-gal treatment. (E) Quantification of ROS levels in (D) ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques: Inhibition

Proteomics analysis of the aging mouse cochlear and the D-gal-induced aging cells. (A) PCA of proteomics data from the cochlear of control and aging mice. (B) Heatmap of DEPs between the control group and the aging group. (C) KEGG enrichment analysis of DEPs between the control group and the aging group. (D) Volcano plot of DEPs between the control group and the D-gal group in HEI-OC1 cells (Up-DEPs shown as red dots; down-DEPs shown as blue dots). (E) KEGG enrichment of upregulated DEPs in the D-gal group. (F) KEGG enrichment of downregulated DEPs in the D-gal group. (G) Volcano plot of DEPs between the control group and the si-FOXG1 group in HEI-OC1 cells (Up-DEPs shown as red dots; down-DEPs shown as blue dots). (H) KEGG enrichment of upregulated DEPs in the si-FOXG1 group. (I) KEGG enrichment of downregulated DEPs in the si-FOXG1 group. (J) KEGG enrichment analysis of the overlapping upregulated DEPs in both the D-gal group and the si-FOXG1 group. (K) KEGG enrichment analysis of the overlapping downregulated DEPs in both the D-gal group and the si-FOXG1 group. (L) Validation results for the top four overlapping upregulated (left four bars) and downregulated (right four bars) DEPs identified in both the D-gal group and the si-FOXG1 group by qRT-PCR ( n = 3). NS, not significant, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Frontiers in Molecular Neuroscience

Article Title: The H3K9me2-FOXG1-microRNA axis reduces cochlear hair cells damage by modulating autophagy in age-related hearing loss

doi: 10.3389/fnmol.2026.1834102

Figure Lengend Snippet: Proteomics analysis of the aging mouse cochlear and the D-gal-induced aging cells. (A) PCA of proteomics data from the cochlear of control and aging mice. (B) Heatmap of DEPs between the control group and the aging group. (C) KEGG enrichment analysis of DEPs between the control group and the aging group. (D) Volcano plot of DEPs between the control group and the D-gal group in HEI-OC1 cells (Up-DEPs shown as red dots; down-DEPs shown as blue dots). (E) KEGG enrichment of upregulated DEPs in the D-gal group. (F) KEGG enrichment of downregulated DEPs in the D-gal group. (G) Volcano plot of DEPs between the control group and the si-FOXG1 group in HEI-OC1 cells (Up-DEPs shown as red dots; down-DEPs shown as blue dots). (H) KEGG enrichment of upregulated DEPs in the si-FOXG1 group. (I) KEGG enrichment of downregulated DEPs in the si-FOXG1 group. (J) KEGG enrichment analysis of the overlapping upregulated DEPs in both the D-gal group and the si-FOXG1 group. (K) KEGG enrichment analysis of the overlapping downregulated DEPs in both the D-gal group and the si-FOXG1 group. (L) Validation results for the top four overlapping upregulated (left four bars) and downregulated (right four bars) DEPs identified in both the D-gal group and the si-FOXG1 group by qRT-PCR ( n = 3). NS, not significant, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Techniques: Control, Biomarker Discovery, Quantitative RT-PCR

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