Microarray Analysis and Biochemical Correlations of Oxidative Stress Responsive Genes in Retinoblastoma

Vandhana, Suryanarayanan; Lakshmi, Thiagavathi Selvaraj Ramyaa; Indra, Dharmu; Deepa, Perinkulam Ravi; Krishnakumar, Subramanian

doi:10.3109/02713683.2012.678544

Cited by 14 publications

(7 citation statements)

References 37 publications

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“…The mechanisms underlying the increase of JAKs and STATs expression under choline deficiency are unknown but might be partially related to the increased reactive oxygen species (ROS). In human retinoblastoma cells, H 2 O 2 , one important ROS induced the expression of JAK3 and STAT4 genes [47]. Our unpublished data showed that choline deficiency increased the ROS levels in the intestine of Jian carp, which supported the hypothesis.…”

Section: Choline Deficiency Induced Inflammation and Regulated Nf-κb And Stat Signaling Molecules In The Intestine Of The Fishsupporting

confidence: 71%

Dietary choline deficiency and excess induced intestinal inflammation and alteration of intestinal tight junction protein transcription potentially by modulating NF-κB, STAT and p38 MAPK signaling molecules in juvenile Jian carp

Jiang

et al. 2016

Fish & Shellfish Immunology

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This study investigated the effects of choline on intestinal mucosal immune and the possible mechanisms in fish by feeding juvenile Jian carp (Cyprinus carpio var. Jian) with graded levels of dietary choline (165-1820 mg/kg diet) for 65 days. The results firstly showed that choline deficiency induced inflammatory infiltration in the proximal intestine (PI), mid intestine (MI) and distal intestine (DI) of fish. Meanwhile, compared with the optimal choline group, choline deficiency decreased the activities of lysozyme and acid phosphatase, contents of complement 3 and IgM in the intestine, downregulated the mRNA levels of antimicrobial peptides (liver-expressed antimicrobial peptide (LEAP) 2A and defensin-3 in the PI and MI, LEAP-2B and hepcidin in the PI, MI and DI), anti-inflammatory cytokines (interleukin (IL) 10 and transforming growth factor β2 in the PI, MI and DI), and signaling molecule IκB in the PI, MI and DI; while upregulated the mRNA levels of pro-inflammatory cytokines (IL-6a and tumor necrosis factor α in the MI and DI, interferon γ2b in the PI and MI, IL-1β and IL-6b in the PI, MI and DI), and signaling molecules (Toll-like receptor 4 in the MI, myeloid differentiation primary response 88 in the PI and MI, Janus kinase 3 and tyrosine kinase 2 in the MI and DI, nuclear factor kappa B (NF-κB), signal transducers and activators of transcription (STAT) 4 and STAT5 in the PI, MI and DI) of juvenile Jian carp, further indicating that choline deficiency caused inflammation and immunity depression in the intestine of fish. But choline deficiency decreased the PI IL-6a mRNA level, and increased the DI LEAP-2A and defensin-3 mRNA levels with unknown reasons. Furthermore, dietary choline deficiency downregulated mRNA levels of tight junction (TJ) proteins (claudin 3c in the PI and MI, claudin 7, claudin 11 and occludin in the PI, MI and DI) and signaling molecule mitogen-activated protein kinases p38 in the PI, MI and DI of juvenile Jian carp, whereas upregulated the mRNA levels of claudin 3b in the MI and DI, and claudin 3c in the DI. Moreover, the excessive choline exhibited negative effects on intestinal immunity and TJ proteins that were similar to the choline deficiency. In summary, dietary choline deficiency or excess caused the depression of intestinal mucosal immune by inducing inflammation and dysfunction of the intestinal physical barrier, and regulating related signaling molecules of fish.

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Section: Choline Deficiency Induced Inflammation and Regulated Nf-κb And Stat Signaling Molecules In The Intestine Of The Fishsupporting

confidence: 71%

Dietary choline deficiency and excess induced intestinal inflammation and alteration of intestinal tight junction protein transcription potentially by modulating NF-κB, STAT and p38 MAPK signaling molecules in juvenile Jian carp

Jiang

et al. 2016

Fish & Shellfish Immunology

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“…In addition, the same changes in cadherin-mediated cell adhesion correlate with the invasive properties of the human retinoblastoma cell lines isolated decades ago, providing a molecular mechanism for these earlier observations" [18]. In another study, it was seen that relating the RB gene expression with the clinico-pathologic features of the tumor tissues, and found that the tumor with invasion of choroid, optic nerve and retinal pigment epithelium, had relatively higher gene expression, when compared with the tumor with only choroidal invasion [19].…”

Section: Discussionmentioning

confidence: 93%

Prognostic significance of retinoblastoma gene mutation in retinoblastoma eye with respect to pathological risk factors

Khan¹,

Mehboob²,

Bukhari³

2013

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Retinoblastoma (Rb) was reported firstly by Benedict is the commonest pediatric intraocular malignant tumor in children younger than 5 years of age. The study was conducted to detect the RB-1 gene for prognostic evaluation in retinoblastoma and to see the frequency of RB-1 gene in our population. This was a retrospective descriptive analytical study. Five years biopsies (January, 2006 to December 2011) of the retinoblastoma, from the Pathology department, was retrieved to see optic nerve involvement in all the retrieved specimens. The study was taken to see the mutation of RB1 gene by immunohistochemistry and PCR. The study plan was approved from Institutional Review Board (IRB) of the University. All the cases showed positivity of abnormal Rb-1 gene proteins expression by Immunohistochemistry staining. On PCR, 51/52 (98%) tumors expressed gene mutation as compared to 100% expression shown by IHC. Out of these, 28/51 (55%) cases showed ONI and ODI with positivity for mutated RB gene. A positive association was seen among RB gene mutation with ONI and ODI (p = 0.05). There were 33/51 (65%) cases who did not show any EOE but showed PCR positivity for RB gene mutation. While there were 18/51 (35%) cases who showed EOE and positivity of PCR for Rb-1 gene mutation and a positive association was seen with EOE and gene mutation (p = 0.005). The most common sequence of mutation was on 13 with 33 cases for double mutation, 12 cases for single and 6 patients for triple pattern of mutation. Most of the double and triple sequences of mutations were associated with ONI, ODI and EOE. We concluded that mutation of RB-1 gene is responsible in causation of the tumors with a positive association with tumor size and tumor extension (optic nerve, and extraocular extension), and mutation affects patients with all ages, both gender and unilateral and bilateral tumors.

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“…Oxidative stress via excess ROS plays a key role in the initiation and progression of carcinogenesis including retinoblastoma. 15 – 18 Aerobic organisms including mammals generate ROS as part of normal aerobic metabolism, and have developed elaborate antioxidant mechanisms for combating oxidative stress. The effective antioxidant defense systems for combating the toxicities of ROS is a family of antioxidant enzymes.…”

Section: Discussionmentioning

confidence: 99%

Morin Induces Heme Oxygenase-1 via ERK-Nrf2 Signaling Pathway

et al. 2013

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Background:Oxidative stress damages to cells or tissues, however, cellular defense systems including heme oxygenase-1 (HO-1) protects them against oxidative stress. Flavonoid compounds can activate cellular defense mechanisms against oxidative stress and it can reduce cell damages. In the present study, the cytoprotective effects of morin (3,5,7,2’,4’-pentahydroxyflavone), in terms of HO-1 enzyme, against the oxidative stress and its involved mechanisms was elucidated.Methods:RT-PCR and western blot analysis were assessed to detect the mRNA and protein expression, respectively. Cell viability was measured by using MTT test. The immunocytochemistry was performed to define location of target protein. Electrophoretic mobility shift assay performed to measure transcription factor-promoter site binding activity.Results:Morin elevated mRNA and protein levels of HO-1 in human lens epithelial cells (HLE-B3). HO-1 inhibitor ZnPP attenuated the protective effect of morin against H2O2-induced cytotoxicity. Morin increased the protein level of transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), which up-regulates HO-1 expression by binding to the antioxidant response element (ARE) within the HO-1 gene promoter. Moreover, morin induced the translocation of Nrf2 from the cytosol into the nucleus. Morin activated extracellular-regulated kinase (ERK), while ERK inhibitor attenuated morin-enhanced Nrf2 and HO-1 expression.Conclusions:Morin activates ERK-Nrf2 signaling cascades in HLE-B3 cells, leading to the up-regulation of HO-1 and cytoprotection against oxidative stress.

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Microarray Analysis and Biochemical Correlations of Oxidative Stress Responsive Genes in Retinoblastoma

Abstract: The study suggests active involvement of redox signaling pathways in the pathogenesis of RB. Consideration of oxidative stress components in the clinical management of RB patients is emphasized.

Cited by 14 publications

References 37 publications

Dietary choline deficiency and excess induced intestinal inflammation and alteration of intestinal tight junction protein transcription potentially by modulating NF-κB, STAT and p38 MAPK signaling molecules in juvenile Jian carp

Dietary choline deficiency and excess induced intestinal inflammation and alteration of intestinal tight junction protein transcription potentially by modulating NF-κB, STAT and p38 MAPK signaling molecules in juvenile Jian carp

Prognostic significance of retinoblastoma gene mutation in retinoblastoma eye with respect to pathological risk factors

Morin Induces Heme Oxygenase-1 via ERK-Nrf2 Signaling Pathway

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