Adenovirus-Mediated Wnt5a Expression Inhibits the Telogen-To-Anagen Transition of Hai

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3675505/Adenovirus-Mediated Wnt5a Expression Inhibits the Telogen-To-Anagen Transition of Hair Follicles in Mice

 

[IDW2BB]

http://www.ncbi.nlm.nih.gov/pubmed/25240110

Wnt5a: A player in the pathogenesis of atherosclerosis and other inflammatory disorders.
Bhatt PM1, Malgor R2.
Author information

Abstract
OBJECTIVE:
The objective of this article is to review the current literature on Wnt5a and its signaling mechanism, along with its role in atherosclerosis. In addition, the significance of Wnt5a as a diagnostic marker and a potential therapeutic target is reviewed. Wnt5a, a secreted glycoprotein, belongs to a family of highly conserved proteins that regulate important processes such as cell fate specification, embryonic development, cell proliferation, migration, and differentiation in a variety of organisms. The complexity of Wnt5a signaling lies in the fact that Wnt5a can bind to different classes of frizzled receptors, receptor tyrosine kinase-like orphan receptor 2, as well as co-receptors such as low density lipoprotein receptor-related protein 5/6. Wnt5a signals primarily through the non-canonical pathway, where it mediates cell proliferation, adhesion, and movement. However, the role of Wnt5a in canonical signaling is still unresolved. Depending on the receptor availability, Wnt5a can serve to activate or inhibit the canonical Wnt signaling pathway. Due to the promiscuous nature of Wnt5a, it has been extremely difficult to fully understand its signaling mechanism. Wnt5a has recently emerged as a macrophage effector molecule that triggers inflammation. Perturbations in Wnt5a signaling have been reported in several inflammatory diseases, particularly in sepsis, rheumatoid arthritis, and atherosclerosis.
CONCLUSION:
Both existing and emerging evidence suggests that the expression of Wnt5a is always up-regulated in these, and possibly other inflammatory disorders. This knowledge can be useful for targeting Wnt5a and/or its receptor and downstream signaling molecules for therapeutic intervention in inflammatory disorders.
Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

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http://www.ncbi.nlm.nih.gov/pubmed/25219536

Over-expression of Wnt5a in mouse epidermis causes no psoriasis phenotype but an impairment of hair follicle anagen development.
Zhu X1, Wu Y, Huang S, Chen Y, Tao Y, Wang Y, He S, Shen S, Wu J, Guo X, Li B, He L, Ma G.
Author information

Abstract
Increased Wnt5a expression has been observed in psoriatic plaques. However, whether Wnt5a over-expression directly causes psoriasis is unknown. In this study, we generated transgenic (TG) mice with epidermal Wnt5a over-expression under the control of the human K14 promoter. The skin of Wnt5a TG mice was not psoriatic, but characterized with normal proliferation and homeostasis of epidermis. Instead, these TG mice displayed impaired hair follicle transition from telogen to anagen, most likely due to impaired canonical Wnt signaling. These results suggest that increased Wnt5a expression alone is inadequate to induce psoriasis in the skin and possible involvement of Wnt5a in hair follicle cycling. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.

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http://www.ncbi.nlm.nih.gov/pubmed/16391828

Alteration of gene expression in response to bone morphogenetic protein-2 in androgen-dependent human prostate cancer LNCaP cells.
Kumagai T1, Tomari K, Shimizu T, Takeda K.
Author information

Abstract
Bone morphogenetic protein (BMP)-2, a multifunctional member of the transforming growth factor (TGF)-beta superfamily with powerful osteoinductive effects, has various biological activities in a variety of cells. We observed that BMP-2 inhibits cell proliferation in the androgen-dependent human prostate cancer cell line, LNCaP. To investigate the mechanism of inhibition of androgen-dependent growth by BMP-2, we compared the gene expression in LNCaP cells treated with dihydrotestosterone (DHT) to that of LNCaP cells treated with DHT and BMP-2, using DNA microarray analysis. Of 8,400 human genes on the gene chip, 38 genes were up-regulated by >2.0-fold and 48 genes were down-regulated by <0.5-fold by treatment with BMP-2. These genes were involved in a variety of cellular functions, including signal transduction, transcription regulation, enzymes, transporters, structural molecules and translation. RT-PCR analysis showed that CH1CL and BMX were up-regulated and DACH1 and WNT5A were down-regulated by treatment with BMP-2. Furthermore, we detected an increase of WNT5A protein in the medium by DHT and inhibition of the increase by BMP-2. In the present study, we identified several BMP-2-responsive genes in LNCaP cells. Further studies of the roles of these genes may clarify the mechanisms underlying the inhibition of cell proliferation by BMP-2 and identify better approaches for the prevention and treatment of prostate cancer.

http://www.ncbi.nlm.nih.gov/pubmed/25225425

From the link:

J Clin Oncol. 2014 Sep 15. pii: JCO.2014.55.4279. [Epub ahead of print]
Relationship Between Male Pattern Baldness and the Risk of Aggressive Prostate Cancer: An Analysis of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial.
Zhou CK1, Pfeiffer RM1, Cleary SD1, Hoffman HJ1, Levine PH1, Chu LW1, Hsing AW1, Cook MB2.
Author information

Abstract
PURPOSE:
Male pattern baldness and prostate cancer appear to share common pathophysiologic mechanisms. However, results from previous studies that assess their relationship have been inconsistent. Therefore, we investigated the association of male pattern baldness at age 45 years with risks of overall and subtypes of prostate cancer in a large, prospective cohort-the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial.
METHODS:
We included 39,070 men from the usual care and screening arms of the trial cohort who had no cancer diagnosis (excluding nonmelanoma skin cancer) at the start of follow-up and recalled their hair-loss patterns at age 45 years. Hazard ratios (HRs) and 95% CIs were estimated by using Cox proportional hazards regression models with age as the time metric.
RESULTS:
During follow-up (median, 2.78 years), 1,138 incident prostate cancer cases were diagnosed, 571 of which were aggressive (biopsy Gleason score ≥ 7, and/or clinical stage III or greater, and/or fatal). Compared with no baldness, frontal plus moderate vertex baldness at age 45 years was not significantly associated with overall (HR, 1.19; 95% CI, 0.98 to 1.45) or nonaggressive (HR, 0.97; 95% CI, 0.72 to 1.30) prostate cancer risk but was significantly associated with increased risk of aggressive prostate cancer (HR, 1.39; 95% CI, 1.07 to 1.80). Adjustment for covariates did not substantially alter these estimates. Other classes of baldness were not significantly associated with overall or subtypes of prostate cancer.
CONCLUSION:
Our analysis indicates that frontal plus moderate vertex baldness at age 45 years is associated with an increased risk of aggressive prostate cancer and supports the possibility of common pathophysiologic mechanisms.
©American Society of Clinical Oncology.
PMID: 25225425 [PubMed - as supplied by publisher]
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