cDNA - Human Tumor Tissue: Skin
- Known as:
- complementary Desoxyribonucleic acid - Human Tumor Tissue: Skin
- Catalog number:
- c1235218-10
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Biochain
- Gene target:
- cDNA - Human Tumor Tissue: Skin
Related genes to: cDNA - Human Tumor Tissue: Skin
- Gene:
- CCL27 NIH gene
- Name:
- C-C motif chemokine ligand 27
- Previous symbol:
- SCYA27
- Synonyms:
- ALP, ILC, CTACK, skinkine, ESkine, PESKY, CTAK
- Chromosome:
- 9p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-30
- Date modifiied:
- 2016-10-05
Related products to: cDNA - Human Tumor Tissue: Skin
Related articles to: cDNA - Human Tumor Tissue: Skin
- Keratinocytes play a crucial role in the pathogenesis of canine atopic dermatitis (cAD). Tumor necrosis factor (TNF)-α, a proinflammatory cytokine, is highly expressed in the lesional skin of dogs with atopic dermatitis. Additionally, interferon (IFN)-γ, a T-helper (Th)1-type cytokine, and interleukin (IL)-13, a Th2-type cytokine, are also detected in the lesional skin during the acute and/or chronic phases of cAD. However, their effects on chemokine expression in canine keratinocytes remain unclear. This study investigated the effects of TNF-α on chemokine mRNA expression in canine keratinocytes and how IFN-γ or IL-13 modulates these responses. Canine progenitor epidermal keratinocyte (CPEK) cells were stimulated with TNF-α alone or in combination with IFN-γ or IL-13. Chemokine mRNA expression was analyzed by real-time PCR. TNF-α induced the mRNA expression of chemokines, including , and . Co-stimulation with IFN-γ enhanced TNF-α-induced and mRNA expression, but reduced TNF-α-induced , and mRNA expression. IL-13 augmented TNF-α-induced mRNA expression, while suppressing TNF-α-induced and mRNA expression. IL-4, another Th2-type cytokine, was also confirmed to have effects similar to those of IL-13. These results indicate that TNF-α induces multiple chemokine genes in canine keratinocytes and that IFN-γ, IL-13, and IL-4 modulate this induction in a chemokine-specific manner, producing both enhancement and suppression. As these findings were obtained exclusively at the mRNA level in a canine keratinocyte cell line, their relevance to the pathogenesis and phases of cAD remains to be determined . - Source: PubMed
Publication date: 2026/09/22
Hasegawa TakehiroKaida YuzukiTakahashi KahoYoshimatsu RinaAndo MioriOhmori Keitaro - Numerous studies have shown that impaired placental angiogenesis results in a spectrum of gestational diseases, posing significant risks to both maternal and fetal health. Yet, the metabolic patterns and underlying mechanisms that govern placental angiogenesis remain poorly understood. Here, we examined the metabolic reprogramming during placental development and the role of its metabolic derivative, lactate, in placental angiogenesis and the associated mechanistic pathways. Firstly, a pronounced metabolic shift toward glycolysis, accompanied by significant lactate accumulation, was identified in the early-stage placenta through targeted metabolomics. Then, converging evidence from inhibition of glycolysis, lactate production, and lactate transport demonstrated that disrupted this metabolic axis significantly impaired placental angiogenesis both in vivo and in vitro. However, supplementation with exogenous NaLa rescued this impairment in both model systems. In addition, mechanistically, lactate contributes to H3K18la modification and placental angiogenesis. Subsequently, integrated analysis of CUT&Tag and RNA-seq data identified CCL27 as a potential transcriptional target of H3K18la. Finally, the regulatory role was further supported by gain- and loss-of-function studies, wherein recombinant CCL27 restored angiogenesis while the receptor antagonist BI-6901 suppressed it, suggesting the involvement of the CCL27 in placental angiogenesis. In summary, our work demonstrates that glycolysis-derived lactate is involved in H3K18la modification and may subsequently contribute to CCL27 expression, potentially supporting placental angiogenesis. This work reveals a novel metabolic-epigenetic pathway that coordinately regulates placental vascular development, informing future targeted strategies for pregnancy complications resulted from impaired placental angiogenesis. - Source: PubMed
Publication date: 2026/09/24
Song JiahaoLi FeiZou WeiZhang YuluCheng YanminYang BeiKuang Haibin - The treatment of immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome has largely focused on immunosuppression with little impact on the atopic manifestations of the disease. Dupilumab therapy has been used successfully in primary atopic diseases and immune regulatory disorders to control type 2 inflammation. Indeed, it has been reported in two prior IPEX cases, but in combination with immunosuppressive agents. Here, we are the first to report the clinical and immunologic impact of dupilumab monotherapy in IPEX. - Source: PubMed
Publication date: 2026/08/17
Alshanti MohammedMacDougall Matthew SGokbak Merve NidaRamachandran AkshayaAlzaabi Amna ArefAlexander Jessie LBacchetta RosaShendi Hiba Mohammed - Major depressive disorder (MDD) is a prevalent mental illness with a significant disease burden. It is characterized by immune-inflammatory dysregulation. - Source: PubMed
Chen TangcongLuo YueyangNiu MengqiLi JingLi MengdieZhang YingqianMaes Michael - Although circadian rhythms are critical regulators of cardiovascular physiopathology, their role in Takotsubo syndrome (TTS) remains poorly understood. This study aimed to investigate the influence of time of day on cardiac hypertrophy and inflammation in a mouse model of TTS induced by isoproterenol (ISO) administration. Female mice were injected with saline (Sal) or ISO at the beginning of the light (ZT0) or dark phase (ZT12). Our data show that mice treated with ISO at ZT12 developed more prominent cardiac hypertrophy and exhibited worse cardiomyocyte calcium handling. This was accompanied by an enhanced accumulation of leukocytes in the hearts of ISO/ZT12 compared with ISO/ZT0 mice. Flow cytometry analysis revealed an exacerbation in the number CD64Ly6CCCR2 monocytes/macrophages at ZT12, indicating a time of day influence on the inflammatory response following ISO administration. Of note, these differences were not secondary to differences in initial tissue injury as assessed by Evans Blue uptake by necrotic cells. However, cardiac expression of was significantly higher in the hearts of ISO/ZT12 than in the hearts of ISO/ZT0, suggesting the involvement of the CCL2/CCR2 signaling axis in the enhanced recruitment of monocytes. Finally, pharmacological and genetic strategies used to prevent CCR2-dependent recruitment of monocytes ameliorated the cardiac hypertrophy induced by ISO at ZT12, indicating that the CCL2/CCR2 signaling axis is crucial to the temporal-dependent effects of ISO. Taken together, our data show a previously unrecognized role of the time of day on cardiac inflammation following adrenergic overload. Using a mouse model of stress-inducible cardiomyopathy, our study reveals that enhanced monocyte influx to the injured heart during the dark phase exacerbates cardiac hypertrophy through activation of the CCL2/CCR2 axis. These findings extend current knowledge on the mechanisms underlying Takotsubo cardiomyopathy and highlight the potential for time of day-based therapeutic strategies. - Source: PubMed
Publication date: 2026/08/01
Sanches BrunoSouza-Neto FernandoPires Giovane L CAbramo HenriqueEliezeck MarcosScalzo Sérgio ASilva Nikolas SantosAmaral Flávio Almeidavan Berlo Jop HGuatimosim SilviaRocha-Resende Cibele