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47
4
Histology of the mesentery
J. CALVIN COFFEY, MIRANDA KIERNAN, AND LEON G. WALSH
Order is the shape upon which beauty depends.
Pearl Buck
AIM
e aim of this chapter is to demonstrate recent ndings
related to the histology of the mesentery and associated
peritoneum. A secondary aim is to highlight the clinical
relevance of these properties.
INTRODUCTION
Remarkably, little data are available on the histology of
the mesentery and associated peritoneal reection. Still
less is known regarding the clinical relevance of mesen-
teric and peritoneal histology. is probably relates to the
erroneous concept that the mesentery functions solely as a
scaff ld for nerves and vessels and as a result has attracted
little attention [1–3]. Recent investigation has increas-
ingly focused on omental and visceral fat leading to the
identication of numerous immunologic functions for
both [4–8]. Data are emerging that supports endocrine
and metabolic roles for adipose tissue in general [9–16].
Similar ndings are emerging in relation to the mesen-
tery in particular, with direct links identifi d between the
mesenteric production of C-reactive protein and systemic
levels of this in disease states [17–22]. Increasing data
indicates that the mesentery is highly active in coordinat-
ing local and systemic physiologic events and is far from
the inert bystander previously thought. is, coupled with
recent clarications of macroscopic anatomy, prompt a
reappraisal of mesenteric histology and its relevance to
clinical practice [23,24].
In order to redress the aforementioned decit, our group
conducted a broad evaluation of mesenteric histology
[25]. Full thickness mesenteric biopsies were examined at
all mesenteric regions from duodenojejunal exure to the
anorectal junction (Figure 4.1). A cadaveric approach was
adopted as a similar study in living patients would endanger
retroperitoneal organs such as the ureters, gonadal vessels,
and duodenum. Samples were examined using a variety
of histologic, immunohistochemical, and electron micro-
scopic approaches to generate a comprehensive appraisal.
is chapter focuses largely on the ndings of this study and
their implications across multiple clinical and nonclinical
sciences.
MESENTERIC MESOTHELIUM AND
TOLDT’S FASCIA: THE MESOFASCIAL
PLANE
Mesenteric histologic appearances are remarkably consistent
from duodenojejunal to anorectal level (Figure 4.1a through
c). e small intestinal mesentery and mobile component of
the mesosigmoid have medial and lateral surfaces. In keep-
ing with the above, both surfaces are covered by mesothe-
lium (Figure 4.2). e transverse mesocolon has an upper
and lower surface that is lined with mesothelium (Figure
4.3). While the right and left mesocolon have an upper sur-
face that is readily apparent, the undersurface of each is
attached to Toldt’s fascia and the underlying retroperito-
neum. Again, both surfaces of the right and left mesocolon
are lined with mesothelium (Figure 4.4).
Aim 47
Introduction 47
Mesenteric mesothelium and Toldt’s fascia: The
mesofascial plane 47
Nomenclature: The visceral andparietal peritoneum 49
Immunohistochemical analysis ofmesenteric
mesothelium 50
Mesenteric connective tissue lattice 51
Mesothelial cell plasticity 53
Future directions 54
Summary 54
References 54
48 Histology of the mesentery
Wherever mesentery attaches to retroperitoneum, a
distinct fascial layer (Toldt’s fascia) occurs between both
(Figure 4.1b and c) [25–27]. Beneath Toldt’s fascia a fur-
ther mesothelial layer covers the retroperitoneum itself.
Variations occur in the composition of Toldt’s fascia [25,26].
e fascia will be discussed in detail in Chapter 5.
Th s arrangement of mesothelium and fascia is impor-
tant as it generates the plane that is exploited in good quality
colorectal surgery. A surgical plane is defi ed as the interface
between two contiguous surfaces. Surgical planes provide an
anatomic roadmap by which structures may be freed from
their normal anatomic attachments to permit safe division
and resection. e plane used most oen in colorectal sur-
gery occurs at the interface between the mesothelium on
the under surface of the mesentery and Toldt’s fascia, that
is, the mesofascial plane. Components of this plane may
Surface
mesothelium
Surface
mesothelium
Deep
mesothelium
Retr
operitoneal
mesothelium
Mesocolon
Mesocolon
(a)
(b)
(c)
Mesocolon and retroperitoneum
Toldt’s fascia
Toldt’s fascia
Toldt’s fascia
Retroperitoneum
Retroperitoneum
Retroperitoneum
1 mm
Mesentery
proper
Figure 4.1 (a) 2.5D snapshot of 3D digital sculpture depicting the histologic structure of the mesentery and underlying
fascia. (b) Photomicrograph demonstrating the mesentery, underlying fascia, and retroperitoneum at the level of the left
mesocolon. (c) Scanning electron micrograph demonstrating the mesentery, fascia, and retroperitoneum at the level of
the right mesocolon.
Nomenclature: The visceral andparietal peritoneum 49
be separated surgically in a manner that allows complete
separation of the mesentery from the posterior abdominal
wall[24].
NOMENCLATURE: THE VISCERAL
ANDPARIETAL PERITONEUM
Mesenteric mesothelium is smooth surfaced, highly
functional, and comprises a single layer of cuboidal-
shaped cells [25]. It closely resembles pleural mesothelium
and is similar to peritoneum elsewhere within the abdo-
men. Manyanatomic texts subdivide the abdominal peri-
toneum into “parietal” and “visceral” regions. Parietal
peritoneum lines the inner aspect of the abdominal wall
while visceral peritoneum covers the abdominal viscera
(including the mesentery) [1–3,27]. us, the mesothelial
covering on either side of the human mesentery corre-
sponds to “visceral peritoneum” (Figure 4.1). In keeping
with the above, mesothelium overlying the retroperito-
neum (i.e.,beneath Toldt’s fascia) corresponds to “pari-
etal peritoneum” (Figure 4.1). It is not uncommon for
these to be referred to as the visceral and parietal fascia,
respectively [28–36]. As they are not anatomic fascia, this
terminology is inaccurate. Moreover, it is also confusing
as the only true fascia in this region is Toldt’s fascia, that
is, the fascia interposed between the visceral and parietal
peritoneum.
Th oughout this book, the terms “visceral” and “parietal”
peritoneum will be adopted and the term “fascia” will be
reserved exclusively for Toldt’s fascia (Figure 4.3) [37].
Mesothelium
Sample
origin
Small intestinal mesentery
Mesothelium
Adipocytes
20,000 µm
(a) (b)
Connec
tive tissue
septation
Small
intestinal
mesentery
Figure 4.2 (a) 2.5D snapshots from a 3D digital model of the mesentery demonstrating the location at which full thickness
biopsies were taken through the small bowel mesentery. (b) Photomicrograph demonstrating the structure of the small
intestinal mesentery.
Transverse mesocolon
Connective tissue
septation
Lower surface
mesothelium
(b)(a)
20,000 µm
Connective
tissue
Upper sur
face
mesothelium
Adipocyte lobule
Sample from
transverse colon
Figure 4.3 (a) 2.5D snapshots from a 3D digital model of the mesentery demonstrating the location at which full thickness
biopsies were taken through the transverse mesocolon. (b) Photomicrograph demonstrating the structure of the trans-
verse mesocolon.
50 Histology of the mesentery
IMMUNOHISTOCHEMICAL ANALYSIS
OFMESENTERIC MESOTHELIUM
Immunohistochemical evaluation of surface mesenteric meso-
thelium demonstrates expression of markers including D2-40
(podoplanin) and CD-35 [26,38]. Few studies have directly
focused on surface marker expression in mesenteric versus
nonmesenteric mesothelium. Indeed, no studies have examined
surface marker expression in mesocolic mesothelium (i.e., vis-
ceral peritoneum), Toldt’s fascia, nor in mesothelium beneath
Toldt’s fascia (i.e., parietal peritoneum). As surface marker
expression relates to cellular functionality, this is a key area for
future research. Table4.1 provides a summary of the surface
markers associated with peritoneal mesothelium in general.
Although it is feasible the properties listed can be extrapolated
to the mesenteric context, this should be investigated.
Left mesocolon
biopsy
Left mesocolon
(a) (b)
Sur
face mesothelium
100 µm
Adipocyte lobule
Connective tissue
lattice
Toldt’s fascia
Retroperitoneum
Left mesocolon
Figure 4.4 (a) 2.5D snapshots from a 3D digital model of the mesentery demonstrating the location at which full thickness
biopsies were taken through the left mesocolon. (b) Photomicrograph demonstrating the structure of the left mesocolon.
Table 4.1 Immunohistochemical markers expressed in surface mesothelium
Study Year Journal Marker Reference
Satelli etal. 2015 Clin Cancer Res 84-1/vimentin [39]
Yokobori etal. 2013 Cancer Res PLS3 [40]
Yung etal. 2011 J Biomed Biotechnol Hyaluronan [41]
Foroutan etal. 2010 J Biol Sci CD45 [42]
CD34
HBME-1
Cytokeratin 18
Rosellini etal. 2007 Folia Biol CKAE1-AE3 [43]
CK19
p63
Ki-67
Vimentin
CD34
HBME-1
Yáñez-Mó etal. 2003 N Engl J Med Cytokeratins [44]
ICAM-1
Yang etal. 1999 Perit Dial Int Cytokeratins [45]
Vimentin
Ho-dac-Pannekeet etal. 1997 Adv Perit Dial CA125 [46]
Mesenteric connective tissue lattice 51
MESENTERIC CONNECTIVE TISSUE
LAT TICE
A connective tissue layer occurs underneath mesenteric
visceral peritoneum. is is the “submesothelial connec-
tive tissue layer.” It is highly variable in thickness and
composition. In some regions, it is well developed, while
in others it is entirely absent (Figure 4.5). For example, it
is well developed on the upper surface of the transverse
mesocolon, where the latter is adherent to the greater
omentum. It is also well developed on the lateral aspect
of mesosigmoid. is distribution appears to correlate
with the presence of congenital adhesions. For example,
congenital adhesions are prominent at the lateral aspect of
the mesosigmoid. ey also cause the greater omentum to
adhere to the upper surface of the transverse mesocolon.
Submesothelial connective tissue
Connec
tive tissue
Undersurface
mesothelium
Surface
mesothelium
Avascular
interpedicular
mesentery
Ileocolic
adipovascular
pedicle
Surface
mesothelium
Septation
Submesothelial connective tissue
Submesothelial
connec
tive tissue
(a)
(b)
(c)
Figure 4.5 (a) Photomicrograph demonstrating the mesenteric surface. This is lined with mesothelium beneath which
there is a connective tissue layer (arrows) and from which connective tissue septations arise. The latter separate adipocyte
compartments. Adipocytes are packaged in a honeycomb-like conformation within compartments. (b)Histologic struc-
ture in an avascular interpedicular region of mesentery. Adipocytes are minimal and both mesothelial surfaces are close.
Thisgenerates a translucent macroscopic appearance (c).
52 Histology of the mesentery
Connective tissue branches, or septae, extend from the
submesothelial connective tissue into the substance of the
mesentery, separating the latter into adipocyte compart-
ments. Adipocytes are packaged in a honeycomb-like con-
formation (Figure 4.5) and together contribute the main
bulk of the mesentery. In certain mesenteric regions, adipo-
cytes are minimal and both mesenteric mesothelial surfaces
come into close apposition (Figure 4.5b,c) [23,25,26].
Macroscopically, these regions are identiable as being near
translucent. is property is of particular surgical relevance
as it enables the surgeon to divide through the mesentery
with minimal bleeding (Figure 4.5c).
Taken together, the connective tissue septae and subme-
sothelial connective tissue layer generate a lattice, the “mes-
enteric connective tissue lattice” (Figure 4.6a and b). is is
present throughout the mesentery. At the gastrointestinal
margin, it is continuous with connective tissue in outer lay-
ers of the gastrointestinal tract (Figure 4.6b and c). Here, the
lattice contributes directly to the formation of the intestinal
serosa. e serosa in turn contributes connective tissue to
the longitudinal and circular smooth muscle layers. Within
the mesentery, the lattice encases vessels contributing to the
adventitia of these.
Where major vessels enter or leave the mesentery, the
connective tissue of the lattice coalesces with that of the
underlying fascia to form a connective tissue cuff or adven-
titia. e perivascular connective tissue cuff is also of surgi-
cal relevance as it means that the mesentery can be readily
cleared from vascular surfaces, with minimal disruption of
either vessel or mesentery.
e submesothelial connective tissue layer is largely
acellular. However, cell clusters occur at points where septa-
tions arise (Figure 4.7a). Analysis of serial sections demon-
strates that on occasion, isolated cell clusters occur. e cells
within these clusters have mesenchymal features, resem-
bling broblast and myobroblasts. is is in keeping with
earlier ndings suggesting that cells within the submeso-
thelial connective tissue layer have surface markers that are
Submesothelial
connective
tissue
(a) (b)
(c) (d)
Connective tissue of
outer muscle layer
Mesenteric
connective
tissue
Mesenteric
connective
tissue
Mesenteric
connective
tissue
*
*
*
Surface
connective tissue
Intestinal
connective
tissue
Intestinal
connective
tissue
Connective tissue of
outer muscle layer
Connective tissue of
inner muscle layer
Mesenteric and intestinal connective tissue
Figure 4.6 (a) 2.5D image from 3D model demonstrating the mesenteric connective tissue lattice and its contiguity with
that in the adjacent gastrointestinal tract. (b) All tissue with exception of the connective tissue has been conceptually
removed from the model in (a) to depict the extent of the connective tissue lattice. (c) Photomicrograph showing connective
tissue contiguity between the mesentery and the gastrointestinal tract. (d) Photomicrograph demonstrating connective tissue
contiguity between deep and supercial muscle layers of the intestinal wall.
Mesothelial cell plasticity 53
intermediate between mesothelial and mesenchymal cells
[23,25,26]. Itisfeasible that mesenchymal cells within these
clusters are derived from overlying mesenteric mesothelium.
e connective tissue lattice also houses a lymphatic net-
work (Figure 4.7b and c). Lymphatic vessels are identiable
in the submesothelial connective tissue monolayer as well
as in septations. e frequency with which lymphatic ves-
sels are identifi d varies (though not signicantly) between
mesenteric regions. In submesothelial connective tissue,
lymphatic vessels measure 10.2 ± 4.1µm in diameter and
have an average radius of diusion of 174.72 ± 97.68 µm.
is means that a lymphatic vessel occurs every 0.17mm
(Figure 4.7b and c). Lymphatic vessels also occur in Toldt’s
fascia where they measure 4.3 ± 3.1µm in diameter and
have a radius of diusion of 165.12 ± 66.26µm. Collectively,
a rich lymphatic network occupies all levels of the mesen-
teric connective tissue lattice and may be vulnerable during
surgery [26].
MESOTHELIAL CELL PLASTICITY
A number of studies have demonstrated submesothelial
connective tissue cells with surface markers normally
observed in cells under transition from one state of dif-
ferentiation to another (i.e., from mesothelial to mesen-
chymal cell types) [39,40,47–49]. eseand other ndings
suggest that mesenteric mesothelium may be plastic and
capable of diffe entiating into multiple mesenchymal cell
types [42,50]. Foroutan etal. examined hematopoietic and
mesenchymal stem markers in mesothelial cells in peri-
toneal dialysate. ese were analyzed by cell culture, ow
cytometry, and immunophenotyping for CD45 and CD34
(hematopoietic stem cell markers), HBME-1 (mesothe-
lial cell marker), and cytokeratin 18 (epithelial marker).
While mesothelial cells expressed classical mesothelial
and epithelial surface markers, they also expressed CD34
(mesenchymal marker) and CD45 (hematopoietic marker)
[42]. Both mesenteric mesothelia and lymphoepithelia are
known to express podoplanin [38,51–53]. Mesothelia else-
where (e.g., hepatic and pleural) can undergo mesothelial-
to-mesenchymal transition [54–56]. Observations such as
these support the intriguing suggestion that mesenteric
mesothelial cells are not inert and could in fact contribute
to the local mesenchymal cellular pool [57–62]. is sug-
gestion is supported by our recent observations related to
the culture of mesenteric mesothelia. If mesenteric meso-
thelia are harvested, purifi d, and cultured, then follow-
ing 2 weeks a mixture of mesenchymal cell types emerges.
is property, when combined with the total surface area
of the extensively plicated mesentery, means that mesen-
teric mesothelium could represent a signicant stem cell
reservoir [63].
Mesenteric connective tissue lattice and lymphatics
Surface
mesothelium
(a)
Mesenchymal
cell cluster
(b)
Surface
mesothelium
(c)
Connective
tissue lattice
Deep
mesothelium
Mesenteric lymph
nodes and channels
with connective
tissue removed
Figure 4.7 (a) Photomicrograph showing the surface mesothelium of the right mesocolon. At certain points mesenchymal
cells clustered as indicated. (b) 3D sculpture demonstrating the connective tissue of the lattice and contained lymphatic
channels. (c) Same model as in (b) but with the connective tissue removed.
54 Histology of the mesentery
Derangements of mesenteric mesothelial plasticity may
contribute to multiple intraabdominal disease processes.
e origin of the cells responsible for adhesion formation
is not known. It is not unreasonable to suggest that surgical
disruption of mesenteric mesothelium may lead to a local-
ized or widespread mesenchymal response that results in
adhesion formation [63,64].
All abdominal wall hernia (out with the acute setting)
have a mesothelial component. Th s could be explained as
follows. As mesothelium proliferates an invagination devel-
ops. Given the secretery properties of mesothelium, the
inner surface of this is highly lubricated and thus permits
both entry and exit of abdominal contents. e cumulative
eect of persistent mechanical pressures (including positive
intraperitoneal pressure) leads to an increase in size of the
mesothelial invagination and ultimately to clinical manifes-
tation of the underlying pathology. Perhaps the best in vivo
model of this phenomenon is the parastomal hernia. Stoma
creation requires formation of a defect in the abdominal wall.
At formation, the local parietal mesothelium is disrupted.
With time, a mesothelial invagination arises that carpets the
subcutaneous tissue and is oen associated with herniation
of adjacent bowel loops. Th s is the parastomal hernia.
Mesothelial-to-mesenchymal transformation may also
contribute to the development of Crohn’s or diverticular dis-
ease [65–69]. In Crohn’s disease, mesenteric lymphangiec-
tasia occurs and correlates with the distribution of mucosal
abnormalities [70–73]. In patients with mesenteric adeni-
tis, a pronounced lymphadenopathy occurs at the ileocecal
mesenteric conuence. Lymph nodes may also develop in
appendices epiploicae [74–76]. Th s is surprising as classic
descriptions indicate that lymph nodes are confi ed to major
vessels. e identifi ation of nodes in appendices epiploices
(i.e., remote from major vessels) maybe further evidence of a
cellular ux involving nearby mesenteric mesothelium.
FUTURE DIRECTIONS
e characterization of mesenteric histology has raised
several suggestions that prompt investigation. ese could
involve a characterization of the role of mesenteric mesothe-
lium in several disease processes including adhesion forma-
tion, hernia development, and Crohn’s disease. e concept
of connective tissue contiguity should be explored in broader
terms. As has been demonstrated to date, the mesenteric con-
nective tissue lattice is contiguous with that of adjacent intes-
tine. e mesenteric connective tissue lattice also contributes
adventitia to contained vessels. ese fi dings suggest that a
systemic connective tissue platform occurs, which receives
inputs from mesenteric and intestinal sources and which
could provide a novel route of disease spread (Figure 4.6).
SUMMARY
e cellular and extracellular composition of the mesentery
is similar from the root region to the anorectal junction.
Multiple levels of continuity (including connective tissue,
vascular, neurologic, and lymphatic) occur between mesen-
tery and adjacent intestinal tract and between mesentery and
associated vessels. Characterization of mesenteric histology
provides opportunities to refresh approaches to several disease
processes including those involving systemic manifestations.
REFERENCES
1. Snell, R.S., Clinical Anatomy by Regions. Lippincott
Williams & Wilkins, 2008, pp. 216, 226, 228, 233,
237,240.
2. Cunningham, D.J., Cunningham’s Textbook of
Anatomy. W. Wood, 1818, pp. 1185, 1208, 1221,
1253, 1423.
3. Arnould-Taylor, W., A Textbook of Anatomy and
Physiology. Stanley Thornes, Surrey, U.K., 1998,
pp.60–68.
4. Hostmann, A. etal., Dendritic cells from human
mesenteric lymph nodes in inammatory and non-
inammatory bowel diseases: Subsets and function
of plasmacytoid dendritic cells. Immunology, 2013.
139(1): 100–108.
5. Bell, S.J. etal., Migration and maturation of human
colonic dendritic cells. J Immunol, 2001. 166(8):
4958–4967.
6. Silva, M.A., Intestinal dendritic cells and epithelial
barrier dysfunction in Crohn’s disease. Inamm
Bowel Dis, 2009. 15(3): 436–453.
7. Baumgart, D.C. etal., Patients with active inamma-
tory bowel disease lack immature peripheral blood
plasmacytoid and myeloid dendritic cells. Gut, 2005.
54(2): 228–236.
8. Kaser, A. etal., Increased expression of CCL20 in
human inammatory bowel disease. J Clin Immunol,
2004. 24(1): 74 –85.
9. Exley, M.A. etal., Interplay between the immune
system and adipose tissue in obesity. J Endocrinol,
2014. 223(2): R41–R48.
10. Fenzl, A. and F.W. Kiefer, Brown adipose tissue and
thermogenesis. Horm Mol Biol Clin Investig, 2014.
19( 1): 25 – 3 7.
11. Kloting, N. and M. Bluher, Adipocyte dysfunction,
inammation and metabolic syndrome. Rev Endocr
Metab Disord, 2014. 15(4): 277–287.
12. Porter, C., M. Chondronikola, and L.S. Sidossis,
The therapeutic potential of brown adipocytes in
humans. Front Endocrinol, 2015. 6: 156.
13. Ozen, G. etal., Human perivascular adipose tissue
dysfunction as a cause of vascular disease: Focus on
vascular tone and wall remodeling. Eur J Pharmacol,
2015. 766: 16–24.
14. Jeanson, Y., A. Carriere, and L. Casteilla, A new role
for browning as a redox and stress adaptive mecha-
nism? Front Endocrinol, 2015. 6: 158.
15. Grundy, S.M., Adipose tissue and metabolic syn-
drome: Too much, too little or neither. Eur J Clin
Invest, 2015. 45(11): 1209 –1217.
References 55
16. Canfora, E.E., J.W. Jocken, and E.E. Blaak, Short-
chain fatty acids in control of body weight and insulin
sensitivity. Nat Rev Endocrinol, 2015. 11(10): 577–591.
17. Declercq, C. etal., Mapping of inammatory bowel
disease in northern France: Spatial variations and
relation to afuence. Inamm Bowel Dis, 2010. 16(5):
807– 812.
18. Henriksen, M. etal., C-reactive protein: A predictive
factor and marker of inammation in inammatory
bowel disease. Results from a prospective popula-
tion-based study. Gut, 2008. 57(11): 1518–1523.
19. Lu, X. etal., Decay-accelerating factor attenuates
C-reactive protein-potentiated tissue injury after
mesenteric ischemia/reperfusion. J Surg Res, 2011.
167(2): e103 –e115.
20. Magro, F., P. Sousa, and P. Ministro, C-reactive
protein in Crohn’s disease: How informative is
it? Expert Rev Gastroenterol Hepatol, 2014. 8(4):
393–408.
21. Peyrin-Biroulet, L. etal., Mesenteric fat in Crohn’s
disease: A pathogenetic hallmark or an innocent
bystander? Gut, 2007. 56(4): 577– 583.
22. Peyrin-Biroulet, L. etal., Mesenteric fat as a source
of C reactive protein and as a target for bacterial
translocation in Crohn’s disease. Gut, 2012. 61(1):
78–85.
23. Culligan, K. etal., The mesocolon: A prospective
observational study. Colorectal Dis, 2012. 14(4):
421–428; discussion 428–430.
24. Coffey, J.C. etal., Mesenteric-based surgery exploits
gastrointestinal, peritoneal, mesenteric and fascial
continuity from duodenojejunal exure to the
anorectal junction—A review. Dig Surg, 2015. 32(4):
291–300.
25. Culligan, K. etal., The mesocolon: A histological and
electron microscopic characterization of the mesen-
teric attachment of the colon prior to and after surgi-
cal mobilization. Ann Surg, 2014. 260(6): 1048 –1056.
26. Culligan, K. etal., A detailed appraisal of mesocolic
lymphangiology—An immunohistochemical and
stereological analysis. J Anat, 2014. 225(4): 463 – 472.
27. Standring, S., Gray’s Anatomy: The Anatomical Basis
of Clinical Practice. Churchill Livingstone/Elsevier,
Edinburgh, Scotland, 2008, pp. 1085, 1099–1111, 1143.
28. Lin, M.B. etal., Understanding the planes of total
mesorectal excision through surgical anatomy of
pelvic fascia. Zhonghua Wei Chang Wai Ke Za Zhi,
2008. 11(4): 308 – 311.
29. Coffey, J.C. and P. Dockery, Colorectal cancer:
Surgery for colorectal cancer—Standardization
required. Nat Rev Gastroenterol Hepatol, 2016.
13(5): 256–257.
30. Thorek, P., C.T. Linden, and N. Swan, Anatomy in
Surgery. Springer, New York, 2012, pp. 327–329, 458,
506, 511, 532.
31. Lin, M. etal., The anatomic basis of total mesorectal
excision. Am J Surg, 201(4): 537–543.
32. Acar, H.I. etal., Dynamic article: Surgical anatomical
planes for complete mesocolic excision and applied
vascular anatomy of the right colon. Dis Colon
Rectum, 2014. 57(10 ) : 116 9 –1175.
33. Gao, Z. etal., An anatomical, histopathological, and
molecular biological function study of the fascias
posterior to the interperitoneal colon and its associ-
ated mesocolon: Their relevance to colonic surgery.
J Anat, 2013. 223(2): 123–132.
34. Sondenaa, K. etal., The rationale behind complete
mesocolic excision (CME) and a central vascular
ligation for colon cancer in open and laparoscopic
surgery: Proceedings of a consensus conference. Int
J Colorectal Dis, 2014. 29(4): 419– 428.
35. Klingensmith, M.E. and W.U.D. Surgery, The
Washington Manual of Surgery. Wolters Kluwer
Health/Lippincott Williams & Wilkins, Philadelphia,
PA, 2008, pp. 199, 207.
36. Roy, H., Short Textbook of Surgery. Jaypee Brothers,
Medical Publishers Pvt. Limited, New Delhi, India,
2010, Chapter 41, p. 260.
37. Culligan, K. etal., Review of nomenclature in colonic
surgery—Proposal of a standardised nomencla-
ture based on mesocolic anatomy. Surgeon, 2013.
11(1):1–5.
38. Ordonez, N.G., D2-40 and podoplanin are highly
specic and sensitive immunohistochemical markers
of epithelioid malignant mesothelioma. Hum Pathol,
2005. 36(4): 372–380.
39. Satelli, A. etal., Epithelial-mesenchymal transitioned
circulating tumor cells capture for detecting tumor
progression. Clin Cancer Res, 2015. 21(4): 899–906.
40. Yokobori, T. etal., Plastin3 is a novel marker for
circulating tumor cells undergoing the epithelial-mes-
enchymal transition and is associated with colorectal
cancer prognosis. Cancer Res, 2013. 73(7): 2059–2069.
41. Yung, S. and T.M. Chan, Pathophysiology of the perito-
neal membrane during peritoneal dialysis: The role of
hyaluronan. J Biomed Biotechnol, 2011. 2011: 180594.
42. Foroutan, T., A. Hosseini, A.A. Pourfatholah, M.
Soleimani, K. Alimoghadam, and N. Mosaffa,
Peritoneal mesothelial progenitor or stem cell. J Biol
Sci, 2010. 10(5): 460.
43. Rosellini, A. etal., Expansion of human mesothelial
progenitor cells in a longterm three-dimensional
organotypic culture of Processus vaginalis peritonei.
Folia Biol, 2007. 53(2): 50–57.
44. Yanez-Mo, M. etal., Peritoneal dialysis and
epithelial-to-mesenchymal transition of mesothelial
cells. NEngl J Med, 2003. 348(5): 403–413.
45. Yang, W.S. etal., Interleukin-1beta stimulates the
production of extracellular matrix in cultured human
peritoneal mesothelial cells. Perit Dial Int, 1999.
19(3): 211–220.
46. Ho-dac-Pannekeet, M.M. etal., Markers of
peritoneal mesothelial cells during treatment with
peritoneal dialysis. Adv Perit Dial, 1997. 13: 17– 22.