Sentence examples for several inflammatory genes from inspiring English sources

Targeted delivery mediated dnIκB transgene expression in endothelial cells inhibited the induced expression of several inflammatory genes, including adhesion molecules, cytokines, and chemokines.

In the elderly, the combination of increased production of reactive oxygen species (ROS) and decreased antioxidant functions, accompanied by an upregulation of several inflammatory genes, such as those coding for interleukin (IL) 1β, IL-6, IL-8, and tumor necrosis factor (TNF) α, leads to a two-pronged attack from altered redox status and dysregulated immune responses1,2.

In addition to the induction of neuropeptide release, an increase in cytosolic Ca2+ can also drive the regulation of the expression of several inflammatory genes, such as those encoding neuropeptides, cytokines, growth factors, prostaglandins (PG), and matrix metalloproteinases (MMPs), which have a possible role in chronic cutaneous inflammation.

We observed suppression of several inflammatory genes, including activating cytokines and iNOS.

Besides that, peroxisome proliferator-activated receptor γ and the liver X receptor α activity are enhanced, leading to the suppressed transcription of several inflammatory genes [27], [28].

Moreover, a crosstalk between the Wnt signalling pathway and the nuclear factor-kappaB pathway has been proposed [22], [23], which regulates the expression of several inflammatory genes implicated in atherosclerosis [24].

Several inflammatory cytokine genes (CXCL1, CXCL2, CXCL3, CCL20, IL8, CCL23, CCL19, CCL21, CCL5) are dysregulated in adenomas.

Moreover, the upregulation of several inflammatory response genes after treatment with inflammatory stimuli was drastically reduced in Parp1 knockout mice [ 112, 114- 116].

In liver cells, binding of TNFα or IL1α to the cellular membrane leads to the activation of NF-κB, which can enter the nucleus and initiate transcription of several inflammatory target genes [ 46].

The inhibitory effect of SRA on expression of Tlr4, Ccl2 and several additional inflammatory genes was confirmed by RT-qPCR (Figure S3).

While CpG methylation can mediate more sustained suppression of certain genes, the promoters of several of the inflammatory genes suppressed in sepsis, including TNF-α, IL-6, IL-12 p40, and iNOS, contain few CpG motifs and are therefore less susceptible to this form of epigenetic regulation.