Developmental methylation pattern regulates porcine GPR120 expression

Hm, Wang; Jd, Ma; Jin, Lan; Yh, Liu; Td, Che; Mz, Li; Xw, Li

doi:10.4238/gmr.15014240

Cited by 3 publications

(3 citation statements)

References 23 publications

(29 reference statements)

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“…Recent decades, numerous studies have revealed that the mechanisms of transcriptional regulation on gene expression were complex, including DNA methylation and transcriptional factors [42][43][44][45]. In present study, bioinformatics analysis showed that there was a CpG island in the promoter of MAPK4.…”

Section: Discussionmentioning

confidence: 51%

NFKB1/NR3C1-MAPK4 axis regulates the pathology of acute lung injury

Mao

Zhou

et al. 2020

Preprint

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BackgroundAcute lung injury (ALI) is a serious disease with highly morbidity and mortality that causes serious health problems worldwide. MAPK4, a member of atypical MAPK family, has been implicated in the development of cancer. Herein, the current study aimed to investigate the possible role of MAPK4 in the pathology of ALI to identify potential candidates for ALI therapy. MethodsMurine ALI model was established in WT or MAPK4 -/mice and the expressions of MAPK4 were measured. The survival ratio of ALI model mice was observed. Moreover, the changes of pathologic injury and infiltration of inflammatory cells, as well as the related signaling pathways, in lung tissues were analyzed. Furthermore, the possible molecular mechanism of MAPK4 expression in ALI was analyzed by massARRAY and EMSA assay. Finally, the effect of MAPK4 silencing using shRNA interference on the pathology of ALI was identified. the expression of MAPK4 by binding to the core sequence of MAPK4 promoter. Importantly, MAPK4-shRNA treatment could significantly reduce the pathology of lung tissues and prolong survival time of ALI mice. Altogether, our study reveals an unknown role of MAPK4 in the pathology of ALI, indicating that MAPK4 might be a new therapeutic target for clinic therapy against ALI. Materials And MethodsMice MAPK4 deficiency (MAPK4 -/-) mice breeding pair in a C57BL/6 background were purchased from The Jackson Laboratory (027666). Animals were housed under specific pathogen-free conditions at Zunyi Medical University. Cell cultureRaw264.7 cells were purchased from Conservation Genetics CAS Kunming Cell Bank (KCB200603YJ), and were cultured in high glucose DEME containing 10% fetal bovine serum at 37°C in 5% CO 2 . Establishment of ALI ModelWT and MAPK4 -/mice (7 to 9 week-old) were challenged with i.p. injection of 10mg/kg LPS (Escherichia coli 0111:B4; Sigma) dissolved in sterile PBS as shown in our previous study [17]. Then the body weight and lung weight index (lung weight/body weight) was detected at indicated time. Bronchoalveolar LavageImmediately after euthanasia, 1 ml aliquots of PBS were slowly infused in the murine lungs through the tracheostomy and then withdrawn gently. This lavage was repeated three times using the same syringe. The collected lavage fluid was stored in a 10ml tube on ice. The fluid was centrifuged at 1000rpm and 4°C for 10 min, and the cell sediment was washed with PBS. The cell-free supernatant was centrifuged again at 14,000g and 4°C for 10 min, stored at −80°C and used for determination of cytokines content via ELISA. To the pellet, red blood lysis buffer (Solarbio, R1010) were used for 15 min and washed with PBS. Next, the pellet was resuspended for analysis. Lung edema determinationLungs from mice were excised and completely dried in the oven at 60°C 24h for calculation of lung wet/dry ratio.

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Section: Discussionmentioning

confidence: 51%

NFKB1/NR3C1-MAPK4 axis regulates the pathology of acute lung injury

Mao

Zhou

et al. 2020

Preprint

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“…In a previous study, DNA methylation, in general, was negatively correlated with gene expression in the endometrium of cattle during early pregnancy (Walker et al, 2013). Recently, Wang et al (2016) revealed that the different methylation CGIs in 5'-untranslated and first exon regions negatively regulated the expression levels of the GPR120 gene in pigs.…”

Section: Discussionmentioning

confidence: 92%

Methylation differences and expression profiles of the caprine DIO3 gene

et al. 2016

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ABSTRACT. DIO3 gene encoding type 3 iodothyronine deiodinase is an imprinted gene, located in the DLK1-DIO3 (delta-like 1 homologtype 3 iodothyronine deiodinase) imprinted domain, and is potentially involved in degrading excessive amounts of thyroid hormone to protect embryogenesis. However, the underlying regulatory mechanism of the imprinted DIO3 gene expression during fetal and neonatal development in goats has not been elucidated. In this study, we explored the DNA methylation patterns of the caprine DIO3 intragenic CpG island and quantified gene expression level in six tissues from Chinese Nanjiang Yellow 3-day old kids. The expression of the DIO3 gene was determined using quantitative reverse transcription-polymerase chain reactions (qRT-PCRs), while the identification of methylation patterns was determined using bisulfite-sequencing PCRs. Modest, and non-significant (P > 0.05), methylation patterns were noted for the DIO3 CpG island methylation in the brain, heart, liver, kidney, lung, and longissimus dorsi tissues (ranging from 26.48 to 34.92%). The expression level of the DIO3 mRNA was significantly higher (P < 0.05) in the liver tissue than in the other five tissues. Pearson's correlation analysis revealed that there was no significant relationship between methylation and gene expression (P > 0.05), which indicated that the expression of the caprine DIO3 gene was likely modified by other regulatory elements. This study identified DNA methylation and expression patterns of the DIO3 gene in goats and provided insights into further regulatory mechanisms of expression and imprinting in the DLK1-DIO3 domain.

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“…It could modulate the expression and closure of genes closely associated with many diseases (e.g., cancer). Thus, it is a critical component of epigenetic machinery (Wang et al, 2016). Tegeder et al (2006) have declared that single-nucleotide polymorphisms (SNPs) in the gene for the GCH1 alter responses to noxious stimuli in healthy humans and susceptibility to neuropathic pain in patients.…”

Section: Discussionmentioning

confidence: 99%

Nitric Oxide in the Spinal Cord Is Involved in the Hyperalgesia Induced by Tetrahydrobiopterin in Chronic Restraint Stress Rats

et al. 2021

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It has been well recognized that exposure to chronic stress could increase pain responding and exacerbate pain symptoms, resulting in stress-induced hyperalgesia. However, the mechanisms underlying stress-induced hyperalgesia are not yet fully elucidated. To this end, we observed that restraint as a stressful event exacerbated mechanical and thermal hyperalgesia, accompanied with up-regulation of nitric oxide (NO) (P < 0.001), GTP cyclohydrolase 1 (GCH1) (GCH1 mRNA: P = 0.001; GCH1 protein: P = 0.001), and tetrahydrobiopterin (BH4) concentration (plasma BH4: P < 0.001; spinal BH4: P < 0.001) on Day 7 in restraint stress (RS) rats. Intrathecal injection of Nω-nitro-L-arginine methyl ester (L-NAME), a non-specific NO synthase inhibitor, or N-([3-(aminomethyl)phenyl]methyl) ethanimidamide, a special inhibitor of inducible NO synthase (iNOS), for seven consecutive days attenuated stress-induced hyperalgesia and decreased the production of NO (P < 0.001). Interestingly, 7-nitro indazole, a special inhibitor of neuronal NO synthase, alleviated stress-induced hyperalgesia but did not affect spinal NO synthesis. Furthermore, intrathecal injection of BH4 not only aggravated stress-induced hyperalgesia but also up-regulated the expression of spinal iNOS (iNOS mRNA: P = 0.015; iNOS protein: P < 0.001) and NO production (P < 0.001). These findings suggest that hyperalgesia induced by RS is associated with the modulation of the GCH1–BH4 system and constitutively expressed spinal iNOS. Thus, the GCH1–BH4–iNOS signaling pathway may be a new novel therapeutic target for pain relief in the spinal cord.

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Developmental methylation pattern regulates porcine GPR120 expression

Cited by 3 publications

References 23 publications

NFKB1/NR3C1-MAPK4 axis regulates the pathology of acute lung injury

NFKB1/NR3C1-MAPK4 axis regulates the pathology of acute lung injury

Methylation differences and expression profiles of the caprine DIO3 gene

Nitric Oxide in the Spinal Cord Is Involved in the Hyperalgesia Induced by Tetrahydrobiopterin in Chronic Restraint Stress Rats

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