Up-regulation of Id1 in peripheral blood of psoriatic patients

Abstract

ABSTRACT. Although the precise causes of psoriasis are unclear, it is widely accepted that psoriasis is a disorder in which factors in the immune system, enzymes, and other biochemical substances that regulate skin cell division are impaired, leading to rapid proliferation of keratinocytes and incomplete keratinization. Expression of the helix-loop-helix transcription factor Id1 (inhibitor of differentiation/DNA binding), functioning as an inhibitor of differentiation, is known to increase in psoriatic skin. However, the molecular involvement of this particular biomarker in the psoriatic immune system remains to be elucidated. We measured Id1 mRNA expression in peripheral blood mononuclear cells (PBMCs) of psoriatic patients and healthy controls using semi-quantitative reverse transcriptase- PCR. The normalized level of Id1 transcripts in psoriatic patients was about 2-fold higher than that in controls (P < 0.05). When we examined the proliferation rate of PBMCs, the stimulation index obtained from the phytohemagglutinin stimulation assay was not significantly different in psoriatic patients. In patients with psoriasis, there was no correlation between the stimulation index and the psoriasis area severity index. We suggest that Id1 has a role in causing psoriatic immune cell symptoms.

Dithranol downregulates expression of Id1 mRNA in human keratinocytes in vitro

“…Consistently, Id1 mRNA was reported to be upregulated in psoriatic involved skin but not in psoriatic uninvolved skin (Mark et al, 2006). Very recently, we revealed that the normalized level of Id1 transcripts in psoriatic patients was approximately twofold higher than that in controls (Ronpirin et al, 2010). Thus, Id1 may be a potential biomarker associated with the pathophysiology of psoriasis.…”

“…We hypothesized that the antipsoriatic drug dithranol could reduce the expression of the Id1 gene in an experimental in vitro model using the HaCaT cell line because Id1 is an elevated biomarker in psoriasis (Bjorntorp et al, 2003;Mark et al, 2006;Ronpirin et al, 2010). This cell line, originally documented by Boukamp et al (1988), is believed to be an appropriate cellular model of psoriasis based on previous reports (Farkas et al, 2001;Tencomnao et al, 2009;George et al, 2010;Saelee et al, 2011;Ronpirin and Tencomnao, 2012).…”

Effects of the antipsoriatic drug dithranol on E2A and caspase-9 gene expression in vitro

“…Various studies have shown that E2A was extremely critical for cell proliferation and differentiation (Yan et al, 1997;Engel and Murre, 2001;Perk et al, Expression of E2A and caspase-9 gene in response to dithranol 2005; Kee, 2009). Although E2A binding partner, Id1, has been revealed to be important in psoriasis according to various reports (Bjorntorp et al, 2003;Mark et al, 2006;Ronpirin et al, 2010), the knowledge concerning the molecular involvement of E2A in psoriasis still remains limited. Apoptosis, another pathway undoubtedly imbalanced in psoriasis, is crucial in the maintenance of skin cell homeostasis as well as in the pathogenesis of certain skin diseases including psoriasis, but only few studies on caspase-9 in psoriasis have been reported to date (Yamamoto and Nishioka, 2003;Oztas et al, 2006).…”

“…In a cellular model of psoriasis such as the HaCaT keratinocyte cell line, the Id1 mRNA was shown to be highly expressed (Langlands et al, 2000). Recently, the molecular role of Id1 was further highlighted in psoriasis since we found that the levels of Id1 transcripts in peripheral blood mononuclear cells of psoriatic patients were approximately 2-fold higher than those in controls (Ronpirin et al, 2010). Of particular interest, the cellular function of the Id1 protein is regulated via binding with other interactors such as E2A proteins (Yan et al, 1997;Engel and Murre, 2001;Perk et al, 2005;Kee, 2009).…”

Computational Systems Biology of Psoriasis: Are We Ready for the Age of Omics and Systems Biomarkers?

“…Among them, SERPINB4 had the highest overexpression with 126-fold difference from nonlesional skin. Other DEGs such as ID1, ID4, KRT16 and HMOX1, which have been previously indicated in psoriasis disease (Hanselmann et al, 2001;Leigh et al, 1995;Ronpirin et al, 2010;Ruchusatsawat et al, 2011;Zebedee et al, 2001) were also identified in the present study.…”