Biomedical Engineering Reference
In-Depth Information
Fig. 9
Translocation of p120 catenin from the juxtamembrane position to cytoplasmic. Let ,
normal pancreatic parenchyma showing linear, crisp membrane staining for p120 in contrast to,
right, the intense cytoplasmic positivity in a solid pseudopapillary tumor. Reprinted from Chet y
et al.
(2008), with permission. © 2008 American Society for Clinical Pathology.
Color image of this i gure appears in the color plate section at the end of the topic.
Inflammation
It is theorized that as squamous epithelial cells, such as cervical epithelium,
mature, they undergo a downregulation of the genes responsible for the synthesis
of adhesion molecules and are exfoliated at the surface (Politi
et al.
2008).
Immunohistochemistry methods have demonstrated that some infections inhibit
the normal downregulation of the surface epithelial cells, resulting in clusters of
cells still tightly bound to each other.
Pathology: Acute Renal Failure
Acute renal failure is characterized by a loss of cell polarity as assessed by
translocation of Na
+
K
+
-ATPase to the apical domain and loss of the barrier
function of the tubular epithelium (Nissenson 1998); importantly, both of these
changes involve disruption of intercellular adhesion, specii cally the cadherin/
catenin complex. Using an
in vitro
model, we have demonstrated that ischemia is
associated with disruption of intercellular adhesions in the proximal tubules of the
a simulated ischemia model in normal rat kidney causes translocation of β-catenin
to a perinuclear location, as seen in Fig. 11, but was not associated with activation
of β-catenin signaling (Chen
et al.
2007). h is result is consistent with several
studies suggesting that loss of cadherin function is not always associated with
activation of β-catenin signaling (Vasioukhin
et al.
2001). Disruption of cadherin/
catenin complexes during acute renal failure is demonstrated
in vivo
, as evidenced
