YAP1/Piezo1涉及淋巴血管在UVR诱导的光衰老过程中的动态变化,进展到状细胞癌
Yuling L Yang1, Chu Zhou1, Qi Chen1
1Institute of Photomedicine, Shanghai Skin Disease Hospital, School of Medicine, Tongji University, Shanghai, China.
Journal of translational medicine
|November 17, 2023
概括
这项研究研究了紫外线辐射 (UVR) 对皮肤的影响,揭示了适应性免疫微环境的变化. 8周和16-18周的关键转折点为皮肤状细胞癌 (cSCC) 的早期预测和干预提供了信息.
科学领域:
- 皮肤病学和瘤学
- 免疫学和癌症生物学
- 分子和细胞生物学分子和细胞生物学
背景情况:
- 皮肤状细胞癌 (cSCC) 是由紫外线引起的损伤引起的.
- 淋巴中心免疫微环境的变化对光衰老至cSCC进展至关重要.
- 了解这些机制可以确定用于早期cSCC预测的目标.
研究的目的:
- 调查在紫外线诱导的光衰老过程中淋巴中心免疫微环境的动态变化,以cSCC.
- 阐明潜在的机制,包括YAP1/VEGFC信号通路和淋巴血管生成.
主要方法:
- 利用TIMER2.0分析YAP1/VEGFC信号在头部和部状细胞癌 (HNSCC) 和其与生存的相关性.
- 在SKH-1无毛小鼠中通过累积的紫外线诱导光衰和cSCC,评估不同时间点的微环境.
- 评估了皮肤表型,淋巴和血管结构,T细胞透,Piezo1和VE-cadherin表达以及淋巴疏通功能.
主要成果:
- YAP1/VEGFC信号通路和淋巴血管 (LV) 密度与HNSCC的进展和存活有关.
- 在小鼠中,UVR暴露在8周 (光衰老) 和16-18周 (癌前阶段) 时显示出明显的转折点.
- LVs,Piezo1表达和免疫细胞透 (CD4 +,CD8 + T细胞) 的动态变化与皮肤状况的进展相关.
结论:
- 淋巴中心的免疫微环境通过YAP1/VEGFC和Piezo1调节适应持续的紫外线.
- 从光衰老到cSCC的进展涉及UVR暴露8周和16-18周的关键转折点.
- 监测YAP1,Piezo1,LVs和免疫细胞动态可以使cSCC的早期识别和及时干预成为可能.
更多相关视频
08:09CUBIC Protocol Visualizes Protein Expression at Single Cell Resolution in Whole Mount Skin Preparations
Published on: August 4, 2016
11.6K
11:32Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter
Published on: March 27, 2020
6.9K
相关概念视频
Nucleotide Excision Repair
3.5K
DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
3.5K
The Intrinsic Apoptotic Pathway
6.6K
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
6.6K
Abnormal Proliferation
4.5K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.5K
