Myofibroblasts. II. Intestinal subepithelial myofibroblasts

Powell, Don W.; Mifflin, Randy C.; Valentich, J. D.; Crowe, Sheila E.; Saada, Jamal I.; West, A. Brian

doi:10.1152/ajpcell.1999.277.2.c183

Cited by 527 publications

(546 citation statements)

References 216 publications

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“…[29][30][31][32] In fact, the features of subepithelial myofibroblasts in lung adenocarcinoma are quite similar to those reported for pericryptal fibroblasts Figure 4 Subepithelial myofibroblasts in invasive lung adenocarcinomas (a-smooth muscle actin staining). In areas of central collapse and fibrosis, the myofibroblastic layer around the neoplastic acinar structure was discontinuous (a).…”

Section: Discussionsupporting

confidence: 55%

“…Pericryptal fibroblasts are more abundant in adenoma than in normal colon, and gradually decrease during the progression from adenoma to intramucosal carcinoma to submucosal invasive carcinoma. [29][30][31][32] In invasive carcinomas they are virtually absent. 29 Pericryptal fibroblasts are also absent in normal gastric mucosa.…”

Section: Discussionmentioning

confidence: 99%

“…[29][30][31][32] In invasive carcinomas they are virtually absent. 29 Pericryptal fibroblasts are also absent in normal gastric mucosa. 33 Interestingly, however, they appear in intestinal metaplastic glands, but disappear in the neoplastic glands of gastric adenocarcinomas of intestinal type.…”

Section: Discussionmentioning

confidence: 99%

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Subepithelial myofibroblast in lung adenocarcinoma: a histological indicator of excellent prognosis

et al. 2009

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We report here the presence of subepithelial myofibroblasts in pure bronchioloalveolar carcinoma and a subset of invasive lung adenocarcinoma. The subepithelial myofibroblasts we describe were observed in a peculiar location beneath the cancer cells in the alveolar septa. Immunohistochemically, they were positive for a-smooth muscle actin and calponin, but negative for desmin and h-caldesmon. To gain insight into their biological significance, we examined 116 surgically resected lung adenocarcinomas. The resected tumors included 13 bronchioloalveolar carcinomas, 20 mixed type adenocarcinomas with bronchioloalveolar carcinoma components, 57 papillary adenocarcinomas, 22 solid adenocarcinomas with mucin, and 4 acinar adenocarcinomas. All specimens were immunostained for a-smooth muscle actin to visualize the myofibroblasts. In all of the pure bronchioloalveolar carcinomas observed, the subepithelial myofibroblasts were completely preserved adjacent to the cancer cells. In mixed adenocarcinomas with bronchioloalveolar carcinoma components, subepithelial myofibroblasts were present in the bronchioloalveolar carcinoma components, but scanty in the invasive areas, where stromal myofibroblasts emerged between the cancer cell nests. Subepithelial myofibroblasts were retained, however, in the invasive areas of a subset of invasive adenocarcinomas. Survival analysis showed that the retention of subepithelial myofibroblasts in these invasive tumors was associated with low rates of lymphatic and vascular invasion, a low rate of lymph node involvement, and an excellent patient survival. These results suggest that subepithelial myofibroblasts increase in bronchioloalveolar carcinomas, but are gradually replaced by typical stromal myofibroblasts during progression into invasive cancer. A subset of invasive adenocarcinomas retains subepithelial myofibroblasts. Analysis of subepithelial myofibroblasts may be helpful in identifying a subset of lung adenocarcinoma with excellent prognosis.

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Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

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Subepithelial myofibroblast in lung adenocarcinoma: a histological indicator of excellent prognosis

et al. 2009

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“…34 Additionally, CB2 knockout mice are more sensitive than wild-type littermates to bleomycin-induced dermal fibrosis. 35 As > 30 % of patients with Crohn ' s disease develop intestinal fibrosis leading to stricture formation, frequently requiring surgical resection, 36 and myofibroblasts are key cells in the process of wound healing and stricture formation in the gut, 37 we investigated the in vitro effects of MAEA on myofibroblasts isolated from intestinal Crohn ' s disease strictures. We found that MAEA reduced collagen production by strictured Crohn ' s disease myofibroblasts and increased their migration ability, thus supporting the view that endocannabinoid pathways might be involved in the fibrogenic process in Crohn ' s disease.…”

Section: Articlesmentioning

confidence: 99%

The endogenous cannabinoid system in the gut of patients with inflammatory bowel disease

et al. 2011

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Activation of cannabinoid receptors (CBs) by endocannabinoids impacts on a number of gastrointestinal functions. Recent data indicate that CB1 agonists improve 2,4-dinitrobenzene sulfonic acid-induced colitis in mice, thus suggesting a role for the endocannabinoid agonist anandamide (AEA) in protecting the gut against inflammation. We here examined the gut endocannabinoid system in inflammatory bowel disease (IBD) patients, and investigated the ex vivo and in vitro effects of the non-hydrolysable AEA analog methanandamide (MAEA) on the mucosal proinflammatory response. The content of AEA, but not of 2-arachidonoyl-glycerol and N-palmitoylethanolamine, was significantly lower in inflamed than uninflamed IBD mucosa, and this was paralleled by lower activity of the AEA-synthesizing enzyme N-acyl-phosphatidylethanolamine-specific phospholipase D and higher activity of the AEA-degrading enzyme fatty acid amide hydrolase. MAEA significantly downregulated interferon-γ and tumor necrosis factor-α secretion by both organ culture biopsies and lamina propria mononuclear cells. Although these results are promising, further studies are needed to determine the role of cannabinoid pathways in gut inflammation.[...

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“…1,6,17,18 CAFs as key factors of abnormal epithelial-stromal interaction and their powerful tumor-supportive effect (eg, increased regulator ligand and extracellular matrix molecule expression) are well known compared with normal stromal cells with similar morphology, that is, subepithelial myofibroblasts. [18][19][20] Tumor cellreleased exosomes are also detectable in the circulation where the plasma level of their specific proteins (eg, CD63 and tumor susceptibility gene 101/TSG101) and miRNA content may be useful as diagnostic and/or prognostic markers in different tumor types including colorectal carcinomas. [21][22][23][24] Our study was designed to analyze the top exosome-specific markers based on change of their tissue mRNA level during colorectal adenomacarcinoma sequence.…”

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confidence: 99%

Exosomes in colorectal carcinoma formation: ALIX under the magnifying glass

et al. 2016

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Exosomes are small membrane vesicles that have important roles in transporting a great variety of bioactive molecules between epithelial compartment and their microenvironment during tumor formation including colorectal adenoma-carcinoma sequence. We tested the mRNA expression of the top 25 exosome-related markers based on ExoCharta database in healthy (n = 49), adenoma (n = 49) and colorectal carcinoma (n = 49) patients using Affymetrix HGU133 Plus2.0 microarrays. Most related genes showed significantly elevated expression including PGK1, PKM, ANXA5, ENO1, HSP90AB1 and MSN during adenoma-carcinoma sequence. Surprisingly, the expression of ALIX (ALG 2-interacting protein X), involved in multivesicular body (MVB) and exosome formation, was significantly reduced in normal vs adenoma (P = 5.02 × 10 − 13 ) and in normal vs colorectal carcinoma comparisons (P = 1.51 × 10 − 10 ). ALIX also showed significant reduction (Po 0.05) at the in situ protein level in the epithelial compartment of adenoma (n = 35) and colorectal carcinoma (n = 37) patients compared with 27 healthy individuals. Furthermore, significantly reduced ALIX protein levels were accompanied by their gradual transition from diffuse cytoplasmic expression to granular signals, which fell into the 0.6-2 μm diameter size range of MVBs. These ALIX-positive particles were seen in the tumor nests, including tumorstroma border, which suggest their exosome function. MVB-like structures were also detected in tumor microenvironment including α-smooth muscle actin-positive stromal cells, budding off cancer cells in the tumor front as well as in cancer cells entrapped within lymphoid vessels. In conclusion, we determined the top aberrantly expressed exosome-associated markers and revealed the transition of diffuse ALIX protein signals into a MVB-like pattern during adenoma-carcinoma sequence. These tumor-associated particles seen both in the carcinoma and the surrounding microenvironment can potentially mediate epithelial-stromal interactions involved in the regulation of tumor growth, metastatic invasion and therapy response.

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Myofibroblasts. II. Intestinal subepithelial myofibroblasts

Cited by 527 publications

References 216 publications

Subepithelial myofibroblast in lung adenocarcinoma: a histological indicator of excellent prognosis

Subepithelial myofibroblast in lung adenocarcinoma: a histological indicator of excellent prognosis

The endogenous cannabinoid system in the gut of patients with inflammatory bowel disease

Exosomes in colorectal carcinoma formation: ALIX under the magnifying glass

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