Search

Objective To determine the relationship between vascular biomarkers reflecting the vascular injury and neoangiogenesis with capillaroscopic changes in systemic sclerosis (SSc). Methods Nailfold video-capillaroscopy (NVC) was performed qualitatively (early, active and late scleroderma patterns) in 72 SSc patients (66 female) fulfilling ACR/EULAR (2013) criteria. Serum samples of patients were collected and analysed by flow cytometer with multiplex kits of sCD40L, tPA, MCP-1, sE-selectin, IL-8, IL-6, VEGF, sP-selectin, TGF-β1 and VCAM at the same time with NVC. Results Compared to healthy subjects; tPA ( p = 0.02), MCP-1 ( p = 0.001), sE-selectin ( p = 0.008) and TGF-β1 ( p = 0.001) levels were significantly higher, however sP-selectin ( p = 0.011) and IL-8 ( p = 0.001) levels were lower in SSc patients. SSc patients were defined according to NVC patterns as ‘early’ ( n = 10), ‘active’ ( n = 37) and ‘late’ ( n = 25). According to NVC patterns of SSc patients, only sCD40L levels were significantly lower in the ‘late’ group ( p = 0.039). The other markers were similar among NVC groups. Conclusions NVC is a useful method for investigating the vascular pathogenesis and severity of SSc. Although the levels were similar to healthy controls in patients with early/active NVC patterns, there were lower sCD40L serum levels in patients with late NVC pattern. CD40L may have a role in the early/active phase of vascular involvement.

The cell surface antigen, CD38, is a 45-kDa transmembrane protein which is predominantly expressed on hematopoietic cells during differentiation. As a bifunctional ectoenzyme, it catalyzes the synthesis of cyclic ADP-ribose (cADPR) from NAD(+) and hydrolysis of either NAD(+) or cADPR to ADP-ribose. All-trans-retinoic acid (RA) is a potent and specific inducer of CD38 in myeloid cells. In this report, we demonstrate that the nuclei of RA-treated human HL-60 myeloblastic cells reveal enzymatic activities inherent to CD38. Thus, GDP-ribosyl cyclase and NAD(+) glycohydrolase activities in the nuclear fraction increased very significantly in response to incubation with RA. With Western blotting, we detected in the nuclear protein fraction from RA-treated cells a approximately 43-kDa protein band which was reactive with the CD38-specific monoclonal antibody OKT10. The expression of CD38 in HL-60 nuclei was also shown with FACScan analysis. RA treatment gave rise to an increase in in vitro ADP ribosylation of the approximately 43-kDa nuclear protein. Moreover, nuclei isolated from RA-treated HL-60 cells revealed calcium release in response to cADPR, whereas a similar response was not observed in control nuclei. These results suggest that CD38 is expressed in HL-60 cell nuclei during RA-induced differentiation.