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Biocompatibility and Biomaterials
Published in Sirshendu De, Anirban Roy, Hemodialysis Membranes, 2017
Platelet adhesion is an essential function in response to vascular injury. Platelets adhere to particulate matter in the bloodstream, bacteria, and microorganisms, as well as artificial surfaces of prosthetic devices, bio-incompatible dialysis membranes, and so on. In fact, platelet adhesion is the first step toward thrombus formation, arresting hemorrhage and permitting wound healing. Platelet aggregation can also be triggered by blood flow or high shear flow conditions. In fact, the Von Willebrand (vWF) factor is used to understand both the phenomena. vWF is a blood glycoprotein that is involved in homeostasis. It has been reported that vWF binds to collagen, tethering platelets to the collagen surface and thus contributing to thrombus formation as well.14
Use of Recombinant DNA Technology for Engineering Mammalian Cells to Produce Proteins
Published in Anthony S. Lubiniecki, Large-Scale Mammalian Cell Culture Technology, 2018
vWF is a large, adhesive, multifunctional glycoprotein that is essential for normal hemostasis (for review, see 198). It is synthesized by endothelial cells and is stored within specialized organelles called Weibel-Palade bodies where it is released upon stimulation. vWF circulates as a series of disulfide-bonded multimers that extend to molecular weights greater than 107. The high molecular weight multimers mediate the adhesion of platelets to subendothelium upon vascular injury. A variety of abnormalities in vWF can result in a condition known as von Willebrand’s disease.
Association of systemic inflammation and coagulation biomarkers with source-specific PM2.5 mass concentrations among young and elderly subjects in central Tehran
Published in Journal of the Air & Waste Management Association, 2021
Abdulmalik Altuwayjiri, Sina Taghvaee, Amirhosein Mousavi, Mohammad H. Sowlat, Mohammad Sadegh Hassanvand, Homa Kashani, Sasan Faridi, Masud Yunesian, Kazem Naddafi, Constantinos Sioutas
vWF is a prognostic marker that can be utilized to predict systemic inflammation and cardiovascular illnesses (Gragnano et al. 2017). Several studies have indicated positive associations of aluminum (i.e., tracer of road dust (Keuken et al. 2013)), and precursors of secondary PM (e.g., SOx, and NOx) with vWF, a biomarker of coagulation (Wu et al. 2012; Zhang et al. 2013a); in concert with our observations in terms of positive associations between abovementioned sources and vWF in the retirement home. Among the elderly group, our study revealed a secondary PM-related increase of 15%--16% in the vWF levels, which is comparable with the results of Zhang et al. (2013a), reporting an 8% increase in vWF associated with IQR increase in NO2 and SO2 concentrations at various time lags. In addition, our statistical findings were in line with the results of Bell et al. (2014), in which the authors reported significantly positive association of PM2.5 road dust with the cardiovascular hospital admissions. Furthermore, results from chamber and atmospheric measurement studies have indicated that the toxicity of primary combustion products increases as they undergo photo-chemical processing due to the increased oxidative potential of the reaction products, i.e., Secondary Organic Aerosol (Jiang et al. 2016; Tuet et al. 2017) compared to the precursors. Additionally, the positive association (Pvalue = .032) of vWF with vehicular emissions among seniors (in the second lag) is consistent with the results of Yuan et al. (2013) and Yue et al. (2007), exhibiting the impact of traffic emissions on increased vWF plasma levels. However, our reported traffic-related increase (around 20%) in the vWF levels was higher than the results of Yuan et al. (2013), in which vehicular emissions contributed to 11.3% (95% CI: 5,17.6%) increase in this biomarker level during the 0–4 days of exposure. Nevertheless, other studies have observed insignificant association of vWF with vehicular sources (Jacobs et al. 2011; Wu et al. 2014). This inconsistency regarding the association of vWF with vehicular emissions was also reflected in Figure 2(a), in which insignificant associations were observed for vehicular sources versus vWF in the first-time lag, despite the significantly positive associations observed in the second lag.
Core genes in lung adenocarcinoma identified by integrated bioinformatic analysis
Published in International Journal of Environmental Health Research, 2023
Liu Yang, Qi Yu, Yonghang Zhu, Manthar Ali Mallah, Wei Wang, Feifei Feng, Qiao Zhang
In addition, our study also found that VWF, PECAM1, TEK, ANGPT1, SCGB1A1, CD36 and SPARCL1 were lower expressed in LUAD and were associated with good overall survival, which need to be further attention. VWF encodes a glycoprotein involved in hemostasis. Once this gene is mutated, it can lead to an inherited bleeding disorder (Favaloro et al. 2018). According to some experimental and clinical studies, immune responses such as chronic inflammation, may influence the development and progression of cancer. VWF is regarded as an anti-tumor factor, which negatively regulates angiogenesis and apoptosis (Franchini et al. 2013). On the contrary, VWF has been reported to promote tumorigenesis of LUAD by modulating inflammatory effects in lung cancer (Liu et al. 2017). As a result, more research on this gene is required. Platelet-endothelial cell adhesion molecule-1 (PECAM1) is a member of the immunoglobulin superfamily located at the endothelial cell–cell junctions (Woodfin et al. 2007). One previous study has revealed that mRNA expression of PECAM1 was significantly higher in clear cell renal cell carcinoma (ccRCC) tissues than that in normal tissues (Yang et al. 2019). PECAM1 was also discovered to be important in ARDS lung repair and regeneration (Villar et al. 2019). The angiogenin receptor TEK is a tyrosine kinase which regulates homeostasis through its own and transphosphoric acid actions, which is regarded as a potential biomarker of ccRCC and lung cancer (Piao et al. 2018; Ha et al. 2019). Additionally, ANGPT1 is one of the key pro-angiogenic factors that enhances endothelial cell migration and capillary-like structure formation, and miRNAs can regulate these genes involved in tumor angiogenesis-dependent growth (Dews et al. 2006; Flores-Perez et al. 2016). Some researchers have the opinion that miRNA can affect many characteristics of breast cancer by targeting key angiogenic gene ANGPT1, which has the reference significance to the LUAD (Flores-Perez et al. 2016). CD36 is a membrane protein receptor located on the cell surface and it belongs to the scavenger receptor B family. By combining with different ligands, it participates in a variety of important physiological and pathological processes. A previous study had reported that changes in CD36 expression are related to NSCLC (Mehan et al. 2012). Thus, CD36 provides new evidence as a therapeutic target for cancer. SPARC-like protein 1 (SPARCL1) is a member of the cysteine-rich acid secreted protein (SPARC) family of cell matrix proteins. Wang et al. found that the expression of SPARCL1 in LUAD was down-regulated, and this gene regulates DNA methylation (Wang et al. 2019). Our study found that SCGB1A1 is related to the prognosis of LUAD patients, but its role in LUAD remains to be explored. Considering these reports and our research, we can conclude that VWF, PECAM1, TEK, ANGPT1, SCGB1A1, CD36 and SPARCL1 play an important prognostic role in LUAD.