Faculty Opinions recommendation of Requirement for the dynein light chain km23-1 in a Smad2-dependent transforming growth factor-beta signaling pathway.

Summary The oocyte growth and development in follicular environment are substantially accompanied by surrounding somatic cumulus (CCs) and granulosa cells (GCs). During these processes, the mammalian gametes reach full maturational stage and may be further successfully fertilized by single spermatozoon. These unique mechanisms are regulated by expression of clusters of genes and their biochemical signaling pathways. In this article we described differential expression pattern of transforming growth factor beta (TGFB) gene superfamily in porcine oocytes before and after in vitro maturation (IVM). We performed Affymetrix® microarray assays to investigate the TGFB-related genes expression profile in porcine immature oocytes and gametes cultured for 44h in vitro. In results we found 419 different genes, 379 genes with lower expression, and 40 genes characterized by increased RNA profile. Moreover, significant up-regulation of 6 genes belonging to TGFB signaling pathway such as: TGFBR3, SMAD4, FOS, KLF10, ID1, MAP3K1 in immature porcine oocytes (before IVM), was also observed. It may be suggested that genes involved in TGFB-related signaling pathway are substantially regulated before IVM. Furthermore, these genes may play a significant role during early stages of nuclear and/or cytoplasmic porcine oocytes maturation. The investigated transcripts may be also recommended as the markers of oocytes maturational capability in pigs.

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Transforming growth factor-beta inhibits aromatase gene transcription in human trophoblast cells via the Smad2 signaling pathway

Reproductive Biology and Endocrinology ◽

10.1186/1477-7827-7-146 ◽

2009 ◽

Vol 7 (1) ◽

pp. 146 ◽

Cited By ~ 8

Author(s):

Hong Zhou ◽

Guodong Fu ◽

Hui Yu ◽

Chun Peng

Keyword(s):

Growth Factor ◽

Signaling Pathway ◽

Gene Transcription ◽

Transforming Growth Factor Beta ◽

Transforming Growth Factor ◽

Trophoblast Cells ◽

Human Trophoblast ◽

Aromatase Gene ◽

Growth Factor Beta ◽

Human Trophoblast Cells

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Role of transforming growth factor-beta signaling pathway in pathogenesis of benign biliary stricture

World Journal of Gastroenterology ◽

10.3748/wjg.14.4949 ◽

2008 ◽

Vol 14 (31) ◽

pp. 4949 ◽

Cited By ~ 4

Author(s):

Zhi-Min Geng ◽

Jian-Bao Zheng ◽

Xiao-Xue Zhang ◽

Jie Tao ◽

Lin Wang

Keyword(s):

Growth Factor ◽

Signaling Pathway ◽

Transforming Growth Factor Beta ◽

Transforming Growth Factor ◽

Biliary Stricture ◽

Benign Biliary Stricture ◽

Growth Factor Beta

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Abstract 425: Doxorubicin Upregulation of the Fibrotic Transforming Growth Factor-beta Pathway

Circulation Research ◽

10.1161/res.119.suppl_1.425 ◽

2016 ◽

Vol 119 (suppl_1) ◽

Author(s):

Trevi A Ramirez ◽

Greg Aune

Keyword(s):

Growth Factor ◽

Signaling Pathway ◽

Transforming Growth Factor Beta ◽

Transforming Growth Factor ◽

Cardiac Fibroblasts ◽

Increased Risk ◽

Pediatric Cancer Patients ◽

Growth Factor Beta ◽

Tgfb Signaling ◽

Old Mice

Childhood cancer survivors are at an increased risk of heart disease as a result of their cancer treatments. Drugs like doxorubicin (DOX) are an effective part of treatment regimens, but have been proven to cause acute and chronic cardiotoxicity (DOX tox). An under-investigated aspect of DOX tox is the interstitial fibrosis that the majority of patients develop. This project aims to better understand the pathology of DOX-induced cardiac fibrosis and the role of the pro-fibrotic transforming growth factor-beta (TGFb) signaling pathway. Research in the area of fibrosis and the effect of DOX on cardiac fibroblasts will increase our understanding of DOX tox. This understanding will allow for improved treatment of pediatric cancer patients by reducing the cardiotoxic sequelae of many standard chemotherapy regimens. Cardiac fibroblasts, isolated from 3 week old mice and treated with 5 μM DOX, showed an increase in nuclear pSMAD compared to control cells via fluorescent immunocytology (2.06 ± 0.26 vs 1.13 ± 0.15, p<0.05). Mice treated with 3 mg/kg DOX injections from 2 weeks to 6 weeks of age showed increased TGFb staining in the left ventricle (1.83 ± 0.34 vs 0.87 ± 0.28, p<0.05) a week after treatment ceased. A subset of mice were followed into old age and sacrificed at 80 weeks. A clear increase in TGFb was seen with age. However, 80 week mice that were exposed to DOX early in life showed a greater increase in TGFb staining compared to untreated 80 week old mice (44.50 ± 2.48 vs 30.93 ± 2.30, p<0.001). Early DOX exposure causes chronic molecular changes as evidenced by acute and chronic changes in signaling molecules in cardiac tissue. Changes in collagen seen in earlier studies and increases in MMP-2 from the literature suggest a cardiac remodeling phenotype in DOX-exposed animals. This project demonstrates that DOX initiates changes to pro-fibrotic pathways, seemingly driven by the TGFb signaling pathway.

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