Ask about this productRelated genes to: CD106 antibody
- Gene:
- VCAM1 NIH gene
- Name:
- vascular cell adhesion molecule 1
- Previous symbol:
- -
- Synonyms:
- CD106
- Chromosome:
- 1p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-10
- Date modifiied:
- 2016-10-05
Related products to: CD106 antibody
Related articles to: CD106 antibody
- Thoracic aortic aneurysm and dissection is one of the most devastating cardiovascular diseases, with limited medical intervention options. This study aims to develop chimeric antigen receptor-engineered CD34 hematopoietic stem/progenitor cells and evaluate their effects on repairing endothelial cell injuries in a murine model. All animal experiments were performed in male mice. We design a chimeric antigen receptor containing a single-chain variable fragment targeting VCAM-1 and a VEGFA activation domain. A ligand-mediated lipid nanoparticle delivery system was used to engineer circulating CD34 cells for transient and tunable chimeric antigen receptor expression. In vitro studies show that the engineered cells exhibit improved differentiation, proliferation, migration, adhesion, and tube formation. They successfully restore endothelial function, strengthened cell junctions, suppressed inflammatory response, and blocked disease progression. This study demonstrates that chimeric antigen receptor technique can effectively equip CD34 hematopoietic stem/progenitor cells to target injured vascular intima, offering a promising approach for treating cardiovascular diseases. - Source: PubMed
Publication date: 2026/04/23
Zhao KaiwenHe YuzhenYao RenqiLi ShuangshuangKong LingxuNiu JinzhuZeng ZanDu PengchengZhu HongqiaoZhao RongLiang TaipingJing ZaipingZhou Jian - Creatinine-based estimated glomerular filtration rate (eGFRcr) and cystatin C-based eGFR (eGFRcys) may be inaccurate for patients with rheumatoid arthritis (RA) due to sarcopenia and inflammation. This study characterized changes in eGFRcys and eGFRcr following two RA treatment regimens and their association with RA disease activity biomarkers. - Source: PubMed
Publication date: 2026/04/20
Fukui ShoInker Lesley ASantacroce Leah MGiles Jon TLiao Katherine PBathon Joan MSolomon Daniel H - Maxim (DrT) is a well-known traditional medicinal and edible plant with hepatoprotective effects. In this study, crude polysaccharides of DrT (DrTPs) were obtained using the water extraction-ethanol precipitation method. Autoimmune hepatitis (AIH) models of both mice and ALM12 cells were produced by ConA. The serum liver function indexes (AST and ALT) were examined by ELISA, and liver tissue pathological changes were observed by HE staining. The hepatoprotective mechanism of DrTP80 was explored by RNA sequencing and verified by detecting the protein expressions using Western blot. As a result, DrTP80 could significantly reduce AST and ALT levels in the injured liver and ALM12 cells. DrTP80 also obviously improved the hepatopathological changes in liver tissue induced by ConA. Furthermore, RNA sequencing detected significant differences in gene expression, and the functions of differential genes were focused on TNF and IL-17 signaling pathways. Based on these two signaling pathways, 13 differentially expressed genes (Vcam1, Atf6b, Akt1, Irf1, Map2k3, Lcn2, Hsp90ab1, Anapc5, Traf4, Fosl1, Jun, Cxcl5, Nfκbia) among NC, CRC, and FP groups were screened and verified by Western blot. In conclusion, our results demonstrated that DrTP80 can alleviate immune liver damage induced by ConA, and its hepatoprotective mechanism may be related to regulating TNF and IL-17 signaling pathways. Our findings indicated that DrTP80 could be exploited as a healthy food supplement for the treatment of immune liver injury. - Source: PubMed
Publication date: 2026/03/24
Guo MinWei SaixueCheng BiaobiaoLi Xiaodong - Vascular endothelial cell dysfunction leads to the breakdown of endothelial barrier integrity, which contributes to sepsis-induced acute lung injury (ALI). The study investigates the role of Cipepofol in regulating endothelial permeability and inflammation during sepsis using a cecal ligation and puncture (CLP) mouse model and human umbilical vein endothelial cells (HUVECs). Our findings demonstrate that Cipepofol treatment inhibits cytoskeletal stress fiber formation and upregulates junction proteins VE-cadherin, thereby preserving endothelial barrier function. These effects were mediated through the γ-aminobutyric acid type A (GABA) receptor α1 subunit (GABA receptor α1). Cipepofol improved sepsis outcomes, including decreased lung injury, leukocyte infiltration, and vascular permeability. Mechanistically, cipepofol-dependent GABA receptor α1 modulated the expression of dual-specificity phosphatase 1 (DUSP1) in lung tissue and endothelial cells of septic mice. DUSP1 knockdown exacerbated p38 and extracellular signal-regulated kinase (ERK)-MAPK signaling and mitochondrial dysfunction, and abolished the protective effects of Cipepofol against lipopolysaccharide (LPS)-induced mitochondrial oxidative stress. Conversely, genetic or pharmacological inhibition of GABA receptor α1 reversed Cipepofol-mediated suppression of p38/ERK-MAPK signaling and reactive oxygen species (ROS) accumulation, confirming DUSP1 as a key downstream mediator. Together, our study unveils that Cipepofol preserves endothelial integrity by depending on GABA receptor α1 to modulate DUSP1 expression, thereby suppressing p38/ERK-MAPK signaling and mitochondrial dysfunction. These findings highlight a potential therapeutic strategy for sepsis-induced ALI. Abbreviations: ALI, acute lung injury; BALF, bronchoalveolar lavage fluid; BCA, bicinchoninic acid; BSA, bovine serum albumin; CLP, cecal ligation and puncture; CIP, Cipepofol; DAPI, 4',6-diamidino-2-phenylindole; DMEM, Dulbecco's modified Eagle's medium; DUSP1, dual-specificity phosphatase 1; ECGS, endothelial cell growth supplement; ECL, enhanced chemiluminescence; ERK, extracellular signal-regulated kinase; FBS, fetal bovine serum; GABA receptor α1, γ-aminobutyric acid type A (GABA) receptor α1 subunit (GABA receptor α1); GAPDH, glyceraldehyde-3-phosphate dehydrogenase; GFP, green fluorescent protein; H&E, hematoxylin and eosin; HRP, horseradish peroxidase; HUVECs, human umbilical vein endothelial cells; ICAM-1, intercellular cell adhesion molecule-1; IL-1β, interleukin-1β; IL-6, interleukin-6; i.p., intraperitoneal; LPS, lipopolysaccharide; LV, lentiviral; MAPK, mitogen-activated protein kinase; MFI, mean fluorescence intensity; MOI, multiplicity of infection; PBS, phosphate-buffered saline; PFA, paraformaldehyde; PTX, Picrotoxin; PVDF, polyvinylidene difluoride; qRT-PCR, quantitative real-time reverse transcription polymerase chain reaction; RIPA, radioimmunoprecipitation assay; ROS, reactive oxygen species; SDS-PAGE, sodium dodecyl sulfate-polyacrylamide gel electrophoresis; SEM, standard error of the mean; shRNA, short hairpin RNA; siRNA, small interfering RNA; SOX17, SRY-box transcription factor 17; TBST, Tris-buffered saline with Tween-20; TNF-α, tumor necrosis factor-α; VCAM-1, vascular cell adhesion molecule-1; VE-cadherin, vascular endothelial cadherin; W/D, wet-to-dry; ZO-1, zonula occludens-1. - Source: PubMed
Publication date: 2026/04/19
Zhou ShutingHe XudongNi XinzheWang AizhongXu Xiaotao - This study investigates the potential mechanism underlying the therapeutic effect of Coptidis Rhizoma-Aucklandiae Radix for ulcerative colitis(UC) in mice from glycocalyx remodeling. The mouse model of UC was established with 2.5% dextran sodium sulfate(DSS). Fifty C57BL/6J mice were randomly assigned to five groups: control, model, sulfasalazine(100 mg·kg~(-1)), low-dose(0.64 g·kg~(-1)) Coptidis Rhizoma-Aucklandiae Radix, and high-dose(1.28 g·kg~(-1)) Coptidis Rhizoma-Aucklandiae Radix. Changes in body weight and hematochezia were monitored throughout the experiment, and the disease activity index(DAI) was calculated accordingly. At the end of the experiment, hematoxylin-eosin(HE) staining was performed to evaluate histopathological changes in the colon tissue. Evans blue dye extravasation was employed to assess colonic vascular permeability. RT-qPCR was conducted to quantify the mRNA levels of inflammatory cytokines, markers of intestinal barrier injury, and glycocalyx-related genes in the colon tissue. Enzyme-linked immunosorbent assay(ELISA) was employed to measure the serum levels of shed hyaluronic acid(HA). Immunofluorescence staining was adopted to detect HA-positive signals in the colonic glycocalyx. Transmission electron microscopy(TEM) was utilized to examine the ultrastructural integrity of colonic vascular endothelial cells and the extent of glycocalyx shedding. The results demonstrated that compared with the control group, the model group exhibited significant body weight loss, marked shortening of the colon, elevated DAI, severe hematochezia, pronounced inflammatory cell infiltration, increased colonic vascular permeability, upregulated expression of pro-inflammatory cytokines including tumor necrosis factor(TNF)-α, interleukin(IL)-6, and IL-1β, downregulated expression of tight junction proteins such as Zonula occludens(ZO)-1, Occludin, and Claudin-5, increased expression of vascular cell adhesion molecule(VCAM)-1, altered expression of glycocalyx-modifying enzymes, specifically increased matrix metalloproteinase 1(MMP1) and hyaluronidase 2(Hyal2) and decreased hyaluronan synthase 2(HAS2), along with substantial shedding of endothelial glycocalyx-derived HA into circulation, as evidenced by elevated serum HA concentrations, and severe ultrastructural damage of colonic vascular endothelial cells with marked glycocalyx degradation as revealed by TEM. In comparison with the model group, both the low-and high-dose Coptidis Rhizoma-Aucklandiae Radix groups showed significantly attenuated weight loss and hematochezia, significantly lowered DAI scores, reduced inflammatory infiltration, improved intestinal barrier function, declined levels of TNF-α, IL-6, and IL-1β, restored expression of ZO-1, Occludin, and Claudin-5, reduced VCAM-1 expression, significantly downregulated expression of MMP1 and Hyal2, significantly increased HAS2 expression, suppressed HA shedding, and preserved endothelial glycocalyx structure with less ultrastructural damage observed under TEM. In summary, Coptidis Rhizoma-Aucklandiae Radix ameliorates UC in mice, potentially through mediating glycocalyx remodeling and thereby protecting the integrity of the intestinal vascular endothelial barrier. - Source: PubMed
Wang Yong-QiWei Yu-ZhuoLiu LiZhu Zi-HangMiao Zhi-WeiXu Yi