IL11 Pre-design Chimera RNAi
- Known as:
- IL11 Pre-design Chimera RNAi
- Catalog number:
- H00003589-R01
- Product Quantity:
- 20 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- IL11 Pre-design Chimera RNAi
Related genes to: IL11 Pre-design Chimera RNAi
- Gene:
- IL11 NIH gene
- Name:
- interleukin 11
- Previous symbol:
- -
- Synonyms:
- IL-11, AGIF
- Chromosome:
- 19q13.42
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-06
- Date modifiied:
- 2016-10-11
Related products to: IL11 Pre-design Chimera RNAi
Related articles to: IL11 Pre-design Chimera RNAi
- Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive fibrotic interstitial lung disease mainly occurs in the elderly, presents limited therapeutic options and necessitating the development of novel drugs. Interleukin-11 (IL-11) belongs to the interleukin-6 (IL-6) family and plays a wide role in fields such as hematopoiesis, immune regulation and tumorigenesis. Recent studies have shown that IL-11 could serve as a potential target for the treatment of IPF and plays a certain role in the aging process. In this study we aims to evaluate the role and mechanism of targeted IL-11 in aging-related pulmonary fibrosis. Firstly, neutralizing antibodies targeting IL-11 were obtained through evaluation and combination of two antibodies with different epitopes can effectively alleviate pulmonary fibrosis in vivo and in vitro. Subsequently, we established pulmonary fibrosis model in aging mice and found that IL-11 was highly expressed in the serum, lung tissues and fibroblasts of fibrotic aging mice. The overexpression or functional loss of IL-11 could significantly change the profibrotic phenotype of senescent lung fibroblasts, and IL-11 neutralizing antibodies could effectively alleviate early and late pulmonary fibrosis in aging mice. Further mechanism studies have confirmed the importance of the TGF-β1/NOX4/IL-11 signaling pathway in regulating the senescence phenotype of lung fibroblasts and aging-related pulmonary fibrosis. In summary, this study elucidate the correlation between IL and 11 and pulmonary fibrosis in aging mice. Both in vitro and in vivo experiments have validated the therapeutic efficacy and molecular mechanisms of IL-11-neutralizing antibodies in pulmonary fibrosis, offering promising insights for future anti-fibrotic drug development. Abbreviations: IL-11, Interleukin-11; IPF, Idiopathic pulmonary fibrosis; TGF-β, Transforming growth factor-β; NOX4, NADPH oxidase-4; SASP, Senescence-associated secretory phenotype; ECM, Extracellular matrix; α-SMA, α-smooth muscle actin; STAT3, Signal transducer and activator of transcription 3; ERK, Extracellular regulated protein kinases; AKT, Protein kinase B; BLM, Bleomycin; WT, Wild-type; KO, Knockout; qRT-PCR, Quantitative real-time polymerase chain reaction; WB, Western blot; hAb, Humanized antibody; mAb, Monoclonal antibody; FVC, Forced vital capacity; CTGF, Connective tissue growth factor; PDGFR-α, Platelet-derived growth factor receptor-α; TNF-α, Tumor necrosis factor-α; Nrf2, NFE2-related factor 2; EMT, Epithelial-mesenchymal transition; HE, Hematoxylin and eosin; PVDF, Polyvinylidene fluoride; GAPDH, Glyceraldehyde-3-phosphate dehydrogenase; siRNA, Small interfering RNA; IL-6, Interleukin-6; MEK, Mitogen-Activated Protein Kinase Kinase; TIME, TGF-β1/IL-11/MEK/ERK; HRP, Horseradish Peroxidase; MLG, Mouse lung fibroblast cell line MLg; NCBI, National Center for Biotechnology Information; Bcl2, BCL2 apoptosis regulator; Bax, BCL2 Associated X, apoptosis regulator; MSC, Mesenchymal Stem Cell; RSK, p90 Ribosomal S6 Kinase; KD, Dissociation Constant; Nin, Nintedanib; CTL, Control; Eto, Etoposide; SA-β-Gal, Senescence-Associated β-Galactosidase. - Source: PubMed
Publication date: 2026/06/27
Miao YangHu Ya-YueXu LiMeng Ling-XinYang YueLiu Zhi-GangYang Zhong-YiLiu Xue-ZeLiu Yu-MingJiao RanXu Ai-GuoGu Xiao-TingZhou Hong-GangLi Xiao-He - Asthma is characterized by persistent airway epithelial dysfunction and remodelling of the reticular basement membrane (RBM). In healthy airways, the RBM is primarily composed of the extracellular matrix (ECM) proteins laminin and collagen-IV, but in remodelled asthmatic airways, the RBM has increased deposition of collagen-I, -III and fibronectin. Here, we systematically compared the effects of collagen-I, -III, -IV, fibronectin, laminin, and bovine serum albumin (BSA) control on bronchial epithelial cells (BECs) from six healthy controls and seven individuals with asthma. Epithelial attachment, spreading and barrier function were assessed in real time over 72 h using electrical cell-substrate impedance sensing. Cell culture supernatants were analyzed for release of epithelial cytokines, thymic stromal lymphopoietin (TSLP), interleukin (IL)-6, IL-8, and IL-11 using ELISA. BECs from both control and asthma donors had faster cell attachment, spreading, and barrier formation on collagen-I, -III, -IV, and fibronectin compared to laminin and BSA. BECs from both control and asthma donors cultured on collagen -I and -III produced more TSLP, but had no effect on IL-6, IL-8, and IL-11 expression. In summary, remodelling of the RBM in asthma may promote epithelial barrier formation whilst simultaneously enhancing epithelial-derived Th2 inflammation through increased TSLP release. - Source: PubMed
Publication date: 2026/06/10
Hsieh AileenBarker-Mulleder JennaYang Chen XiFouadi MayHackett Tillie-Louise - Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a disease of unknown etiology associated with chronic severe fatigue and neurological symptoms, including dizziness, sleep disturbances, cognitive impairment and pain. There are no reliable blood biomarkers available for ME/CFS, possibly due to the lack of specific pathogenesis, even though Epstein-Barr Virus (EBV) has been suspected. We quantified the levels of interleukin-11 (IL-11) in the serum of female ME/CFS patients (n = 40; mean age 51 years) and age- and gender-matched healthy control subjects (n = 38; mean age 43), as well as matrix metalloproteinase-9 (MMP-9) in ME/CFS patients (n = 18; mean age 57 years old) and healthy control subjects (n = 18; mean age 53 years old), using an enzyme-linked immunosorbent assay (ELISA). We hypothesized that mast cells (MC) stimulated by EBV may be involved. MC are unique tissue immune cells that have been implicated in ME/CFS. MC were grown from human umbilical cord blood CD34 stem cells and incubated with recombinant (rEBV) protein, following which the release of MMP-9 was assayed in the cell culture supernatant media by ELISA. There was a significant increase in serum levels of IL-11 and MMP-9 in ME/CFS patients compared to control subjects. MCs stimulated by rEBV protein released a high amount of MMP-9 compared to control cells. In conclusion, IL-11, MMP-9 and MCs may be involved in ME/CFS individuals. - Source: PubMed
Publication date: 2026/06/05
Chinnappan BaskaranKempuraj DuraisamyAenlle Kristina KMiddleton AshleyDay Katie SKothuru Sai PuneethJoshi Rhitik SamirKlimas Nancy GTheoharides Theoharis C - Effective treatment of pulmonary diseases remains constrained by the scarcity of delivery systems capable of selective tissue targeting. Herein, we report a lung-targeting platform created through the structural repurposing of hemoglobin (Hb). Acidic heating enables a conformational shift of Hb from α-helix to β-sheet, leading to its self-assembly into fibrils (HbFs). Unexpectedly, intravenously injected HbFs exhibit rapid and specific accumulation in the lungs. Cryo-electron microscopy (cryo-EM) structure determination revealed a fibril surface rich in positively charged residues, which facilitates two key functions: selective binding to circulating platelets via a hitchhiking mechanism for lung targeting, and efficient electrostatic complexation with mRNA. In a therapeutic application, HbFs loaded with mRNA encoding an interleukin-11 single-chain fragment variable (IL-11 scFv) were administered in a murine model of bleomycin-induced pulmonary fibrosis. The formulation achieved lung-specific delivery with predominant uptake by pulmonary fibroblasts, enabling sustained local IL-11 scFv expression. Consequently, treatment significantly suppressed fibroblast activation and migration, attenuated collagen deposition, restored lung function. This work establishes HbFs as a novel protein‑based vehicle for targeted mRNA delivery, leveraging natural cellular trafficking pathways to enable localized therapy for lung disorders. - Source: PubMed
Publication date: 2026/06/12
Liu XihuaLi SaiyaWu GuodongLi ShuangjianHuang Long ShuangLi XiaoyangZhao YiguoLu WeiSun CuixiaCao QinFang YapengCao Yiping - Lung cancer is a leading cause of cancer-related mortality, with metastasis significantly reducing patient survival. Interleukin 11 (IL11), a member of the IL-6 cytokine family, has been associated with cancer progression, yet its role in non-small cell lung cancer (NSCLC) metastasis remains unclear. This study analyzed public datasets and demonstrated that IL11 is upregulated in NSCLC and correlates with lymphatic metastasis and poor prognosis. Functional assays revealed that IL11 enhances lung cancer cell migration through upregulation of matrix metalloproteinase 12 (MMP12). Mechanistically, IL11 acts via the IL11 receptor subunit alpha (IL11RA)/ IL6 cytokine family signal transducer (IL6ST) complex to activate the PI3K/Akt/NF-κB signaling pathway, which in turn drives MMP12 expression and promotes metastatic behavior. Notably, the clinically approved selective estrogen receptor modulator bazedoxifene effectively inhibited IL11-induced signaling, reduced MMP12 levels, and suppressed cancer cell migration in vitro. In an orthotopic lung cancer mouse model, IL11 knockdown significantly reduced tumor growth and intrapulmonary spread, accompanied by decreased IL11, MMP12, and phosphorylated NF-κB p65 levels in lung tissues. These findings uncover a novel IL11-driven pathway contributing to metastatic behavior in NSCLC and identify the IL11/IL11RA/IL6ST axis as a potential therapeutic target.Schematic representation of bazedoxifene-mediated suppression of IL11-induced pro-metastatic signaling in lung cancer. Non-small cell lung cancer (NSCLC) cells secrete IL11, which binds to the IL11RA/IL6ST receptor complex and activates the PI3K/Akt signaling pathway. This activation enhances NF-κB transcriptional activity, leading to upregulated MMP12 expression and promoting lung cancer cell migration. Notably, bazedoxifene effectively blocks IL11-induced PI3K/Akt activation, thereby suppressing NF-κB signaling and reducing MMP12 expression, which ultimately attenuates NSCLC metastasis. - Source: PubMed
Publication date: 2026/06/11
Lee Chiang-WenLin Shih-SenChang Tsung-MingLin Zih-ChanChiang Yao-ChangChi Miao-ChingPeng Kuo-TiFang Mei-LingLiu Ju-Fang