Differential Expression of Serum Proinflammatory Cytokine TNF-α and Genetic Determinants of TNF-α, CYP2C19*17, miR-423 Genes and Their Effect on Coronary Artery Disease Predisposition and Progression

Almassabi, Rehab F.; Mir, Rashid; Javid, Jamsheed; AbuDuhier, Faisel M.; Almotairi, Reema; Alhelali, Marwan H.; Algehainy, Naseh; Alsaedi, Basim S. O.; Albalawi, Salem Owaid; Elfaki, Imadeldin

doi:10.3390/life13112142

Cited by 2 publications

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References 52 publications

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“…Moreover, TNF-α induces the secretion of metalloproteinases (MMPs) by macrophages under the control of microRNAs. MMPs catalyze the destruction of interstitial collagen, which leads to thinning and weakening of the fibrous capsule, thereby making the plaque unstable and increasing the risk of plaque rupture and thrombosis ( Almassabi et al, 2023 ).…”

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confidence: 99%

The association of TNF-alpha secretion and mtDNA copy number in CD14+ monocytes of patients with obesity and CHD

Tolstik,

Kirichenko,

Markin

et al. 2024

Front. Mol. Biosci.

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IntroductionMitochondrial dysfunction may be one of the causes of inflammatory activation of monocytes and macrophages, which leads to excessive secretion of inflammatory mediators and the development of chronic inflammation.AimsThe study was aimed to evaluate the secretion of inflammatory cytokine tumor necrosis factor-α (TNF-α) in the primary culture of monocytes, and to analyze its relationship with the number of mitochondrial DNA (mtDNA) copies in the blood of patients with coronary heart disease (CHD) and obesity.Materials and methods108 patients with obesity and concomitant CHD and a control group of 25 participants were included in the study. CD14+ monocytes were isolated by a standard method in a ficoll-urographin gradient, followed by separation using magnetic particles. The number of mtDNA copies was estimated using qPCR.ResultsIt was demonstrated that the number of mtDNA copies was significantly increased in groups of patients with CHD and obesity + CHD in comparison with control group. mtDNA copy number positively correlated with basal and LPS-stimulated TNF-α secretion, the most significant correlation was found in the group of patients with CHD and obesity.ConclusionThus, the change in mtDNA copy number in CD14+ monocytes which indicates the presence of mitochondrial dysfunction, confirm the direct involvement of mitochondria in the violation of the inflammatory response of monocytes revealed in this study as an increased secretion of inflammatory cytokine TNF-α.

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Section: Introductionmentioning

confidence: 99%

The association of TNF-alpha secretion and mtDNA copy number in CD14+ monocytes of patients with obesity and CHD

Tolstik,

Kirichenko,

Markin

et al. 2024

Front. Mol. Biosci.

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Exploring the Association of Biochemical Characterization and Genetic Determinants of TNF-α, CXCR2, and CCR5 Delta 32 Mutation with Predisposition to Polycystic Ovary Syndrome

Almasoudi,

Hussain,

Almotairi

et al. 2024

Life

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PCOS is a heterogeneous, multifactorial endocrine disorder with a complex pathophysiology. It is a globally rising infertility disorder that affects a large percentage of women of reproductive age, with a relatively high prevalence of 8–13%. Genome-wide association studies have revealed associations of genetic variations with many diseases, including PCOS. The cellular activity of IL8 is mediated by the receptor CXCR2, and transcription of IL8 is controlled by TNF-α. Therefore, this study aimed to investigate the association of TNF-α, CCR5-delta32, and CXCR2 gene variations with PCOS. Methodology: In this case control study, we used amplification-refractory mutation system (ARMS)-PCR to detect and determine the presence of the polymorphic variants TNF-α, CCR5-delta32, and CXCR2 in the study subjects. These gene polymorphs may serve as critical candidate gene variants in PCOS pathogenesis and therapeutics. Results: The case–control study’s findings revealed that the majority of the biochemical and endocrine serum biomarkers examined in the investigation—including lipids (LDL, HDL, and cholesterol), T2DM markers (fasting glucose, free insulin, and HOMA-IR), and hormones (FSH, LH, testosterone, and progesterone)—exhibited statistically significant changes in PCOS patients. The distributions of TNF-α (rs1800629), CCR5-delta32, and CXCR2 (rs2230054) genotypes analyzed within PCOS patients and healthy controls in the considered population were significant (p < 0.05). The heterozygosity of CXCR2-CA, TNF-α GA, and CCR5(WT+Δ32*) genotypes was significantly associated with PCOS susceptibility, with high OR and p < 0.05 in the codominant model. Similarly, the A allele of the TNF-α and CXCR2 genes, along with the CCR5Δ32*(mutant) allele, was significantly associated with PCOS susceptibility, with high OR and p < 0.05. Likewise, the CXCR2 (CA+AA) vs CC genotype was associated with increased susceptibility to PCOS, with OR 2.25, p < 0.032. Conclusions: Our study concludes that TNF-α rs1800629G>A, CXCR2-rs2230054C>T, and CCR5-Delta32 rs333 are potential loci for developing PCOS in the Tabuk population. These findings might eventually be useful in identifying and classifying those who are at risk for PCOS. To validate these results, it is advised that further longitudinal studies be conducted in diverse ethnic populations and with larger sample sizes.

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Differential Expression of Serum Proinflammatory Cytokine TNF-α and Genetic Determinants of TNF-α, CYP2C19*17, miR-423 Genes and Their Effect on Coronary Artery Disease Predisposition and Progression

Cited by 2 publications

References 52 publications

The association of TNF-alpha secretion and mtDNA copy number in CD14+ monocytes of patients with obesity and CHD

The association of TNF-alpha secretion and mtDNA copy number in CD14+ monocytes of patients with obesity and CHD

Exploring the Association of Biochemical Characterization and Genetic Determinants of TNF-α, CXCR2, and CCR5 Delta 32 Mutation with Predisposition to Polycystic Ovary Syndrome

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