Role of Alpha-Smooth Muscle Actin and Fibroblast Activation Protein Alpha in Ovarian Neoplasms

2018 ◽  
Vol 83 (4) ◽  
pp. 381-387 ◽  
Author(s):  
Ana Carolinne da Silva ◽  
Millena Prata Jammal ◽  
Renata Margarida Etchebehere ◽  
Eddie Fernando Candido Murta ◽  
Rosekeila Simões Nomelini
Keyword(s):  
Smooth Muscle ◽  
Ovarian Neoplasms ◽  
Smooth Muscle Actin ◽  
Fibroblast Activation Protein ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin ◽  
Fibroblast Activation ◽  
Fibroblast Activation Protein Alpha

scholarly journals Alpha Smooth Muscle Actin (αSMA) Immunohistochemistry Use in the Differentiation of Pancreatic Cancer from Chronic Pancreatitis

2021 ◽  
Vol 10 (24) ◽  
pp. 5804
Author(s):  
Katarzyna Winter ◽  
Monika Dzieniecka ◽  
Janusz Strzelczyk ◽  
Małgorzata Wągrowska-Danilewicz ◽  
Marian Danilewicz ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Smooth Muscle ◽  
Chronic Pancreatitis ◽  
Smooth Muscle Actin ◽  
Healthy Tissue ◽  
Pancreatic Stellate Cells ◽  
Resected Specimen ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin

Aim: Fibrosis is observed both in pancreatic cancer (PDAC) and chronic pancreatitis (CP). The main cells involved in fibrosis are pancreatic stellate cells (PSCs), which activate alpha smooth muscle actin (αSMA), which is considered to be the best-known fibrosis marker. The aim of the study was to evaluate the expression of the αSMA in patients with PDAC and CP as the possible differentiation marker. Methods: We enrolled 114 patients undergoing pancreatic resection: 83 with PDAC and 31 with CP. Normal fragments of resected specimen from 21 patients represented the control tissue. The immunoexpressions of αSMA were detected in tissue specimens with immunohistochemistry (Abcam antibodies, GB). Results: Mean cytoplasmatic expression of αSMA protein in PDAC stromal cells was significantly higher compared to CP: 2.42 ± 0.37 vs 1.95 ± 0.45 (p < 0.01) and control group 0.61 ± 0.45 (p < 0.01). Strong immunoexpression of the αSMA protein was found in the vast majority (80.7%) of patients with PDAC, in about half (58%) of patients with CP, and not at all in healthy tissue. The expression of αSMA of different intensity was found in all patients with PDAC and CP, while in healthy tissue was minimal or absent. In PDAC patients, αSMA expression was significantly higher in tumors of diameter higher than 3 cm compared to smaller ones (p = 0.017). Conclusions: Presented findings confirm the significant role of fibrosis in both PDAC and CP; however, they do not confirm the role of αSMA as a marker of differentiation.

Rat liver ferritin selectively inhibits expression of alpha-smooth muscle actin in cultured rat lipocytes

1996 ◽  
Vol 270 (2) ◽  
pp. G370-G375 ◽  
Author(s):  
G. A. Ramm ◽  
R. S. Britton ◽  
R. O'Neill ◽  
H. D. Kohn ◽  
B. R. Bacon
Keyword(s):  
Smooth Muscle ◽  
Rat Liver ◽  
Protein Production ◽  
Smooth Muscle Actin ◽  
Inhibitory Effect ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin ◽  
Potent Effect ◽  
Liver Ferritin

The role of ferritin in lipocyte activation is unknown. This study examined the effect of rat liver ferritin (RLF), human recombinant H-ferritin (HrHF), human recombinant L-ferritin (HrLF), apo-ferritin (apo-RLF), and hemin on lipocyte activation. Lipocytes were cultured on uncoated plastic and were incubated with these agents for 7 days, at concentrations ranging from 10(-14) to 10(-7) M (0.5 to 50 microM for hemin). Collagen/noncollagen protein production and lipocyte proliferation were determined by [3H]proline and [3H]thymidine incorporation, respectively, and the expression of alpha-smooth muscle actin (alpha-SMA) and desmin was determined by Western blot. RLF, at concentrations ranging from 10(-10) to 10(-7) M, decreased alpha-SMA expression by 65-88%. Apo-RLF, HrHF, and HrLF decreased alpha-SMA by 17-45% at 10(-7) and 10(-8) M. Hemin (10 or 50 microM) inhibited alpha-SMA by 37 and 54%, respectively. Desmin expression was not altered by ferritin or hemin. Collagen and noncollagen protein production were not altered by either RLF or apo-RLF. Lipocyte proliferation was decreased by 54, 32, and 40%, by 10(-7) M RLF, HrHF, and HrLF, respectively, whereas apo-RLF had no effect. Thus RLF inhibited lipocyte alpha-SMA expression, which may be due to an effect of sequestered iron, since neither apo-RLF, HrHF, nor HrLF had a potent effect on alpha-SMA expression and all are essentially iron-free. The inhibitory effect of iron-loaded RLF on alpha-SMA expression suggests that tissue ferritin does not initiate lipocyte activation in iron overload, but rather may have a suppressive action on this process.

Role of stromal myofibroblasts in invasive breast cancer: stromal expression of alpha-smooth muscle actin correlates with worse clinical outcome

Breast Cancer ◽  
2010 ◽  
Vol 19 (2) ◽  
pp. 170-176 ◽  
Author(s):  
Masako Yamashita ◽  
Tomoko Ogawa ◽  
Xinhui Zhang ◽  
Noriko Hanamura ◽  
Yumi Kashikura ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Smooth Muscle ◽  
Clinical Outcome ◽  
Invasive Breast Cancer ◽  
Smooth Muscle Actin ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin
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