The Joseph Rowntree Charitable Trust: A Study in Quaker Philanthropy and Adult Education 1904-1954

(A) Neurite formation in SY5Y cells in response to 13cRA. Representative phase contrast images depicting extension of neurites in response to 13cRA treatment after 6 days and 10 days. Long neurites were observed when cells were treated with 13cRA. (B) Statistical analysis of neurite outgrowth following 13cRA treatment in SY5Y cells. Length of neurites from three to five representative fields of 13cRA treated cells were measured in μm and compared with neurites from untreated cells. Neurites were measured (μm-micrometer) from at least three independent experiments, and p-values were calculated by one-way ANOVA using Prism followed by Tukey’s post-test. (DOC 208 kb

Additional file 4: Figure S4 of Retinoic acid-induced CHD5 upregulation and neuronal differentiation of neuroblastoma

(A) Detection of neurites in NB69 cells in response to retinoic acid. Representative phase contrast images of NB69 cells showing long neurites upon 13cRA treatment for 6 and 10 days. (B) Statistical analysis of various neurites upon 13cRA treatment in NB69 cells. Length of neurites from various selected fields were measured in μm and compared with neurites from untreated cells. Neurites were measured (μm-micrometer) from at least three independent experiments and p-values were calculated by one-way ANOVA using Prism followed by Tukey’s post-test. (DOC 296 kb

Additional file 2: Figure S2. of Retinoic acid-induced CHD5 upregulation and neuronal differentiation of neuroblastoma

Effect of 13cRA on cell proliferation by SRB assay. SY5Y and NB69 cells were plated on 96 well plates and treated with or without 10 ΟM retinoic acid. Plates were harvested after 2, 5, and 7 days of 13cRA treatment. Cell viability was analyzed by an SRB assay measuring optical density (OD). Cell lines treated with 13cRA showed lower OD, indicating reduced cell number compared to untreated control cells. (DOC 46 kb

Additional file 5: Figure S5. of Retinoic acid-induced CHD5 upregulation and neuronal differentiation of neuroblastoma

(A) Neurite inhibition by CEP-701 in SY5Y-TrkA cells. Representative phase contrast images of SY5Y-TrkA cells depicting extension of neurites in response to 13cRA treatment after 4 days, and subsequent neurite inhibition following 100 nM CEP-701 treatment (μm-micrometer) (B) Statistical analysis of neurite outgrowth following 13cRA as well as CEP-701 treatment of SY5Y-TrkA cells. Length of neurites (μm-micrometer) from three to five representative fields of 13cRA and CEP-701 treated cells were measured in μm and compared with neurites from untreated cells. P-values were calculated by one-way ANOVA using Prism followed by Tukey’s post-test. (DOC 148 kb

Additional file 6: Table S1. of Retinoic acid-induced CHD5 upregulation and neuronal differentiation of neuroblastoma

Nucleotide sequences of primers used in this study (DOCX 15 kb

Developmental regulation of DUOX1 expression and function in human fetal lung epithelial cells.

The purpose of this study was to determine the expression and cellular functions of the epithelial NADPH oxidase DUOX1 during alveolar type II cell development. When human fetal lung cells (gestational age 11-22 wk) were cultured to confluency on permeable filters, exposure of cells to a hormone mixture (dexamethasone, 8-Br-cAMP, and IBMX, together referred to as DCI) resulted in differentiation of cells into a mature type II phenotype as assessed by expression of lamellar bodies, surfactant proteins, and transepithelial electrical parameters. After 6 days in culture in presence of DCI, transepithelial resistance (2,616 +/- 529 Omega.cm(2)) and potential (-8.5 +/- 0.6 mV) indicated epithelial polarization. At the same time, treatment with DCI significantly increased the mRNA expression of DUOX1 ( approximately 21-fold), its maturation factor DUOXA1 ( approximately 12-fold), as well as DUOX protein ( approximately 12-fold), which was localized near the apical cell pole in confluent cultures. For comparison, in fetal lung specimens, DUOX protein was not detectable at up to 27 wk of gestational age but was strongly upregulated after 32 wk. Function of DUOX1 was assessed by measuring H(2)O(2) and acid production. Rates of H(2)O(2) production were increased by DCI treatment and blocked by small interfering RNA directed against DUOX1 or by diphenylene iodonium. DCI-treated cultures also showed increased intracellular acid production and acid release into the mucosal medium, and acid production was largely blocked by knockdown of DUOX1 mRNA. These data establish the regulated expression of DUOX1 during alveolar maturation, and indicate DUOX1 in alveolar H(2)O(2) and acid secretion by differentiated type II cells.Journal ArticleResearch Support, N.I.H. ExtramuralResearch Support, Non-U.S. Gov'tSCOPUS: ar.jinfo:eu-repo/semantics/publishe