Interestingly, recently published data by our group utilizing murine models of infection and trauma do not completely support this severely exacerbated gene expression pattern in mice of advanced age, although restoration of genomic homeostasis is certainly delayed [ 10, 11].
As shown above, inhibition of USP18 exacerbated IFN α-induced chemokine expression but double knockdown of USP18 and STAT1 or STAT2 reverted this effect for all the chemokines tested.
The lack of IL-6 expression was associated with exacerbated steatosis in HFD conditions.
In our study, stage 4 microglia and MHC II expression was associated with exacerbated neurodegeneration and motor symptoms.
Previous study shows aldehyde dehydrogenase 2 (ALDH2) plays a critical role in myocardial protection against ischemia, and down-regulation of ALDH2 expression is associated with exacerbated myocardial ischemia injury [ 1].
Exposing astrocytes with reduced PPAR expression to amyloid-β exacerbated production of the inflammatory molecules TNFα (tumour necrosis factor α), IL-6, iNOS (inducible nitric oxide synthase), and COX-2 (cyclo-oxygenase 2) compared with wild-type astrocytes (Benito et al., 2012).
Thus, C/EBPβ defects augment TNFα expression, which contributes to the exacerbated osteoclastogenesis.
In contrast, patients with both diseases showed significant higher BRINP3 gene expression, which can reflects the potential exacerbated reaction that BRINP3 can induct in the chronic periodontitis process.
We recently demonstrated that loss of Fra-1 leads to exacerbated bleomycin-induced pulmonary fibrosis, accompanied by enhanced expression of various inflammatory and fibrotic genes.
