Effects of sex hormones on inflammatory response in male and female vascular endothelial cells

Annibalini, Giosuè; Agostini, Deborah; Calcabrini, Cinzia; Martinelli, Chiara; Colombo, Evelin; Guescini, Michele; Tibollo, Pasquale; Stocchi, Vilberto; Sestili, Piero

doi:10.1007/s40618-014-0118-1

Cited by 37 publications

(32 citation statements)

References 24 publications

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“…This agrees with studies showing sex differences in clinical markers of inflammation [14]. Interestingly, the ratio of DE pro-inflammatory to anti-inflammatory genes in males were higher than in females, also in agreement with studies on human endothelial cells showing greater pro-inflammatory effects of androgens over estrogens [15]. We analyzed the BSL male sub-cohort pro-inflammatory genes in T2D and CJP, and found only 3 inflammatory genes (LUM, WISP2, ARTN) with sex-dimorphic expression at comparable effect sizes in either T2D or CJP with respect to BSL (Fig 1c) suggesting that the pro-inflammatory gene signature is unlikely to be caused solely by a subset of donors in BSL that are suffering from inflammatory conditions unreported in the clinical record.…”

Section: Pro-inflammatory Gene Signaturessupporting

confidence: 91%

Transcriptome analysis of the human tibial nerve identifies sexually dimorphic expression of genes involved in pain, inflammation and neuro-immunity

Ray

Khan

Wangzhou

et al. 2018

Preprint

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Section: Pro-inflammatory Gene Signaturessupporting

confidence: 91%

Transcriptome analysis of the human tibial nerve identifies sexually dimorphic expression of genes involved in pain, inflammation and neuro-immunity

Ray

Khan

Wangzhou

et al. 2018

Preprint

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“…; sex identified: Annibalini et al . ) where the receptor expression was not detectable. In the study by Annibalini et al .…”

Section: Discussionmentioning

confidence: 98%

Sex differences influencing micro‐ and macrovascular endothelial phenotype in vitro

Huxley

Kemp

Schramm

et al. 2018

The Journal of Physiology

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Vascular endothelial cells (EC) are heterogeneous with respect to phenotype, reflecting at least the organ of origin, location within the vascular network and physical forces. As an independent influence on EC functions in health or aetiology, susceptibility, and progression of dysfunction in numerous disease states, sex has been largely ignored. The present study focussed on EC isolated from aorta (macrovascular) and skeletal muscle vessels (microvascular) of age-matched male and female rats under identical conditions of short-term (passage 4) culture. We tested the hypothesis that genomic sex would not influence endothelial growth, wound healing, morphology, lactate production, or messenger RNA and protein expression of key proteins (sex hormone receptors for androgen and oestrogens α and β; platelet endothelial cell adhesion molecule-1 and vascular endothelial cadherin mediating barrier function; α β and N-cadherin influencing matrix interactions; intracellular adhesion molecule-1 and vascular cell adhesion molecule-1 mediating EC/white cell adhesion). The hypothesis was rejected because the EC origin (macro- vs. microvessel) and sex influenced multiple phenotypic characteristics. Statistical model analysis of EC growth demonstrated an hierarchy of variable importance, recapitulated for other phenotypic characteristics, with predictions assuming EC homogeneity < sex < vessel origin < sex and vessel origin. Furthermore, patterns of EC mRNA expression by vessel origin and by sex did not predict protein expression. Overall, the present study demonstrated that accurate assessment of sex-linked EC dysfunction first requires an understanding of EC function by position in the vascular tree and by sex. The results from a single EC tissue source/species/sex cannot provide universal insight into the mechanisms regulating in vivo endothelial function in health, and no less in disease.

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“…The effect of male and female sex hormones on HUVECs has been extensively studied to elucidate mechanisms behind sex-specific morbidities in cardiovascular disease. For example, androgens have been shown to have a pro-inflammatory effect by amplifying the effect of TNF-α in both male and female HUVECs [16]. …”

Section: Discussionmentioning

confidence: 99%

Differential sex-specific effects of oxygen toxicity in human umbilical vein endothelial cells

Zhang

Lingappan

2017

Biochemical and Biophysical Research Communications

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Despite the well-established sex-specific differences in the incidence of bronchopulmonary dysplasia (BPD), the molecular mechanism(s) behind these are not completely understood. Pulmonary angiogenesis is critical for alveolarization and arrest in vascular development adversely affects lung development. Human neonatal umbilical vein endothelial cells (HUVECs) provide a robust in vitro model for the study of endothelial cell physiology and function. Male and Female HUVECs were exposed to room air (21% O2, 5% CO2) or hyperoxia (95% O2, 5% CO2) for up to 72 hr. Cell viability, proliferation, H2O2 production and angiogenesis were analyzed. Sex-specific differences in the expression of VEGFR2 and modulation of NF-kappa B pathway were measured. Male HUVECs have decreased survival, greater oxidative stress and impairment in angiogenesis compared to similarly exposed female cells. There is differential expression of VEGFR2 between male and female HUVECs and greater activation of the NF-kappa B pathway in female HUVECs under hyperoxic conditions. The results indicate that sex differences exist between male and female HUVECs in vitro after hyperoxia exposure. Since endothelial dysfunction has a major role in the pathogenesis of BPD, these differences could explain in part the mechanisms behind sex-specific differences in the incidence of this disease.

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Effects of sex hormones on inflammatory response in male and female vascular endothelial cells

Cited by 37 publications

References 24 publications

Transcriptome analysis of the human tibial nerve identifies sexually dimorphic expression of genes involved in pain, inflammation and neuro-immunity

Transcriptome analysis of the human tibial nerve identifies sexually dimorphic expression of genes involved in pain, inflammation and neuro-immunity

Sex differences influencing micro‐ and macrovascular endothelial phenotype in vitro

Differential sex-specific effects of oxygen toxicity in human umbilical vein endothelial cells

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