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Fig. 4.9 In vitro matrigel assays to compare the ability of meprin
null and wild-type leukocytes
b
to infiltrate matrigel. Meprin
null ( filled square ) or age- and strain-matched wild-type ( open
square ) mesenteric lymph node leukocytes (1.7 10 5 /well) were incubated in the upper well of
triplicate matrigel chambers, with 10 nMMCP-1 (a) or 10 nMMIP-1 a (b) in the lower reservoir of
the matrigel chamber. After 18 h, the filters were stained to reveal those cells that infiltrated
through the matrigel and onto the filter. The infiltrating cells were counted in 5-20 fields
(*, p < 0.05, n ΒΌ 15). (c) Matrigel assays were performed to detect meprin b and the macro-
phage-specific protein F4/80 on wild-type leukocytes infiltrating matrigel. The filters were incu-
bated with PE-conjugated anti-F4/80 mAb ( red , c) or isotype control ( red , d) and rabbit antimeprin
b antisera (c) or rabbit nonimmune sera (d), followed by FITC-conjugated donkey antirabbit IgG
( green ). Horscht stain was used as a nuclear counterstain ( blue ) (Crisman et al. 2004 )
b
evidence that polymorphisms in the human meprin
gene are associated with IBD,
especially ulcerative colitis (Banerjee et al. 2009 ). These findings coupled with the
observation that meprin
a
mRNA is significantly lower in inflamed tissue of IBD
patients, strongly implicates a lack of meprin
a
in the pathogenesis of the disease.
a
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