scholarly journals HYALURONIC ACID PATHWAY EXPRESSION IN PAIRED EUTOPIC ENDOMETRIAL AND ENDOMETRIOMA CELLS

2021 ◽  
Vol 116 (3) ◽  
pp. e202-e203
Author(s):  
Kathryn M. Goldrick ◽  
Jennifer F. Knudtson ◽  
Mubeen Sultana ◽  
Rajeshwar Rao Tekmal ◽  
Robert S. Schenken
2021 ◽  
Vol 116 (3) ◽  
pp. e208
Author(s):  
Kathryn M. Goldrick ◽  
Jennifer F. Knudtson ◽  
Robert S. Schenken ◽  
Mubeen Sultana ◽  
Randal D. Robinson ◽  
...  

2019 ◽  
Vol 5 (12) ◽  
pp. eaaw7099 ◽  
Author(s):  
Alec M. DeSimone ◽  
John Leszyk ◽  
Kathryn Wagner ◽  
Charles P. Emerson

Facioscapulohumeral muscular dystrophy (FSHD) is linked to epigenetic derepression of the germline/embryonic transcription factor DUX4 in skeletal muscle. However, the etiology of muscle pathology is not fully understood, as DUX4 misexpression is not tightly correlated with disease severity. Using a DUX4-inducible cell model, we show that multiple DUX4-induced molecular pathologies that have been observed in patient-derived disease models are mediated by the signaling molecule hyaluronic acid (HA), which accumulates following DUX4 induction. These pathologies include formation of RNA granules, FUS aggregation, DNA damage, caspase activation, and cell death. We also observe previously unidentified pathologies including mislocalization of mitochondria and the DUX4- and HA-binding protein C1QBP. These pathologies are prevented by 4-methylumbelliferone, an inhibitor of HA biosynthesis. Critically, 4-methylumbelliferone does not disrupt DUX4-C1QBP binding and has only a limited effect on DUX4 transcriptional activity, establishing that HA signaling has a central function in pathology and is a target for FSHD therapeutics.


2006 ◽  
Vol 104 (6) ◽  
pp. 396-408 ◽  
Author(s):  
Shenandoah Robinson ◽  
Qing Li ◽  
Anne DeChant ◽  
Mark L. Cohen

1997 ◽  
Vol 12 (10) ◽  
pp. 1657-1663 ◽  
Author(s):  
Osamu Ishida ◽  
Yoshiya Tanaka ◽  
Isao Morimoto ◽  
Masaharu Takigawa ◽  
Sumiya Eto

1996 ◽  
Vol 09 (02) ◽  
pp. 60-5 ◽  
Author(s):  
N. Hope ◽  
P. Ghosh ◽  
S. Collier

SummaryThe aim of this study was to determine the effects of intra-articular hyaluronic acid on meniscal healing. Circular defects, 1.0 mm in diameter, were made in the anterior third of the medial meniscus in rabbits. In one joint, 0.4 ml hyaluronic acid (Healon®) was instilled, and in the contralateral (control) joint, 0.4 ml Ringer’s saline. Four rabbits were killed after four, eight and 12 weeks and the menisci examined histologically. By eight weeks most of the lesions had healed by filling with hyaline-like cartilage. Healing was not improved by hyaluronic acid treatment. The repair tissue stained strongly with alcian blue, and the presence of type II collagen, keratan sulphate, and chondroitin sulphate was demonstrated by immunohistochemical localisation. In contrast to the circular defects, longitudinal incisions made in the medial menisci of a further six rabbits did not show any healing after 12 weeks, indicating that the shape of the lesion largely determined the potential for healing.The effect of hyaluronic acid on meniscal healing was tested in a rabbit model. With one millimeter circular lesions in the medial meniscus, healing by filling with hyalinelike cartilage was not significantly affected by the application of hyaluronic acid intra-articularly at the time of surgery, compared to saline controls, as assessed histologically four, eight and 12 weeks after the operation.


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