Altogether, these data suggested that TfR/CD71 overexpression and ERK1/2 and PI3K/AKt/mTOR activation were engaged in HMC proliferation induced by IgA1 from HSP patients, which might be related to the mesangial injury of HSPN.
Spearman correlation analysis shows that: (i) AOPPs and Gd-IgA1 in HSP patients are positively correlated; both of them are positively correlated with the disease severity scores; (ii) AOPPs are negatively correlated with the relative expression value (RQ) of Cosmc mRNA.
In this respect, idiopathic IgAN and Henoch Schonlein Purpura have been the object of studies revealing a pathogenetic role of aberrant glycosylation of IgA1 molecules.
In addition, the bax and P53 expression were up-regulated and the Bcl-2 expression was down-regulated in HUVEC co-cultured with IgA1 isolated from HSP patients for 24 hours.
Henoch-Schönlein purpura nephritis (HSPN) is the most serious long-term complication of Henoch-Schönlein purpura and aberrant galactosylation of IgA1 plays a role in its development.
Abnormalities of immunoglobulin A1 (IgA1) glycosylation have been described in patients with IgA nephropathy (IgAN), whether primitive or secondary to Henoch-Schönlein purpura.