An article published this year in “The
FASEB Journal” using our “Apoptosis Detection Kit FITC”, by our customers from the University-Hospital
of Verona, Italy, in the analysis of how Heparanase regulates the M1
polarization of renal macrophages and their crosstalk with renal epithelial
tubular cells after ischemia/reperfusion injury. Congrats and Thanks.
Summay:
Heparanase (HPSE) is part of the biologic network
triggered by ischemia/reperfusion (I/R) injury, a complication of renal
transplantation and acute kidney injury. During this period, the kidney or
graft undergoes a process of macrophages recruitment and activation. HPSE may
therefore control these biologic effects. We measured the ability of HPSE and
its inhibitor, SST0001, to regulate macrophage polarization and the crosstalk
between macrophages and HK-2 renal tubular cells during in vitro hypoxia/reoxygenation
(H/R). Furthermore, we evaluated in
vivo renal inflammation,
macrophage polarization, and histologic changes in mice subjected to
monolateral I/R and treated with SST0001 for 2 or 7 d. The in vitro experiments showed
that HPSE sustained M1 macrophage polarization and modulated apoptosis, the
release of damage associated molecular patterns in post-H/R tubular cells, the
synthesis of proinflammatory cytokines, and the up-regulation of TLRs on both
epithelial cells and macrophages. HPSE also regulated M1 polarization induced
by H/R-injured tubular cells and the partial epithelial–mesenchymal transition
of these epithelial cells by M1 macrophages. All these effects were prevented
by inhibiting HPSE. Furthermore, the inhibition of HPSE in vivo reduced
inflammation and M1 polarization in mice undergoing I/R injury, partially restored
renal function and normal histology, and reduced apoptosis. These results show
for the first time that HPSE regulates macrophage polarization as well as renal
damage and repair after I/R. HPSE inhibitors could therefore provide a new
pharmacologic approach to minimize acute kidney injury and to prevent the
chronic profibrotic damages induced by I/R.—Masola, V., Zaza, G., Bellin, G.,
Dall’Olmo, L., Granata, S., Vischini, G., Secchi, M. F., Lupo, A., Gambaro, G.,
Onisto, M. Heparanase regulates the M1 polarization of renal macrophages and
their crosstalk with renal epithelial tubular cells after ischemia/reperfusion
injury.
Reference:
Product link:
Apoptosis Detection Kit FITC
http://www.immunostep.com/apoptosis/3727-anxvkf-100t.html
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