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Related articles to: 2'-PDE antibody
- The treatment of oral submucosal fibrosis (OSF) is challenging owing to the complex pathogenesis. It is characterized by excessive collagen deposition in the subepithelium along with epithelial damage. Betel nut chewing is considered a major cause of OSF. We previously found that phosphodiesterase 12 (PDE12) was involved in the oral mucosal epithelial barrier damage, promoting the occurrence of OSF. Early growth response 1 (EGR1), a well-characterized transcription factor, has been implicated in the development of fibrotic diseases, including oral fibrosis. This study aimed to explore the effects and underlying mechanisms of PDE12 overexpression on oral epithelial cells in OSF. Overexpression of PDE12 was employed to verify its critical role in mitochondrial dysfunction and oral mucosal epithelial barrier disruption in HOKs. Subsequently, electrophoretic mobility shift assay and chromatin immunoprecipitation analysis were performed to demonstrate that EGR1 interacted with the promoter of the PDE12 gene, thereby upregulating its expression in HOKs. By combining EGR1 silencing and PDE12 overexpressing strategies, our study confirmed that PDE12-induced impairment of mitochondrial function and oral mucosal epithelial barrier was dependent on EGR1. These findings suggest that regulating the expression of PDE12 through EGR1 could alleviate arecoline-induced epithelial injury, thereby inhibiting the development of OSF and offering a potential therapeutic strategy to combat OSF. - Source: PubMed
Publication date: 2026/04/16
Peng JingChen LinlinXie JinmeiWang XiWang XuerouChen CailianWang RongXie Xi - Sepsis-associated acute kidney injury (SA-AKI) is a severe complication characterized by inflammation, hemodynamic instability, and organ dysfunction, with high morbidity and mortality. Despite advances in supportive care, targeted therapies remain limited. Given the critical role of cAMP signaling in immune regulation and cellular homeostasis, this study explored the therapeutic potential of dipyridamole, a phosphodiesterase (PDE) inhibitor, mitigating SA-AKI. - Source: PubMed
Publication date: 2025/11/14
Xing JiaLin GengChen Zhao-XuanZhao Wan-TingMo Shu-WenZhai Xiao-YueZhang Jie - Phosphodiesterase 12 (PDE12), also known as 2'-PDE, is a key molecule in the 2-5A antiviral system and a member of the endonuclease-exonuclease-phosphatase (EEP) superfamily of deadenylases. Current research on PDE12 mainly focuses on mitochondrial mRNA degradation, mitochondrial protein translation, and the related human diseases caused by mitochondrial oxidative phosphorylation disruption. However, the biological role and molecular mechanisms of PDE12 in human cancers remains unclear. In the present study, we found that PDE12 was highly expressed in gastric cancer tissues and gastric cancer cell lines. Gain- and loss-of-function experiments confirmed that PDE12 promoted the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of gastric cancer cells. PDE12 also promoted G1-S phase transition of gastric cancer cells by regulating the expression of G1 phase-specific Cyclin D1/CDK4 and Cyclin E/CDK2. Our further studies indicated that PDE12 positively regulated the expression of TRPM8 channel-associated factor 2 (TCAF2), which functioned as an oncogene in gastric cancer progression. TCAF2 knockdown significantly suppressed gastric cancer cell proliferation, migration and invasion, and reversed the promoting effect of PDE12 overexpression on gastric cancer cell growth and metastasis. Furthermore, our findings revealed a novel mechanism by which PDE12/TCAF2 axis promoted gastric cancer progression by activating the JAK2/STAT3 signaling pathway. Taken together, our data strongly indicate that PDE12 exerts an oncogenic function in gastric cancer progression at least partly via activating the TCAF2/JAK2/STAT3 signaling axis. These findings provide new insights into the tumorigenesis and metastasis of gastric cancer, and suggest that PDE12 may serve as a novel therapeutic target for gastric cancer. - Source: PubMed
Publication date: 2025/07/06
Liu Yi-JinSong Huan-XiLi Jia-HuiWang Xin-YaNie Xiao-FeiZhang Li-Na - Oxidative phosphorylation (OXPHOS) is a major energy resource occurring in mitochondria. Targeting OXPHOS-related genes has emerged as potential targets for cancer therapy. This study aimed to explore the significance of OXPHOS-related genes in breast cancer (BRCA). - Source: PubMed
Publication date: 2025/01/23
Xia Man-ZhiDong Shu-FengWang Chun-Lei - Mitochondrial DNA (mtDNA)-encoded RNA molecules undergo extensive processing to generate mature RNA, including removal of spurious poly-A tails by phosphodiesterase12 (PDE12). A new study by Van Haute and colleagues (Van Haute et al, 2024) describes the first pathogenic variants in the human PDE12 gene. The 3 missense mutations that were identified each carry severe phenotypic consequences that correlate with the presence or not of residual PDE12 protein, show cell-type-specific adaptive responses, and specificity in the mtDNA-encoded electron transport chain subunits that are most affected. These new data demonstrate the necessity of PDE12 for life, and provide invaluable insights into RNA processing in mitochondria. - Source: PubMed
Publication date: 2024/11/20
Yu ChenxiaoTigano MarcoSeifert Erin L