Serum tumor necrosis factor-α, interleukin-6, monocyte chemotactic protein-1 and paraoxonase-1 profiles in women with endometriosis, pcos, or unexplained infertility

Younis, A.I.; Hawkins, Kristina C.; Mahini, Halleh; Butler, Warren L.; Garelnabi, Mahdi

doi:10.1007/s10815-014-0237-9

Cited by 46 publications

(53 citation statements)

References 43 publications

(65 reference statements)

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“…PCOS presents with acne symptoms together with polycystic ovaries, oligo‐anovulation and hyperandrogenism . Hyperandrogenism likely drives acne in PCOS, although as it is a proinflammatory disease, immune genes and cytokines could likewise predispose to acne symptoms (Table ) . A number of GWASs have been performed for PCOS .…”

Section: Human Disorders That Cause Acne‐like Phenotypesmentioning

confidence: 99%

“…127,128 Hyperandrogenism likely drives acne in PCOS, although as it is a proinflammatory disease, immune genes and cytokines could likewise predispose to acne symptoms (Table 1). [129][130][131][132][133] A number of GWASs have been performed for PCOS. [134][135][136][137][138] Hormonal therapies are a well-tolerated and effective way to control acne with and without endocrine disorders.…”

Section: Endocrine System Syndromesmentioning

confidence: 99%

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What does acne genetics teach us about disease pathogenesis?

2019

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Summary Background Acne vulgaris is a highly prevalent inflammatory skin disorder with a complex pathogenesis, characterized by comedones, papules, pustules and nodules. Familial preponderance clearly indicates a genetic basis for acne vulgaris, but until recently solid genetic associations were lacking. Results The advent of high‐resolution genotyping array technologies has allowed for large‐scale studies with both family‐based and cross‐sectional designs. These studies have revealed genetic loci encompassing genes that could be active in biological pathways and processes underlying acne vulgaris. However, specific functional consequences of those variants remain elusive. In parallel, investigations into rare disorders and syndromes that incorporate features of acne or acne‐like lesions have recently accelerated our understanding of disease pathogenesis. The genes revealed by these rare disorders highlight mechanisms cardinal for pilosebaceous biology and therefore anchor our insights from genetic association studies for acne vulgaris. Conclusions The next phase of research will require more in‐depth mechanistic investigations of loci and genes implicated in acne phenotypes to define the key molecular players driving the disorder. Concurrently, new treatments for acne vulgaris could be developed by dissecting the candidate molecular pathways to identify druggable targets.

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Section: Human Disorders That Cause Acne‐like Phenotypesmentioning

confidence: 99%

Section: Endocrine System Syndromesmentioning

confidence: 99%

What does acne genetics teach us about disease pathogenesis?

2019

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“…PON1 activity is decreased in several pathological conditions (diabetes type II, coronary heart disease, rheumatoid arthritis, hyperthyroidism, Alzheimer, and others), as well as in workers exposed to OPs independently or have a PON1 genetic polymorphism (Mackness et al, 1998;Brophy et al, 2002;Ferr e et al, 2002;Paragh et al, 2002;Tanimoto et al, 2003;Deakin and James, 2004;Costa et al, 2005;S€ ozmen et al, 2007;Araoud et al, 2010;Hofmann et al, 2010;Gbandjaba et al, 2012;Gugliucci et al, 2012;Gungor et al, 2013). In this sense, Younis et al (2014) reported that circulating IL-6, MCP-1 and PON1 levels are influenced by ovarian stimulation. On the other hand, Bobin-Dubigeon et al (2013) observed that in patients with metabolic syndrome, the levels of inflammatory markers, with the exception of sTNF-R2, were significantly higher, while PON1 activity was significantly lower.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of human paraoxonase 1 (PON1) by organophosphate pesticides in HepG2 cells

Medina-Díaz

Ponce-Ruíz

Ramírez-Chávez

et al. 2016

Environmental Toxicology

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Paraoxonase 1 (PON1) is a calcium-dependent esterase synthesized primarily in the liver and secreted into the plasma where it is associated with high-density lipoproteins (HDL). PON1 hydrolyzes and detoxifies some toxic metabolites of organophosphorus compounds (OPs) such as methyl parathion and chlorpyrifos. Thus, PON1 activity and expression levels are important for determining susceptibility against OPs poisoning. Some studies have demonstrated that OPs can modulate gene expression through interactions with nuclear receptors. In this study, we evaluated the effects of methyl parathion and chlorpyrifos on the modulation of PON1 in Human Hepatocellular Carcinoma (HepG2) cells by real-time PCR, PON1 activity assay, and western blot. The results showed that the treatments with methyl parathion and chlorpyrifos decreased PON1 mRNA and immunoreactive protein and increased inflammatory cytokines in HepG2 cells. The effects of methyl parathion and chlorpyrifos on the downregulation of PON1 gene expression in HepG2 cells may provide evidence of OPs cytotoxicity related to oxidative stress and an inflammatory response. A decrease in the expression of the PON1 gene may increase the susceptibility to OPs intoxication and the risk of diseases related to inflammation and oxidative stress. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 490-500, 2017.

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“…161 The genes related to inflammatory cytokines and chronic inflammation such as TNF-a, interleukin (IL)-6, IL-1A and IL-1B might also become possible candidate genes correlated with PCOS. [162][163][164][165][166] Although studies for the inflammation cytokines and PCOS have shown mixed results, several GWAS concerning PCOS identified several susceptibility loci and SNPs (Table 10). [167][168][169][170][171] Identifying the genetic pathways involved in PCOS may provide a better understanding of the mechanism causing PCOS and the correlation with inflammatory cytokines and acne vulgaris.…”

Section: Polycystic Ovary Syndrome (Pcos)mentioning

confidence: 99%

Genetic architecture of acne vulgaris

Lichtenberger

Simpson

Smith

et al. 2017

Acad Dermatol Venereol

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Acne vulgaris is a ubiquitary skin disease characterized by chronic inflammation of the pilosebaceous unit resulting from bacterial colonization of hair follicles by Propionibacterium acnes, androgen-induced increased sebum production, altered keratinization and inflammation. Here, we review our current understanding of the genetic architecture of this intriguing disease. We analysed genomewide association studies (GWAS) and candidate genes studies for acne vulgaris. Moreover, we included GWAS studies for the associated disease polycystic ovary syndrome (PCOS). Overall, the available data revealed sixteen genetic loci flagged by single nucleotide polymorphisms (SNPs), none of which has been confirmed yet by independent studies. Moreover, a GWAS for PCOS identified 21 susceptible loci. The genetic architecture is complex which has been revealed by GWAS. Further and larger studies in different populations are required to confirm or disprove results from candidate gene studies as well to identify signals that may overlap between different populations. Finally, studies on rare genetic variants in acne and associated diseases like PCOS may deepen our understanding of its pathogenesis.

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Serum tumor necrosis factor-α, interleukin-6, monocyte chemotactic protein-1 and paraoxonase-1 profiles in women with endometriosis, pcos, or unexplained infertility

Cited by 46 publications

References 43 publications

What does acne genetics teach us about disease pathogenesis?

What does acne genetics teach us about disease pathogenesis?

Downregulation of human paraoxonase 1 (PON1) by organophosphate pesticides in HepG2 cells

Genetic architecture of acne vulgaris

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