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Transcriptional expression and gelatinolytic activity of matrix metalloproteinases in Henoch–Schonlein purpura
Author(s) -
Mahajan N,
Bisht D,
Dhawan V,
Singh S,
Minz RW
Publication year - 2010
Publication title -
acta pædiatrica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 115
eISSN - 1651-2227
pISSN - 0803-5253
DOI - 10.1111/j.1651-2227.2010.01781.x
Subject(s) - henoch schonlein purpura , medicine , matrix metalloproteinase , extracellular matrix , zymography , vasculitis , immunology , peripheral blood mononuclear cell , gelatinase , disease , biology , biochemistry , in vitro , microbiology and biotechnology
Aim: Accelerated extracellular matrix breakdown caused by the increased activity of matrix metalloproteinases (MMPs) has been implicated in several rheumatological disorders and systemic vasculitides, especially Takayasu’s arteritis and Kawasaki disease. Therefore, the aim of the present study was to investigate the potential role of MMPs in Henoch–Schonlein purpura (HSP), an acute type of systemic vasculitis in children. Methods: We studied the activity of MMP‐2 and MMP‐9 in the sera using gelatin zymography and the transcriptional expression in peripheral blood mononuclear cells using semi‐quantitative RT‐PCR in 20 patients with HSP in acute and convalescent phase and in 20 healthy children, who were siblings of the subjects with same age group. Results: All 20 children with HSP showed increased levels of serum activity of MMP‐2 and MMP‐9 in acute phase as compared with their convalescent phase [MMP‐2 (p > 0.05); MMP‐9 (p > 0.05)] and their control counterparts [MMP‐2 (p < 0.001); MMP‐9 (p < 0.001)]. Similarly, transcriptional expression of MMPs was found to be higher in the acute phase of HSP than in convalescent phase [MMP‐2 (p < 0.05); MMP‐9 (p < 0.001)] and in their healthy controls [MMP‐2 (p < 0.001); MMP‐9 (p < 0.01)]. Conclusion: The presence of excessive transcriptional expression and gelatinolytic activity of MMPs may be downstream to the actual aetiopathogenetic factors.