CNTF, Human Protein
- Known as:
- CNTF, Human Protein
- Catalog number:
- z02745-20
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- CNTF Human Protein
Related genes to: CNTF, Human Protein
- Gene:
- CNTF NIH gene
- Name:
- ciliary neurotrophic factor
- Previous symbol:
- -
- Synonyms:
- HCNTF
- Chromosome:
- 11q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-01-07
- Date modifiied:
- 2016-10-05
Related products to: CNTF, Human Protein
Related articles to: CNTF, Human Protein
- Scaffold-based retinal pigment epithelium (RPE) transplantation is a candidate approach to preserve or recover vision for macular degeneration. Electrospun poly(ε-caprolactone) (PCL)/Gelatin (Gel) scaffolds have demonstrated support for cellular proliferation and function, yet their inadequate mechanical performance compromises surgical handling and deliverability. In this study, we incorporated low-oxidation graphene oxide (GO) into electrospun PCL/Gel scaffolds and evaluated their performance for human embryonic stem cell (hESC)-derived RPE cell transplantation. We found that the incorporation of low-oxidation GO improved scaffolds' WCA from 45.47 ± 8.44° to 27.48 ± 1.42° and tensile strength from 1.60 ± 0.06 MPa with an ultimate strain of 16% to 1.75 ± 0.07 MPa with an elongation at break of 44%, while maintaining fibrous formability and biocompatibility. The PCL/Gel/GO scaffolds supported RPE-specific protein expression (MITF, PAX6, CRALBP, ZO-1) and established favorable cell polarity, as indicated by apical Na/K-ATPase. Transmission electron microscopy assay also showed that the hESC-RPE cells on PCL/Gel/GO scaffolds formed apical microvilli. RNA-seq revealed the preservation of trophic factors and phagocytic function on PCL/Gel/GO scaffolds, which was further validated by augmented expression levels of CNTF, IGF1, and VEGFA, as well as improved fluorescent microsphere uptake capacity. Furthermore, the enhanced mechanical properties of the PCL/Gel/GO scaffold eliminated the need for additional treatment before implantation and facilitated surgical handling during implantation. In addition, the scaffold did not cause any observable short-term retinal dysfunction, indicating good short-term feasibility. Collectively, the scaffold structural features, RPE functional profiles, and surgical findings establish PCL/Gel/GO scaffolds as a versatile platform, warranting further investigation into their application in scaffold-based cell therapy for the treatment of macular degeneration. - Source: PubMed
Publication date: 2026/07/17
Wu WeiCao YujiaLi QiyouHu ShuyunWong Daniel Soo LinBarathi Veluchamy AmuthaLingam GopalWang LiqiangXue JiajiaLiu Zengping - Macular telangiectasia Type 2 (MacTel 2) is a bilateral retinal disease characterized by progressive neurodegenerative and telangiectatic changes in the macula. Its subtle early presentation and overlap with a variety of retinal conditions often lead to diagnostic uncertainty and delayed intervention. As clinical understanding of MacTel 2 has evolved, advanced imaging modalities such as optical coherence tomography, fundus autofluorescence, fundus fluorescein angiography, and optical coherence tomography angiography have become essential tools for accurate diagnosis and differentiation from mimicking disorders. Key features such as parafoveal telangiectatic vessels, pigment plaques, and ellipsoid zone loss help establish the diagnosis, while multimodal imaging enhances confidence in distinguishing MacTel from its many masqueraders. The recent Food and Drug Administration approval of a long-acting ciliary neurotrophic factor implant has marked a significant advancement in the treatment of MacTel, highlighting the urgent need for timely recognition. In this review, we propose a practical, algorithm-based framework for diagnosing MacTel 2, with an emphasis on key clinical and imaging features and common diagnostic pitfalls. By improving recognition of characteristic patterns and differentiating features, this article aims to support clinicians in making confident, early diagnoses and implementing appropriate management strategies for MacTel 2. - Source: PubMed
Publication date: 2026/06/30
Shiromani SakshiGandhi PriyankaMohan SashwanthiVenkatesh RameshHatcher KensingtonChhablani Jay - Administration of ciliary neurotrophic factor (CNTF) reduces food intake and body weight in both humans and experimental animals, where it also ameliorates hyperglycemia, hyperinsulinemia, and dyslipidemia. To exert its anti-obesogenic and anti-diabetogenic effects, CNTF targets brain feeding centers as well as multiple peripheral organs inducing the phosphorylation of the transcription factor signal transducer and activator of transcription 3 (p-STAT3). However, data showing which peripheral cytotypes are specifically targeted by exogenous CNTF in vivo in metabolically relevant organs are currently lacking. Here, we first evaluated the gene expression levels of the subunits of the tripartite CNTF receptor (Cntfr) complex, that is, the Cntfrα, the leukemia inhibitory factor receptor β (Lifrβ) and the glycoprotein 130 (gp130), by quantitative real-time PCR in metabolically relevant organs of adult male mice: gastrointestinal (GI) tract, pancreas, liver, visceral and subcutaneous white (WAT) and interscapular brown adipose tissue (iBAT), skeletal muscle and the sciatic nerve. We then quantified p-STAT3 by Western blotting in these organs after intraperitoneal administration of CNTF (0.3 mg/kg) or saline. Finally, we mapped CNTF-responsive cells by immunohistochemistry, followed by morphometric quantification and confocal microscopy in both CNTF- and saline-treated mice. Lifrβ and gp130 were ubiquitously detected across all the investigated organs; the Cntfrα showed the highest expression levels in the skeletal muscle, sciatic nerve, and iBAT, whereas it was found to be expressed to a lesser extent in the other sites. Administration of CNTF led to a significant increase of p-STAT3/STAT3 protein ratio in all organs examined, except the duodenum, and induced a distinctive pattern of cell nuclear p-STAT3 immunoreactivity. Notably, along the analyzed GI tract, CNTF induced nuclear STAT3 phosphorylation in neurons of the submucosal and myenteric plexuses of the enteric nervous system and in contractile cells of the muscularis externa, where the response peaked in the mesenteric gut and colon. In the pancreas, CNTF triggered a higher activation within the endocrine component compared to the exocrine parenchyma. In the liver, CNTF induced STAT3 phosphorylation not only in parenchymal cells but also in sinusoids and resident macrophages. The cytokine activated p-STAT3 in subcutaneous and visceral white adipocytes, but also in brown adipocytes, with a prominent response observed in the beige subcutaneous adipocytes; adipose-resident macrophages and endothelial cells of numerous blood vessels were also CNTF-responsive. Lastly, in skeletal muscle, a major site for glucose/lipid utilization, CNTF induced widespread nuclear p-STAT3 immunoreactivity in muscle fibers and in connective and Schwann cells of the peripheral nerves, including the sciatic nerve, supplying the gastrocnemius. In conclusion, our data indicate that CNTF acts across diverse cytotypes within metabolically relevant organs and tissues, likely fostering its peripheral metabolic effects through this cellular heterogeneity. - Source: PubMed
Publication date: 2026/06/25
Galli ChiaraColleluori GeorgiaPerugini JessicaScopini EdoardoSeveri IleniaGrandin GaiaGiordano Antonio - To identify proteomic signatures underlying 3-year progression from impaired fasting glucose (IFG) to diabetes. - Source: PubMed
Rooney Mary REchouffo Tcheugui Justin BChen JingshaWalker Keenan ABallantyne Christie MBoerwinkle EricKelly Tanika NNdumele Chiadi EPankow James SGrams Morgan EPost Wendy SGanz Peter JWood Alexis CRotter Jerome ISelvin ElizabethCoresh Josef - Management of glaucoma is now at an inflection point with a new generation of therapeutic candidates, whilst targeting intraocular pressure-independent strategies is challenged by the landmark Phase III failure of memantine regarding trial design and endpoint sensitivity. Preclinical research has identified promising targets including glutamate excitotoxicity, neurotrophic factor deprivation, and mitochondrial dysfunction, with nicotinamide emerging as a leading candidate due to its ability to robustly protect RGCs by supporting NAD levels and bioenergetics. Current clinical efforts are expanding into metabolic repurposing with agents (eg metformin and semaglutide), sustained-delivery systems with neurotrophic factors (eg ciliary neurotrophic factor implant), and functional enhancers (eg citicoline). To bridge the translational gap, the field is integrating new endpoints with higher sensitivity (eg advanced assessment of photopic negative response), AI-guided endpoint selection (eg graph attention neural network), novel biomarkers (eg detection of apoptotic retinal cells and neurofilament light chain in aqueous humor), and precision medicine frameworks (eg polygenic risk scores and multi-omics analysis) to develop the first clinically validated neuroprotective treatments for glaucoma. - Source: PubMed
Publication date: 2026/06/16
Rho SeungsooWilliams Pete A