9-cis retinoic acid improves developmental competence and embryo quality during in vitro maturation of bovine oocytes through the inhibition of oocyte tumor necrosis factor-α gene expression1

2011 ◽  
Vol 89 (9) ◽  
pp. 2759-2767 ◽  
Author(s):  
G. K. Deb ◽  
S. R. Dey ◽  
J. I. Bang ◽  
S. J. Cho ◽  
H. C. Park ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Tumor Necrosis ◽  
In Vitro Maturation ◽  
Tumor Necrosis Factor Α ◽  
Embryo Quality ◽  
Developmental Competence ◽  
Factor Α ◽  
Bovine Oocytes ◽  
Necrosis Factor

254 9-cis RETINOIC ACID INHIBITS CUMULUS CELL APOPTOSIS DURING IN VITRO MATURATION OF BOVINE OOCYTES THROUGH INHIBITION OF AP-1 PATHWAY

2011 ◽  
Vol 23 (1) ◽  
pp. 225
Author(s):  
G. K. Deb ◽  
S. R. Dey ◽  
J. I. Bang ◽  
S. J. Cho ◽  
T. H. Kwon ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Tumor Necrosis Factor ◽  
Oocyte Maturation ◽  
Tumor Necrosis ◽  
In Vitro Maturation ◽  
Tumor Necrosis Factor Α ◽  
Cumulus Cell ◽  
Factor Α ◽  
Necrosis Factor

Cumulus cells (CC) play a critical role in oocyte maturation and fertilization via gap junctions. The oocyte itself maintains CC health to favour oocyte maturation via the secretion of paracrine growth factors. However, the antiapoptotic effects of oocyte-secreted factors follow a gradient from the site of the oocytes. Moreover, degrees of CC apoptosis are inversely related to the in vitro embryo development. Therefore, inhibition of CC apoptosis is important for efficient in vitro embryo development. The beneficial effects of retinoic acid (RA) during in vitro embryo production are well known in different species. However, the effect of RA on CC apoptosis is yet to be elucidated. All-trans RA and 9-cis RA are the natural components of retinoids, and all-trans RA are metabolized to 9-cis RA for physiological function. Therefore, the objective of the present study was to evaluate the effect of 9-cis RA on the mechanism for inhibition of apoptosis in CC. Slaughterhouse cumulus–oocyte complexes (COC) were matured in vitro in TCM-199-based in vitro maturation medium containing 0 or 5 mM 9-cis RA for 23 to 24 h (15 COC/100 μL droplet) at 38.5°C and 5% CO2 in air with maximum humidity. Following in vitro maturation, COC of a droplet were fixed in 4% paraformaldehyde for TUNEL staining using In Situ Cell Death Detection Kit (Roche, Budapest, Hungary). The proportion of apoptotic cells was estimated using Olympus Soft Imaging Solutions GmBH (Olympus, Münster, Germany). The COC of the remaining droplet were denuded. The CC were frozen and stored at –80°C. The CC of 3 different cultures were pooled, and total RNA was extracted using RNeasy Mini Kit (Qiagen, Valencia, CA, USA). Total RNA was reverse transcribed into cDNA using Omniscript Reverse Transcription kit (Qiagen). Relative expression of candidate genes was quantified using SYBER green real-time PCR with ΔΔ CT method. The expression was normalized against β-actin, glyceraldehyde 3-phosphate dehydrogenase, and 18s rRNA genes expression. The PCR efficiencies were calculated using relative calibration curves following 10-fold dilution series at 5 measuring points. Data were analysed for one-way ANOVA. The proportion of apoptotic cells was low in the 9-cis RA group (1.3 v. 3.3% of total CC; P < 0.05). Expression of tumor necrosis factor-α (11.1 v. 1.0; P < 0.001), caspase9 (2.0 v. 1.0; P < 0.01), and caspase3 (2.1 v. 1.0; P < 0.001) genes was down-regulated in the 9-cis RA group, whereas expression of Bcl2 gene was increased (1.0 v. 2.6 fold; P < 0.05). Moreover, the expression of c-fos gene of AP-1 pathway was down-regulated (1.9 v. 1 fold; P < 0.05) in the 9-cis RA group. Retinoic acid suppressed the expression of NF-kB, which in turn inhibits tumor necrosis factor-α-mediated caspase activity. However, the expression of NF-kB in CC was not affected by 9-cis RA (1.1 v. 1.0; P > 0.05). In conclusion, the present study indicated that 9-cis RA may inhibit cumulus cell apoptosis through suppression of AP-1 pathway. This work was partly supported by a scholarship from the BK21 program, the KRF (KRF-2008-211-F00011), the IPET (108068-03-1-SB010), and the KOSEF (10525010001-05N2501-00110).

In vitro regulation of rat Sertoli cell transferrin expression by tumor necrosis factor α and retinoic acid

1999 ◽  
Vol 148 (1-2) ◽  
pp. 163-170 ◽  
Author(s):  
F. Sigillo ◽  
F. Guillou ◽  
I. Fontaine ◽  
M. Benahmed ◽  
B. Le Magueresse-Battistoni
Keyword(s):  
Retinoic Acid ◽  
Tumor Necrosis Factor ◽  
Sertoli Cell ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals In Vivo and in Vitro Evidence for the Involvement of Tumor Necrosis Factor-α in the Induction of Leptin by Lipopolysaccharide*

Endocrinology ◽  
1998 ◽  
Vol 139 (5) ◽  
pp. 2278-2283 ◽  
Author(s):  
Brian N. Finck ◽  
Keith W. Kelley ◽  
Robert Dantzer ◽  
Rodney W. Johnson
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Ectopic HOXB4 overcomes the inhibitory effect of tumor necrosis factor-α on Fanconi anemia hematopoietic stem and progenitor cells

Blood ◽  
2009 ◽  
Vol 113 (21) ◽  
pp. 5111-5120 ◽  
Author(s):  
Michael D. Milsom ◽  
Bernhard Schiedlmeier ◽  
Jeff Bailey ◽  
Mi-Ok Kim ◽  
Dandan Li ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Fanconi Anemia ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Ectopic Expression ◽  
Hematopoietic Stem ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

AbstractEctopic delivery of HOXB4 elicits the expansion of engrafting hematopoietic stem cells (HSCs). We hypothesized that inhibition of tumor necrosis factor-α (TNF-α) signaling may be central to the self-renewal signature of HOXB4. Because HSCs derived from Fanconi anemia (FA) knockout mice are hypersensitive to TNF-α, we studied Fancc−/− HSCs to determine the physiologic effects of HOXB4 on TNF-α sensitivity and the relationship of these effects to the engraftment defect of FA HSCs. Overexpression of HOXB4 reversed the in vitro hypersensitivity to TNF-α of Fancc−/− HSCs and progenitors (P) and partially rescued the engraftment defect of these cells. Coexpression of HOXB4 and the correcting FA-C protein resulted in full correction compared with wild-type (WT) HSCs. Ectopic expression of HOXB4 resulted in a reduction in both apoptosis and reactive oxygen species in Fancc−/− but not WT HSC/P. HOXB4 overexpression was also associated with a significant reduction in surface expression of TNF-α receptors on Fancc−/− HSC/P. Finally, enhanced engraftment was seen even when HOXB4 was expressed in a time-limited fashion during in vivo reconstitution. Thus, the HOXB4 engraftment signature may be related to its effects on TNF-α signaling, and this pathway may be a molecular target for timed pharmacologic manipulation of HSC during reconstitution.

scholarly journals Tumor Necrosis Factor-α-Induced Protein 8-Like 2 Negatively Regulates Innate Immunity Against RNA Virus by Targeting RIG-I in Macrophages

2021 ◽  
Vol 12 ◽  
Author(s):  
Ziqi Zou ◽  
Mengyao Li ◽  
Yunlian Zhou ◽  
Jiaying Li ◽  
Ting Pan ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Retinoic Acid ◽  
Viral Infection ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Rna Virus ◽  
Type I ◽  
Factor Α ◽  
Necrosis Factor ◽  
Inducible Gene

A systematic and flexible immunoregulatory network is required to ensure the proper outcome of antiviral immune signaling and maintain homeostasis during viral infection. Tumor necrosis factor-α-induced protein 8-like 2 (TIPE2), a novel immunoregulatory protein, has been extensively studied in inflammatory response, apoptosis, and cancer. However, the function of TIPE2 in antiviral innate immunity is poorly clarified. In this study, we reported that the expression of TIPE2 declined at the early period and then climbed up in macrophages under RNA virus stimulation. Knockout of TIPE2 in the macrophages enhanced the antiviral capacity and facilitated type I interferon (IFN) signaling after RNA viral infection both in vitro and in vivo. Consistently, overexpression of TIPE2 inhibited the production of type I IFNs and pro-inflammatory cytokines, and thus promoted the viral infection. Moreover, TIPE2 restrained the activation of TBK1 and IRF3 in the retinoic acid inducible gene-I (RIG-I)-like receptors (RLR) signaling pathway by directly interacting with retinoic acid inducible gene-I (RIG-I). Taken together, our results suggested that TIPE2 suppresses the type I IFN response induced by RNA virus by targeting RIG-I and blocking the activation of downstream signaling. These findings will provide new insights to reveal the immunological function of TIPE2 and may help to develop new strategies for the clinical treatment of RNA viral infections.

Interleukin-6 and tumor necrosis factor α levels after bisphosphonates treatment in vitro and in patients with malignancy

Bone ◽  
1996 ◽  
Vol 18 (2) ◽  
pp. 133-139 ◽  
Author(s):  
A. Sauty ◽  
M. Pecherstorfer ◽  
I. Zimmer-Roth ◽  
P. Fioroni ◽  
L. Juillerat ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor
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