scholarly journals Activin A Is Anti-Lymphangiogenic in a Melanoma Mouse Model

2015 ◽  
Vol 135 (1) ◽  
pp. 212-221 ◽  
Author(s):  
Magdalena Heinz ◽  
Heide Leb Niederleithner ◽  
Emmi Puujalka ◽  
Ana Soler-Cardona ◽  
Michael Grusch ◽  
...  
Keyword(s):  
2019 ◽  
Author(s):  
Lily Huang ◽  
Chris Schoenherr ◽  
Lili Wang ◽  
Xialing Wen ◽  
Joyce McClain ◽  
...  

2019 ◽  
Vol 66 (1.2) ◽  
pp. 123-127 ◽  
Author(s):  
Kana Kasai ◽  
Takeshi Kato ◽  
Yuri Kadota ◽  
Otgontsetseg Erdenebayar ◽  
Kaoru Keyama ◽  
...  

Placenta ◽  
2015 ◽  
Vol 36 (8) ◽  
pp. 926-931 ◽  
Author(s):  
R. Lim ◽  
S. Adhikari ◽  
S. Gurusinghe ◽  
B. Leaw ◽  
R. Acharya ◽  
...  
Keyword(s):  

PLoS ONE ◽  
2015 ◽  
Vol 10 (4) ◽  
pp. e0124325 ◽  
Author(s):  
Sandy Stayte ◽  
Peggy Rentsch ◽  
Kong M. Li ◽  
Bryce Vissel

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A53-A54
Author(s):  
Pauline Xu ◽  
Mikyoung You ◽  
Yi Luan ◽  
Maya Eldani ◽  
Soonkyu Chung ◽  
...  

Abstract Background: Pancreatic ductal adenocarcinoma (PDAC) is currently the third leading cause of cancer death in the United States and is projected to become the second leading cause by the year 2030. Prognosis for patients with metastatic disease remains dismal. Cancer cachexia is seen in over 85% of PDAC patients who often have the most severe degrees of cachexia and experience adipose tissue loss prior to skeletal muscle loss early in the disease process. Several factors have been proposed to induce cachectic symptoms in human patients, including inhibin subunit βA, or activin A. Hypothesis: While muscle wasting has been the most frequently studied mechanism in cachexia research, changes in adipose tissue are increasingly understood as important components of body weight loss in cachectic patients. We hypothesized that there is a correlation between the marked increase in activin A production in PDAC patients and the remodeling of adipose tissue and consequent cancer-associated cachectic state. Experimental Design: We measured serum activin A levels of a cohort of PDAC patients and analyzed the expression of activin A in tumor-derived cell lines and biopsies of both humans and mice. We further investigated the effect of activin A on remodeling of adipose tissue secondary to tumor progression in PDAC patients and an orthotopic murine model. Results: We observed that PDAC cell lines express and secrete activin A. We recognized a loss of adipose tissue mass and adipocyte diameter in PDAC patients and our orthotopic PDAC mouse model in relation to increased circulating activin A. We also noted that both exogenous activin A and conditioned medium from pancreatic tumor-derived cell lines dampened adipocyte differentiation and lipid droplet formation via reduction of PPARγ expression in mouse mesenchymal stem cells. These treatment conditions also reduced lipid droplet size without upregulating traditional markers of adipose tissue browning and lipolysis such as UCP-1 and ATGL in mature mouse adipocytes. PPARγ, UCP-1, and ATGL expression are also heavily downregulated in adipose tissue of PDAC patients. Furthermore, our studies revealed that the expression of extracellular matrix proteins such as collagen I and fibronectin is dramatically upregulated in adipose tissue of PDAC patients and our orthotopic PDAC mouse model. Thus, we found that there is a clear correlation between elevated levels of activin A and the progression of cancer-associated cachexia in PDAC. Discussion: Our results reveal an imperative role of activin A in relation to the loss and remodeling of adipose tissue in the progression of cachexia in PDAC patients.


Author(s):  
H. D. Geissinge ◽  
L.D. Rhodes

A recently discovered mouse model (‘mdx’) for muscular dystrophy in man may be of considerable interest, since the disease in ‘mdx’ mice is inherited by the same mode of inheritance (X-linked) as the human Duchenne (DMD) muscular dystrophy. Unlike DMD, which results in a situation in which the continual muscle destruction cannot keep up with abortive regenerative attempts of the musculature, and the sufferers of the disease die early, the disease in ‘mdx’ mice appears to be transient, and the mice do not die as a result of it. In fact, it has been reported that the severely damaged Tibialis anterior (TA) muscles of ‘mdx’ mice seem to display exceptionally good regenerative powers at 4-6 weeks, so much so, that these muscles are able to regenerate spontaneously up to their previous levels of physiological activity.


1998 ◽  
Vol 13 (11-s4) ◽  
pp. S178-S184 ◽  
Author(s):  
PETER KONTUREK ◽  
TOMASZ BRZOZOWSKI ◽  
STANISLAW KONTUREK ◽  
ELZBIETA KARCZEWSKA ◽  
ROBERT PAJDO ◽  
...  

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