Human PDGF-AB Protein Vector: HEK293
- Known as:
- Human PDGF-AB Protein Vector: HEK293
- Catalog number:
- 10185-HCyH
- Product Quantity:
- 10μg
- Category:
- -
- Supplier:
- Provo
- Gene target:
- Human PDGF- Protein Vector: HEK293
Related genes to: Human PDGF-AB Protein Vector: HEK293
- Gene:
- PDGFA NIH gene
- Name:
- platelet derived growth factor subunit A
- Previous symbol:
- -
- Synonyms:
- PDGF1, PDGF-A
- Chromosome:
- 7p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
- Gene:
- PDGFRA NIH gene
- Name:
- platelet derived growth factor receptor alpha
- Previous symbol:
- -
- Synonyms:
- CD140a, PDGFR2, GAS9
- Chromosome:
- 4q12
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-19
- Date modifiied:
- 2019-04-23
- Gene:
- PDGFRB NIH gene
- Name:
- platelet derived growth factor receptor beta
- Previous symbol:
- PDGFR
- Synonyms:
- JTK12, CD140b, PDGFR1
- Chromosome:
- 5q32
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: Human PDGF-AB Protein Vector: HEK293
Related articles to: Human PDGF-AB Protein Vector: HEK293
- The prevalence of diabetes mellitus (DM) is increasing daily worldwide. DM patients suffer from numerous complications, including the development of chronic wounds that can lead to amputation. These complications necessitate innovative approaches. As part of these innovative approaches, this study synthesized four chalcone derivatives and evaluated their activities in an in vitro diabetic wound model. Several spectroscopic techniques, including 1 H and 13 C NMR and HR-MS, were used to confirm the structures of the newly synthesized compounds. After investigating the inhibition of α-glucosidase in HDF-1 cells treated with D-glucose (50 mM), MTT tests and scratch tests were performed. Tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), total antioxidant status (TAS), and procollagen type-1 were analyzed using an ELISA kit. Additionally, proliferation (Ki67), inflammatory (Nuclear factor kappa B; NFκB), and growth factor (Platelet-derived growth factor subunit A; PDGFA) markers in fibroblasts were assessed by immunohistochemistry. All compounds exhibited strong α-glucosidase inhibitory activity, with IC₅₀ values ranging from 1.115 to 1.612 µg/mL. Cytotoxicity analysis demonstrated that all compounds were biocompatible, maintaining over 85% cell viability in HDF-1 cells. Under diabetic conditions, treatment significantly improved cell viability and promoted wound closure, particularly in C4. In addition, the compounds reduced pro-inflammatory cytokines TNF-α and IL-1β while increasing TAS and procollagen type I levels. Immunocytochemical findings revealed enhanced Ki67 and PDGFA expression and decreased NFκB activation in treated groups. Molecular docking analysis supported the experimental findings by demonstrating favorable binding interactions with α-glucosidase. In conclusion, chalcone derivatives-particularly compound C4-promote diabetic wound healing through multitarget mechanisms involving anti-inflammatory, antioxidant, and pro-regenerative effects, highlighting their strong therapeutic potential. - Source: PubMed
Publication date: 2026/05/08
Demirbağ BurcuÜnver HakanKara AyçaNecip AdemYıldırım Metin - Cellular senescence is a multifaceted stress response marked by stable proliferative arrest and the secretion of diverse biologically active factors, collectively known as the senescence-associated secretory phenotype (SASP). The senescent phenotype is remarkably variable and subject to various regulatory influences. We previously demonstrated that mitochondrial dysfunction induced by diverse stimuli, including the loss of sirtuin 3 (SIRT3), leads to the hyperactivation of AMPK and p53, culminating in senescence while concurrently suppressing much of the proinflammatory SASP. Here, we extend our findings by revealing that the absence of SIRT3 can suppress segments of the SASP even in the absence of p53. Intriguingly, SIRT3 deficiency renders cells resistant to stimulation by exogenous cytokines, such as interleukin-1. Fibroblasts derived from Sirt3 knockout mice exhibit a diminished SASP, including reduced levels of Pdgfa, and these mice display impaired wound healing and a more expansive granulation area. Furthermore, aged Sirt3 knockout mice show disrupted patterns of senescence relative to wild type controls, including increases in senescence markers in adipose tissue, but surprisingly also decreases in liver and heart. Collectively, these data underscore a role for SIRT3 in orchestrating cellular senescence phenotypes, shedding light on its regulatory influence beyond the p53-dependent pathway. - Source: PubMed
Publication date: 2026/05/06
Kura NiharikaMogck Bronwyn AJezak Samantha TVelarde Michael CWiley Christopher D - Tumor-associated Tie2-expressing monocytes/macrophages (TEMs) have been implicated in promoting angiogenesis and metastasis in colorectal cancer (CRC), yet the molecular mechanisms linking TEMs infiltration to tumor metastasis and progression remain incompletely defined. This study investigated the distribution of TEMs in CRC and their association with gene expression profiles, microvessel density (MVD), and clinical outcomes. Immunohistochemistry on 30 formalin-fixed paraffin-embedded (FFPE) primary CRC samples revealed that TEMs, which characteristically express tyrosine kinase with immunoglobulin and epidermal growth factor homology domains 2 (Tie2) receptor and CD14, preferentially localize to perivascular regions and are associated with higher histological grade, tumor size, lymph node metastasis, and increased MVD. However, Tie2/CD14 macrophages and CD68 tumor-associated macrophages (TAMs) showed uniform stromal distribution. Gene set enrichment analysis (GSEA) of in silico transcriptomic datasets of metastatic CRC (mCRC) identified enrichment of pathways related to cell-cell recognition, calcium signaling, transcription regulation, and metalloexopeptidase activity in Tie2/CD14 tumors. Subsequent qRT-PCR validation on FFPE primary CRC samples confirmed significant upregulation of C-C chemokine receptor 7 (CCR7), platelet-derived growth factor A (PDGFRA), CBP/p300-interacting transactivator with glutamic acid/aspartic acid-rich carboxyl-terminal domain 2 (CITED2), and carboxypeptidase E (CPE) in TEMs regions. Notably, angiopoietin1 (Ang1), but not angiopoietin2 (Ang2), was significantly elevated in TEMs primary tumors. Kaplan-Meier analysis on 1336 CRC patients indicated that high expression of CITED2, CPE, and Ang2 is associated with reduced overall survival. Collectively, these findings suggest that TEM infiltration is linked to transcriptional regulation, biological processes, and enzymatic programs in CRC, potentially contributing to tumor progression and poor prognosis, and highlight CCR7, PDGFRA, CITED2, CPE, and Ang1 as candidate biomarkers for further mechanistic exploration. - Source: PubMed
Publication date: 2026/04/19
Ali Eman Amin MAltaie Alaa MuayadAlhamidi Reem SamiAli NivalBoghossian AnaniaAlmazrouei MarwaMohan Vidya BijoshBendardaf RiyadMohamed RawiaTalaat Iman MHamoudi Rifat - Angiogenesis is a pivotal process for tumor progression and metastasis in non-small cell lung cancer (NSCLC). However, the molecular mechanisms by which WNT1-inducible signaling pathway protein 3 (WISP-3) contributes to NSCLC angiogenesis remain poorly defined. This study investigated the role of WISP-3 in regulating pro-angiogenic signaling in lung adenocarcinoma (LUAD) cells. Conditioned medium from H1299 and A549 cells treated with recombinant WISP-3 (0-100 ng/mL) significantly and dose-dependently enhanced the tube formation of human umbilical vein endothelial cells (HUVECs). WISP-3 selectively upregulated platelet-derived growth factor A (PDGF-A) expression at both mRNA and protein levels in NSCLC cell lines, while other angiogenic factors remained unaffected. Notably, knockdown of PDGF-A using siRNA markedly abolished WISP-3-induced HUVEC tube formation, confirming PDGF-A as a critical mediator in this process. Mechanistically, WISP-3 rapidly triggered the phosphorylation of p38 and JNK signaling pathways. These activations led to the phosphorylation of the transcription factor c-Jun, which in turn promoted PDGF-A gene expression. Pharmacological inhibition of p38 (Adezmapimod), JNK (SP600125), or c-Jun (T-5224) effectively suppressed WISP-3-induced c-Jun activation, PDGF-A expression, and subsequent angiogenesis. Collectively, our findings identify a novel WISP-3/p38-JNK/c-Jun/PDGF-A signaling axis that drives vascular remodeling in NSCLC. Targeting WISP-3 or its downstream effectors may represent a promising therapeutic strategy for anti-angiogenic treatment in lung cancer. - Source: PubMed
Publication date: 2026/03/25
Chang En-MingLin Syuan-LingCheng Ching-YuanTang Chih-HsinChen Yu-ChenLee Chiang-WenLin Chih-Yang - Differentiating between malignant and benign biliary strictures remains a clinical challenge because current diagnostic tools have limited sensitivity. The detection of tumour-related biomarkers directly in bile, which is in close contact with the lesion, may enhance diagnostic accuracy. This study aimed at evaluating the diagnostic and prognostic values of biliary concentrations of VEGF, PDGF-AA, IGF and MMPs in patients with extrahepatic cholangiocarcinoma (CCA), pancreatic ductal adenocarcinoma (PDAC), or benign obstruction. - Source: PubMed
Gigante EUntereiner VCaruso SRhaiem RGrados LBoulagnon-Rombi CAdam SSockalingum G DGarnotel RThiefin G