Biomedical Engineering Reference
In-Depth Information
are obtained from human and mouse enteric nervous progenitors and applied to
mouse aganglionic bowel locating in aganglionic area, differentiating and restoring
normal contraction rate [
53
].
SCs have been also studied in ischemic colitis. In an animal model produced by
partial intestinal obstruction and ligation of marginal vessels, BM-MNCs were
directly injected on ischemic colonic wall; macroscopic and microscopic colitis
severity scores and whole-gut transit time decreased and capillary and myenteric
plexus density increased, both significantly compared with controls. Transplanted
cells were detected in all intestinal layers but authors could not demonstrate SCs
differentiation into vascular or neural cells [
54
].
Regarding fecal incontinence , there are studies on the application of BM-MSCs
for surgical damage and repair in rats [
55
], on muscle SCs for cryolesion in rats
[
56
], on myoblasts transplanted to mice after surgical damage [
57
] and with human
umbilical cord matrix and BM-MSCs from rabbit in rabbits [
58
]. A recently
published paper on a rabbit model of external sphincter surgical damage studied
delayed autologous muscle progenitor cells injection without surgical repair.
Authors found SCs in the sphincter, regenerated myotubes and a significant
decrease in interstitial fibrosis and higher Ki-67-positive cells in SCs group
(without cd-34 cells infiltration); manometry and electromyography showed also a
statistically significant improvement 4 weeks after cell injection [
59
]. Our group is
working with animal models of this condition with ASCs.
12.7.5 Inflammatory Bowel Disease
12.7.5.1 Crohn's Disease
Several studies have been performed. We highlight three murine models: one uses
murine and human ASCs [
60
], another applies BM-HSCs topically [
61
] and the
third compares HSCs and MSCs [
62
]. Generally, an improvement has been
reported. Studies have focussed on the regenerative and trophic role (providing
VEGF and TGF-b1-) [
61
,
63
], and immunoregulation [
64
] as therapeutic
mechanisms. Two good reviews on this topic are provided by Dryden et al. [
65
]
and by Lanzoni et al. [
66
]. More studies are needed to confirm the results.
12.7.5.2 Ulcerative Colitis
This condition has been tested later than Crohn's provided better treatments results
and that experimental models usually reproduce better Crohn's (transmural) than
Ulcerative Colitis (mucosal). Recent studies have suggested microvascular dys-
function and endothelial barrier defect or impaired contribution of BM-EPCs (by
decreased release and/or impaired homing to colon) as critical pathogenic mech-
anisms. All are ideas for SCs application [
67
].
