Potential of Sphingosine-1-phosphate in Preventing SARS-CoV-2 Infection by Stabilizing and Protecting Endothelial Cells | Chapter 1 | Diagnostic and Treatment Advances in COVID-19 and SARS-CoV-2

 Coronavirus disease 2019, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has spread worldwide, resulting in over 250 million infections and >5 million deaths. Most antiviral drugs and vaccines have shown limited efficacy against SARS-CoV-2. Clinical data revealed that except for the large number of self-healing mild cases, moderate and severe cases mostly survived after supportive treatment but not specific drug administration or vaccination. The endothelial system is the first physiological barrier, and its structural stability is of critical importance in conferring disease resistance. Membrane lipid components, particularly sphingosine-1-phosphate (S1P), play a central role in stabilizing the cell membrane.

Here, we used “Boolean Operators” such as AND, OR, and NOT, to search for relevant research articles in PubMed, then reviewed the potential of S1P in inhibiting SARS-CoV-2 infection by stabilizing the endothelial system, this is the major aim of this review work.

Reportedly, vasculitis and systemic inflammatory vascular diseases are caused by endothelial damage resulting from SARS-CoV-2 infection. S1P, S1P receptor (SIPR), and signaling were involved in the process of SARS-CoV-2 infection, and S1P potentially regulated the function of EC barrier, in turn, inhibited the SARS-CoV-2 to infect the endothelial cells, and ultimately has the promising therapeutic value to coronavirus disease 2019.

Taken together, we conclude that maintaining or administering a high level of S1P will preserve the integrity of the EC structure and function, in turn, lowering the risk of SARS-CoV-2 infection and reducing complications and mortality.

Author(s) Details:

Zhang Rongzhi,
Department of Anesthesiology, Lanzhou University Second Hospital, Lanzhou, Gansu, China.

Wang Qiang,
Gansu Medical College, Pingliang, Gansu, China.

Yang Jianshe,
Department of Anesthesiology, Lanzhou University Second Hospital, Lanzhou, Gansu, China, Gansu Medical College, Pingliang, Gansu, China and Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai, China.

Please see the link here: https://stm.bookpi.org/DTACSC/article/view/9551

Toxicity Preventive Potential of Anti-Inflammatory CeO2 Nanoparticles in HUVE Cells | Chapter 8 | Recent Trends in Chemical and Material Sciences Vol.7

The mechanism behind cerium oxide nanoparticles' (CeO2 NPs) cytoprotective capability against cytotoxic nitric oxide (NO) donors and H2O2 is currently unknown. The lipopolysaccharide (LPS)-induced cytokines IL-1 and TNF- were dramatically reduced by CeO2 NPs that had been synthesised and described. Because NP-induced ROS/NO did not cause toxicity in HUVE cells, the main goal of this investigation was to determine the capacities of CeO2 NPs in terms of signalling effects that could have happened owing to reactive oxygen species (ROS) and/or NO. Two NO-donors were used in conjunction with CeO2 NPs in human umbilical vein-derived endothelial (HUVE) cells to achieve this goal. To our knowledge, there has been little investigation on CeO2 NPs' modulatory ability against known NO-donors. SNP (sodium nitroprusside, #ab145732 from Abcam plc, Cambridge, UK) and DETA-NO (Z)-1-[N-(2-Aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate or DETA-NONOate #ab144627 from Abcam plc, Cambridge, UK) were the two NO donors utilised in this The IC50s of two NO donors (DETA-NO; 1250 110 M and sodium nitroprusside (SNP; 950 89 M) as well as the IC50 of H2O2 (120 7 M) were used to assess cytoprotective capacity and its underlying mechanism. Total ROS (as a collective marker of hydrogen peroxide, superoxide radical, hydroxyl radical, and other ROS) was assessed using DCFH-DA, and significant ROS was deciphered using a specialised probe DHE. The data demonstrated that signalling processes mediated primarily by and/or NO are responsible for CeO2 NPs at 100 g/mL ameliorating toxicity. The fact that NP exposure had no effect on mitochondrial membrane potential (MMP) and that CeO2 NPs-mediated recovery of MMP loss caused by exogenous NO donors and H2O2 suggested that NP-mediated generation was extra-mitochondrial. The mechanism behind the NP-induced gain in GSH and persistent cytoplasmic ROS is partially explained by data on activated glutathione reductase (GR) and unchanged glutathione peroxidase (GPx) activity. Instead of being inhibited by CeO2 NP administration, cells may develop the ability to tolerate exogenously generated toxicity due to increased antioxidant capacity due to non-cytotoxic ROS and/or NO generation.

Author(s) Details:

Mohd Javed Akhtar,
King Abdullah Institute for Nanotechnology, King Saud University, Riyadh-11451, Saudi Arabia.


Maqusood Ahamed,
King Abdullah Institute for Nanotechnology, King Saud University, Riyadh-11451, Saudi Arabia.

Please see the link here: https://stm.bookpi.org/RTCAMS-V7/article/view/6101

Inspiration from New Discoveries in Vascular Endothelial Cell Growth: A Bold Conjecture about Mature Cell Growth | Chapter 4 | Current Approaches in Science and Technology Research Vol. 4

 Scientists have been trying to figure out how to speed up the proliferation of endothelial cells (EC) in vascular biomaterials and devices so that they can repair, regenerate, or build an endothelial monolayer as quickly as feasible. By directly encouraging EC growth on the surface while suppressing smooth muscle cells (SMC) and macrophages, a variety of approaches have been devised to achieve this goal. However, a 2017 discovery that the endothelium monolayer in regenerated tissues does not come into touch with implanted biomaterials provided us with new inspiration, and offered the idea of "spatiotemporal orderliness of function" to describe macrophage actions. This objective phenomena and law should be followed by SMC and EC on implanted biomaterials in time and space, as well as the functionalities endowed for the implants' surfaces. In the following research, we discovered a series of new mysteries of EC growth, much to our amazement. These minor subtleties, which are often overlooked in scientific research, have the potential to provide new guidelines for universal mature cell proliferation, in addition to explaining the causes for varied blood implantation failures.

Author(s) Details

Jingan Li
School of Materials Science and Engineering & Henan Key Laboratory of Advanced Magnesium Alloy, Zhengzhou University, 100 Science Road, Zhengzhou 450001, PR China.

Yachen Hou
School of Materials Science and Engineering & Henan Key Laboratory of Advanced Magnesium Alloy, Zhengzhou University, 100 Science Road, Zhengzhou 450001, PR China.

Kun Zhang
School of Life Science, Zhengzhou University, 100 Science Road, Zhengzhou 450001, PR China.

View Book :- https://stm.bookpi.org/CASTR-V4/article/view/1038