mouse keratinocytes
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2022 ◽  
Vol 3 (1) ◽  
pp. 101052
Author(s):  
Keiko Sakamoto ◽  
Shubham Goel ◽  
Atsuko Funakoshi ◽  
Tetsuya Honda ◽  
Keisuke Nagao

2021 ◽  
Vol 22 (4) ◽  
Author(s):  
Sung Lee ◽  
Liliana Rodriguez ◽  
Rima Majumdar ◽  
Paula De Marval ◽  
Marcelo Rodriguez‑puebla
Keyword(s):  
Aurora B ◽  

2021 ◽  
Author(s):  
Lipei Liu ◽  
Megumi Watanabe ◽  
Norikazu Minami ◽  
Mohammad Yunizar ◽  
Tetsuo Ichikawa

Abstract Metal allergy is one of the typical immune disorders encountered during the application of dental/medical materials and has a highly complex pathogenic mechanism. Semaphorin 3A (Sema3A), a member of the semaphorin family, is reported to be involved in various immune disorders. However, its role in metal allergy has not been clarified yet. Herein, we show that Sema3A promoted nickel (Ni) allergy by mediating tumor necrosis factor-alpha (TNF-α) production and mitogen-activated protein kinase (MAPK) activation in keratinocytes. Sema3A was upregulated in NiCl2-stimulated mouse keratinocytes and in Ni allergy-induced mouse ear tissue. TNF-α production and MAPK activation were altered when Sema3A was suppressed in keratinocytes. The specific deletion of Sema3A in keratinocytes alleviated Ni allergy and regulated the macrophage polarization towards an anti-inflammatory direction. Our results demonstrate that Sema3A promotes the development of metal allergy and should be explored as a potential target for the prevention and treatment of metal allergy.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Amit Mittal ◽  
Mike Wang ◽  
Aurobind Vidyarthi ◽  
Diana Yanez ◽  
Gabriela Pizzurro ◽  
...  

AbstractCutaneous squamous cell carcinomas (cSCC) are among the most commonly diagnosed malignancies, causing significant morbidity and mortality. Tumor-associated macrophage (TAM) expression of arginase is implicated in tumor progression, and therapeutic use of arginase inhibitors has been studied in various cancers. However, investigating potential cSCC immunotherapies including arginase inhibition in pre-clinical models is hampered by the lack of appropriate tumor models in immunocompetent mice. PDV is a cSCC cell line derived from chemical carcinogenesis of mouse keratinocytes. PDVC57 cells were derived from a PDV tumor in C57BL/6 (B6) mice. Unlike PDV, PDVC57 tumors grow consistently in B6 mice, and have increased TAMs, decreased dendritic and T cell intra-tumor infiltration. Arginase inhibition in cSCC tumors using Nω-hydroxy-nor-arginine (nor-NOHA) reduced tumor growth in B6 mice but not immunodeficient Rag1-deficient mice. nor-NOHA administration increased dendritic and T cell tumor-infiltration and PD-1 expression. The combination of nor-NOHA and anti-PD-1 therapy with nivolumab enhanced anti-PD-1 therapeutic efficacy. This study demonstrates the therapeutic potential of transcutaneous arginase inhibition in cSCC. A competent immune microenvironment is required for tumor growth inhibition using this arginase inhibitor. Synergistic co-inhibition of tumor growth in these results, supports further examination of transcutaneous arginase inhibition as a therapeutic modality for cSCC.


2020 ◽  
Author(s):  
Rosario Avolio ◽  
Marta Inglés-Ferrandiz ◽  
Annagiulia Ciocia ◽  
Sarah Bonnin ◽  
Anna Ribó ◽  
...  

SUMMARYOncogene-induced senescence (OIS) is a form of stable cell cycle arrest elicited in cells as a response to oncogenic stimulation. OIS must be bypassed for transformation, but the mechanisms of OIS establishment and bypass remain poorly understood, especially at the post-transcriptional level. Here we show that the RNA binding protein UNR/CSDE1, previously involved in melanoma metastasis, unexpectedly enables OIS in primary mouse keratinocytes that have been challenged by over-expression of oncogenic H-Ras. Depletion of CSDE1 leads to senescence bypass, cell immortalization and tumor formation in vivo, indicating that CSDE1 behaves as a tumor suppressor. Using iCLIP-Seq, RNA-Seq and polysome profiling we have uncovered two independent molecular branches by which CSDE1 contributes to OIS. On one hand, CSDE1 enhances the senescence-associated secretory phenotype (SASP) by promoting the stability of SASP factor mRNAs. On the other hand, CSDE1 represses the synthesis of the pro-oncogenic RNA binding protein YBX1. Importantly, depletion of YBX1 from immortal keratinocytes rescues senescence and uncouples proliferation arrest from the SASP, revealing multilayered post-transcriptional mechanisms exerted by CSDE1 to control senescence. Our data uncover a novel function of CSDE1, and highlight the relevance of post-transcriptional control in the regulation of senescence.


2020 ◽  
Vol 153 (4) ◽  
pp. 225-237
Author(s):  
Shoji Miyazono ◽  
Takahito Otani ◽  
Kayoko Ogata ◽  
Norio Kitagawa ◽  
Hiroshi Iida ◽  
...  

Molecules ◽  
2019 ◽  
Vol 24 (12) ◽  
pp. 2344
Author(s):  
Chang ◽  
Soo ◽  
Chen ◽  
Shyur

The v-raf murine sarcoma viral homolog B1 (BRAF) inhibitor drug vemurafenib (PLX4032) is used to treat melanoma; however, epidemiological evidence reveals that it could cause cutaneous keratoacanthomas and squamous cell carcinoma in cancer patients with the most prevalent HRASQ61L mutation. In a two-stage skin carcinogenesis mouse model, the skin papillomas induced by 7,12-dimethylbenz[a]anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA) (DT) resemble the lesions in BRAF inhibitor-treated patients. In this study, we investigated the bioactivity of Mentha aquatica var. Kenting Water Mint essential oil (KWM-EO) against PDV cells, mouse keratinocytes bearing HRASQ61L mutation, and its effect on inhibiting papilloma formation in a two-stage skin carcinogenesis mouse model with or without PLX4032 co-treatment. Our results revealed that KWM-EO effectively attenuated cell viability, colony formation, and the invasive and migratory abilities of PDV cells. Induction of G2/M cell-cycle arrest and apoptosis in PDV cells was also observed. KWM-EO treatment significantly decreased the formation of cutaneous papilloma further induced by PLX4032 in DT mice (DTP). Immunohistochemistry analyses showed overexpression of keratin14 and COX-2 in DT and DTP skin were profoundly suppressed by KWM-EO treatment. This study demonstrates that KWM-EO has chemopreventive effects against PLX4032-induced cutaneous side-effects in a DMBA/TPA-induced two-stage carcinogenesis model and will be worth further exploration for possible application in melanoma patients.


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