Ask about this productRelated genes to: VEGFB antibody
- Gene:
- VEGFB NIH gene
- Name:
- vascular endothelial growth factor B
- Previous symbol:
- VRF
- Synonyms:
- VEGFL
- Chromosome:
- 11q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-26
- Date modifiied:
- 2015-07-22
Related products to: VEGFB antibody
Related articles to: VEGFB antibody
- Pathological H-type angiogenesis in medial subchondral bone plays a critical role in Knee Osteoarthritis (KOA); however, the cellular crosstalk remains unclear. We investigated whether osteoblast-derived hypoxia-inducible factor-1 alpha (HIF-1α) drives medial vascular remodeling via vascular Endothelial Growth Factor A (VEGFA) paracrine signaling to Endothelial Cells (ECs). - Source: PubMed
Publication date: 2026/07/29
Chen BoWang JibingJin XingMeng ZhaoxiangBin Jamaludin Mohamad Ikhwan - We hypothesized that arboviruses impair the placental expression of key functional markers implicated in fetal brain development. Singleton placentae (n = 54) affected by chikungunya (CHIKV, n = 12), dengue (DENV, n = 8), zika (ZIKV, n = 15), or healthy controls (HC, n = 15) were analysed. Immunohistochemical quantification of key transporter systems, cell turnover markers, and signalling pathways related to extracellular matrix remodelling, vascular maintenance, and nutrient sensing was undertaken. Maternal age and BMI were lower in CHIKV/ZIKV, whereas birth weight was reduced in DENV pregnancies compared with HC. CHIKV/ZIKV exhibited reduced syncytiotrophoblast area, CHIKV/DENV showed reduced syncytial knot area, whereas DENV showed increased fetal blood vessel and reduced connective tissue areas. Histopathology detected predominantly mild vascular and stromal lesions across groups, with DENV placentae exhibiting moderate congestion in 100% of cases. Decreased expression of P-gp, BCRP, ABCA1 and SNAT2 were detected in all groups. CHIKV/ZIKV also exhibited decreased GLUT1, while ZIKV showed reduced SNAT1 expression. MCT8 expression was significantly elevated in CHIKV. Placental Ki-67 was increased in CHIKV/ZIKV, indicating altered trophoblast turnover. VEGFB expression was reduced and p-mTOR signalling was increased across all arbovirus-exposed placentae, while MMP9 expression was unchanged. Principal components analysis (PCA) distinguished infected from uninfected groups based on placental functional markers related to fetal brain development, but not on histomorphometry. Arboviral-infected placentae showed distinct structural remodelling and altered transporter expression, potentially increasing fetal brain vulnerability and long-term neurodevelopmental risks, even in the absence of neonatal symptoms. KEY POINTS: Virus-specific placental histomorphometric changes were detected, including altered syncytiotrophoblast/syncytial knot, connective tissue and fetal blood vessel areas. Arboviruses reduced the placental efflux transporters P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) and disrupted the expression of ABCA1, SNAT2, GLUT1 and SNAT4 nutrient transporters, while ZIKV additionally reduced SNAT1 expression. Placental functional adaptation to arboviral infection comprised changes in the expression of placental markers of proliferation (Ki-67), angiogenesis (VEGFB), and nutrient sensing (p-mTOR). Arbovirus-exposed placentae exhibited greater functional alterations rather than overt structural pathology, suggesting potential subclinical effects on fetal neurodevelopment, even in the absence of major neonatal abnormalities. - Source: PubMed
Publication date: 2026/07/31
Andrade Cherley B VBloise EnrricoSilva Natália LBraga Jair R SCoelho Sharton V ANascimento Veronica M OImperio Guinever ENunes Camila O SCunha Antônio J L APascoal-Xavier Marcelo AArruda Luciana BPrata-Barbosa ArnaldoConnor Kristin LOrtiga-Carvalho Tania M - : Recurrent pregnancy loss (RPL) is frequently linked to antiphospholipid antibodies, yet many affected women are seronegative for the classical (Sydney) criteria antibodies. In a previously characterized cohort, an extended antiphospholipid antibody panel was positive in 79% of women with RPL, with the strongest associations for antibodies against prothrombin, annexin V and β-glycoprotein I. Whether this association reflects molecular endometrial dysfunction was unclear. : To examine endometrial expression of ten decidualization- and inflammation-related genes in women with RPL, stratified by APL status, focusing on the dominant antibody specificity: anti-β-glycoprotein I. : Thirty-nine women with RPL (≥2 losses), a subsample of a published 100-patient cohort, underwent mid-luteal Pipelle endometrial biopsy followed by RT-PCR for , , , , , , , , and . Antibodies were measured by antiphospholipid 10 Dot line immunoblot (Generic Assays, Germany). The analysis used Mann-Whitney U, Fisher's exact test, Benjamini-Hochberg correction and ROC analysis. : Antibody prevalence in the subsample matched the parent cohort (Pearson r = 0.999). Of ten transcripts, only showed a nominally significant reduction in APL+ women (median ΔCt -2.04 vs. -1.30; = 0.037; rank-biserial r = -0.47); this signal did not survive Benjamini-Hochberg correction (q = 0.372). The signal was specific to anti-βGPI ( = 0.064; AUC 0.700), not to annexin V or prothrombin. A cut-off of ΔCt ≤ -1.60 identified APL+ status with 73% sensitivity, 78% specificity and OR 9.62 (95% CI 1.64-56.4; = 0.015). clustered with (ρ = 0.65) and (ρ = 0.70). : Anti-β-glycoprotein I antibodies, the dominant APL specificity in RPL, are associated with reduced endometrial expression. This exploratory data outline a candidate molecular pathway linking extended antiphospholipid serology to impaired endometrial receptivity. - Source: PubMed
Publication date: 2026/07/12
Khalmirzaeva MadinaOmarova GulzhakhanKurmanova AlmagulKurmanova GaukharAnartayeva GainiZhankina ZhamilyaTulesheva AidanaVeliyeva AinuraJarikova BotakuzDzheksembekova Alfiya - The characteristics of diabetic vascular complications are impaired angiogenesis, which leads to hindlimb ischemia. Although astragaloside IV (AS-IV) can promote angiogenesis, its poor targeting to endothelial progenitor cells (EPCs) limits its therapeutic effect. Here, we developed liposomes modified with iRGD to load AS-IV (Lp-iRGD@AS-IV) to enhance its delivery and explored its mechanism. Lp-iRGD@AS-IV and fluorescently labeled liposomes were prepared, and their phenotypic characteristics were detected. The study results showed that the uptake efficiency of Lp-iRGD@AS-IV by EPCs was higher than that of Lp@AS-IV. In a diabetic mouse hindlimb ischemia model induced by streptozotocin, Lp@AS-IV and Lp-iRGD@AS-IV improved cell damage, increased capillary density, and reduced reactive oxygen species accumulation. However, the therapeutic effect of Lp-iRGD@AS-IV was more significant than that of Lp@AS-IV. Lp-iRGD@AS-IV attenuated high glucose-induced inhibitory effect on cell viability, migration, and invasion capability of EPCs. Additionally, we analyzed the regulatory effects of the Hippo-YAP/TAZ signaling pathway in diabetic vascular complications. AS-IV increased the expression of vascular growth factors (VEGFa, VEGFb, VEGFc, FGF, and Ang-1), eNOS, and osteopontin, and enhanced glucose-lipid metabolism, via activating the upstream Hippo signaling pathway while inactivating the downstream YAP/TAZ activity. In conclusion, Lp-iRGD@AS-IV significantly enhanced the delivery of AS-IV to EPCs and improved hindlimb ischemia in diabetic mice. AS-IV can restore diabetes-associated impaired angiogenesis through the Hippo-YAP/TAZ pathway. Lp-iRGD@AS-IV may be a targeted therapy for diabetic vascular complications. - Source: PubMed
Publication date: 2026/07/24
Zeng ChuruoLi QinxiaGuo DongweiXiong WuZou XiaolingLi WeiBin JieWang XiupingZhang ZihaoXue BingqianHu RuoweiZhang Xi - Diabetic kidney disease (DKD) remains a leading cause of end-stage kidney disease despite advances with renin-angiotensin system blockade, sodium-glucose cotransporter 2 inhibitors, finerenone, and glucagon-like peptide-1 receptor agonists. Therapeutic monoclonal antibodies may offer a targeted strategy to modulate inflammatory, fibrotic, metabolic, and vascular pathways involved in DKD. This review summarizes the mechanistic rationale, clinical evidence, translational barriers, and future prospects of antibody-based therapies for DKD. - Source: PubMed
Publication date: 2026/07/09
Yang Xiu HongLiu YaoFu Chen ShengJin Hui MinYe Zhi Bin