Proliferation of a-Smooth Muscle Actin-containing Stromal Cells (Myofibroblasts) in the Lamina Propria Subjacent to Intraepithelial Carcinoma of the Esophagus

2001 ◽  
Vol 36 (1) ◽  
pp. 86-91
Author(s):  
S. Tsuzuki, H. Ota, M. Hayama, A. S
Keyword(s):  
Smooth Muscle ◽  
Lamina Propria ◽  
Stromal Cells ◽  
Smooth Muscle Actin ◽  
Muscle Actin ◽  
Carcinoma Of The Esophagus ◽  
Intraepithelial Carcinoma

Epithelial Cells and Their Neighbors I. Role of intestinal myofibroblasts in development, repair, and cancer

2005 ◽  
Vol 289 (1) ◽  
pp. G2-G7 ◽  
Author(s):  
D. W. Powell ◽  
P. A. Adegboyega ◽  
J. F. Di Mari ◽  
R. C. Mifflin
Keyword(s):  
Lamina Propria ◽  
Information Flow ◽  
Stromal Cells ◽  
Smooth Muscle Actin ◽  
Distant Metastases ◽  
Muscle Actin ◽  
Mural Cells ◽  
Intestinal Neoplasms ◽  
Extracellular Matrix Molecules

Intestinal myofibroblasts are α-smooth muscle actin-positive stromal cells that exist as a syncytium with fibroblasts and mural cells in the lamina propria of the gut. Through expression and secretion of cytokines, chemokines, growth factors, prostaglandins, and basal lamina/extracellular matrix molecules, as well as expression of adhesion molecules and receptors for many of the same soluble factors and matrix, myofibroblasts mediate information flow between the epithelium and the mesenchymal elements of the lamina propria. With the use of these factors and receptors, they play a fundamental role in intestinal organogenesis and in the repair of wounding or disease. Intestinal neoplasms enlist and conscript myofibroblast factors and matrix molecules to promote neoplastic growth, carcinoma invasion, and distant metastases.

Stromal Incorporation of VEGFR-1+, CD68+ and α-SMA+ Hemangiogenic Cells Correlates with Histologic Subtype in Non-Hodgkin’s Lymphoma.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 1930-1930 ◽  
Author(s):  
Jia Ruan ◽  
Elizabeth Hyjek ◽  
Andrea T. Hooper ◽  
Loic Vincent ◽  
Pouneh Kermani ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Stromal Cells ◽  
Smooth Muscle Actin ◽  
Hematopoietic Cells ◽  
Hodgkin's Lymphoma ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin ◽  
Stromal Compartment ◽  
Non Hodgkin's Lymphoma ◽  
Benign Hyperplasia

Abstract BACKGROUND: Tumor stromal environment has been increasingly recognized to contribute to tumorigenesis. Vascular endothelial growth factor receptor-1+ (VEGFR-1+) hematopoietic cells and alpha-smooth muscle actin+ (α-SMA+) stromal cells both contribute to tumor neo-angiogenesis. However, their roles in promoting neo-angiogenesis specifically in human lymphomas remain unknown. METHODS: We examined the spatial localization of vascular and stromal cells expressing CD34 (vasculature), α-SMA (stromal cells), VEGFR-1 (hematopoietic cells and neo-vessels) and CD68 (myelomonocytic hematopoietic cells) by immunohistochemistry in 42 cases of non-Hodgkin’s lymphoma (NHL) specimens, which include diffuse large B-cell lymphoma (DLBCL, n=28), Burkitt lymphoma (BL, n=2), follicular lymphoma (FL, n=7), and chronic lymphocytic leukemia / small lymphocytic lymphoma (CLL/SLL, n=5). RESULTS: There was a significant increase in CD68+ hematopoietic cells and a profound increase in the tissue hemangiogenic index, as defined by the degree of infiltration of both VEGFR-1+ neo-vessels and CD68+ cells, in aggressive lymphomas including DLBCL as compared to the indolent subtypes. Specifically, CD68 cell counts (mean±S.E. in 200X high power field (HPF)) for aggressive vs. indolent vs. benign hyperplasia were: 235.48±16.91 (n=30) vs. 35.98±4.48 (n=12) vs. 79.06±12.41 (n=5), p<0.0001 by ANOVA test; hemangiogenic index for DLBCL vs. CLL vs. FL: 18.14±1.27% (n=5) vs. 3.39±0.97% (n=4) vs. 6.08±1.26% (n=5), p< 0.0001. Transformed DLBCL (from indolent subtypes) had a similar increase in CD68+ cells compared to de novo DLBCL (193.97±58.10 (n=5) vs. 241.77±18.15 (n=23), p=0.81). In DLBCL, CD68+ cells were localized to the peri-endothelial region of the VEGFR-1+ neo-vessels and stromal compartment. Remarkably, although the expression of alpha-smooth muscle actin (α-SMA) was barely detectable in the aggressive subtypes, there was a profound diffuse increase of α-SMA throughout the stromal compartment of CLL/SLL. Surprisingly, there was no correlation between the CD34+ microvessel density (MVD) and the lymphoma subtypes (aggressive vs. indolent vs. benign hyperplasia: 39.29±3.42 vs. 41.88±5.38 vs. 47.92±5.84, p=0.61). CONCLUSIONS: These data introduce the novel concept that the extent of vessel density has no correlation with the histologic grade of lymphomas. However, the stromal hemangiogenic index, as quantified by the incorporation of CD68+, VEGFR-1+, and α-SMA+ cells, correlates with NHL subtypes. Increased incorporation of pro-angiogenic CD68+ cells and diminished localization of α-SMA+ cells to the peri-vascular zone may contribute to enhanced neo-angiogenesis and tumor growth in DLBCL; while decrease in the CD68+ cells and increase in the α-SMA+ cells may promote neo-vessel stability in CLL/SLL. Thus stromal hemangiogenic components in lymphoma could potentially be targeted for therapeutic intervention.

scholarly journals Docetaxel Conjugate Nanoparticles That Target α-Smooth Muscle Actin–Expressing Stromal Cells Suppress Breast Cancer Metastasis

2013 ◽  
Vol 73 (15) ◽  
pp. 4862-4871 ◽  
Author(s):  
Mami Murakami ◽  
Mark J. Ernsting ◽  
Elijus Undzys ◽  
Nathan Holwell ◽  
Warren D. Foltz ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Smooth Muscle ◽  
Stromal Cells ◽  
Cancer Metastasis ◽  
Smooth Muscle Actin ◽  
Breast Cancer Metastasis ◽  
Muscle Actin

TGFβ-1 and epithelial-mesenchymal interactions promote smooth muscle gene expression in bone marrow stromal cells: Possible application in therapies for urological defects

2008 ◽  
Vol 31 (11) ◽  
pp. 951-959 ◽  
Author(s):  
C. Becker ◽  
T. Laeufer ◽  
J. Arikkat ◽  
G. Jakse
Keyword(s):  
Bone Marrow ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Smooth Muscle Actin ◽  
Muscle Actin ◽  
Muscle Gene Expression ◽  
Muscle Gene

Purpose For regenerative and cellular therapies of the urinary tract system, autologous bladder smooth muscle cells (SMCs) have several limitations, including constricted in vitro proliferation capacity and, more importantly, inability to be used in malignant conditions. The use of in vitro (pre-)differentiated multipotential adult progenitor cells may help to overcome the shortcomings associated with primary cells. Methods By mimicking environmental conditions of the bladder wall, we investigated in vitro effects of growth factor applications and epithelial-mesenchymal interactions on smooth muscle gene expression and on the morphological appearance of adherent bone marrow stromal cells (BMSCs). Results Transcription growth factor beta-1 (TGFβ-1) upregulated the transcription of myogenic gene desmin and smooth muscle actin-γ2 in cultured BMSCs. Stimulatory effects were significantly increased by coculture with urothelial cells. Prolonged stimulation times and epigenetic modifications further enhanced transcription levels, indicating a dose-response relationship. Immunocytochemical staining of in vitro-differentiated BMSCs revealed expression of myogenic protein α-smooth muscle actin and desmin, and changes in morphological appearance from a fusiform convex shape to a laminar flattened shape with filamentous inclusions similar to the appearance of bladder SMCs. In contrast to the TGFβ-1 action, application of vascular endothelial growth factor (VEGF) did not affect the cells. Conclusions The combined application of TGFβ-1 and epithelial-mesenchymal interactions promoted in vitro outgrowth of cells with a smooth muscle-like phenotype from a selected adherent murine bone marrow-derived cell population.

α-Smooth muscle actin–positive perisinusoidal stromal cells in human hepatocellular carcinoma

Hepatology ◽  
1994 ◽  
Vol 19 (4) ◽  
pp. 895-903 ◽  
Author(s):  
Hideaki Enzan ◽  
Hiromi Himeno ◽  
Shinichi Iwamura ◽  
Saburo Onishi ◽  
Toshiji Saibara ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Smooth Muscle ◽  
Stromal Cells ◽  
Smooth Muscle Actin ◽  
Human Hepatocellular Carcinoma ◽  
Muscle Actin
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