Blood Physiology: Molecular Mechanisms of Vascular Wall Functioning, 2nd Volume

Topic Information

Dear Colleagues,

The functional state of the vascular wall is very important for maintaining one’s health and preventing diseases. It reacts very sensitively to external influences, and the development of any deviations from the physiological optimum in the internal organs can impact the synthesis of the hemostatically important substances of disaggregation, in addition to anticoagulant and fibrinolytic activity. Generally, in vascular activity studies, a human is the object of the study. This is due to the high clinical significance of the development of vascular dysfunctions in humans, which can lead to thrombophilia. It is known that many dysfunctional and pathological processes disrupt the metabolism and synthesis of biologically significant substances in the vascular wall. This situation can worsen blood rheology, promote hypoxia, inhibit tissue metabolism and significantly increase the risk of thrombosis. Recently, various productive animals have become the object of study of the activity of the vascular wall. This allows researchers to search for opportunities to influence the level of substances formed in the vascular wall that control the state of capillary blood flow and, as a result, metabolism in tissues and the degree of realization of the productive potential of any farm animal. The collected information on the functioning of the vascular wall indicates the need for additional research aimed at revealing the fine mechanisms of the functioning of the vascular wall in humans and productive animals. In addition, it is necessary to search for approaches that can stimulate the biological processes in the walls of blood vessels, significantly increasing their activity. In humans, this can help to reduce the risk of thrombotic events, thereby prolonging one’s life. Strengthening the activity of the vascular wall in productive animals can help to significantly increase the level of their productive properties. For this reason, the purpose of this Special Issue is to bring together and comprehend the results of the most recent observations on the mechanisms of the functioning of the vascular wall in humans and animals, considering the effectiveness of various options at improving overall health and increasing vitality.

Prof. Dr. Ilya Nikolaevich Medvedev
Dr. Svetlana Zavalishina
Dr. Vorobieva Nadezhda Viktorovna
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Biomedicines biomedicines	3.9	5.2	2013	15.3 Days	CHF 2600
Cells cells	5.1	9.9	2012	17.5 Days	CHF 2700
Current Issues in Molecular Biology cimb	2.8	2.9	1999	16.8 Days	CHF 2200
International Journal of Molecular Sciences ijms	4.9	8.1	2000	18.1 Days	CHF 2900
Life life	3.2	4.3	2011	18 Days	CHF 2600

MDPI Topics is cooperating with Preprints.org and has built a direct connection between MDPI journals and Preprints.org. Authors are encouraged to enjoy the benefits by posting a preprint at Preprints.org prior to publication:

1. Immediately share your ideas ahead of publication and establish your research priority;
2. Protect your idea from being stolen with this time-stamped preprint article;
3. Enhance the exposure and impact of your research;
4. Receive feedback from your peers in advance;
5. Have it indexed in Web of Science (Preprint Citation Index), Google Scholar, Crossref, SHARE, PrePubMed, Scilit and Europe PMC.

Published Papers (9 papers)

Order results

Content type Publication Date

Result details

Normal Extended Compact

Journals

All Biomedicines Cells CIMB IJMS Life

Show export options expand_more Show export options expand_less

Select all

Export citation of selected articles as:

Plain Text BibTeX BibTeX (without abstracts) Endnote Endnote (without abstracts) Tab-delimited RIS

Error

Oops... you haven't selected anything for export.

Ok

clear

attachment

Supplementary material:
Supplementary File 1 (ZIP, 1010 KiB)

17 pages, 5483 KiB  

Open AccessArticle

Increased Collagen I/Collagen III Ratio Is Associated with Hemorrhage in Brain Arteriovenous Malformations in Human and Mouse

by Zahra Shabani, Joana Schuerger, Xiaonan Zhu, Chaoliang Tang, Li Ma, Alka Yadav, Rich Liang, Kelly Press, Shantel Weinsheimer, Annika Schmidt, Calvin Wang, Abinav Sekhar, Jeffrey Nelson, Helen Kim and Hua Su

Cells 2024, 13(1), 92; https://doi.org/10.3390/cells13010092 - 1 Jan 2024

Cited by 1 | Viewed by 1821

Abstract

Background: The increase in the collagen I (COL I)/COL III ratio enhances vessel wall stiffness and renders vessels less resistant to blood flow and pressure changes. Activated microglia enhance inflammation-induced fibrosis. Hypotheses: The COL I/COL III ratio in human and mouse brain arteriovenous [...] Read more.

Background: The increase in the collagen I (COL I)/COL III ratio enhances vessel wall stiffness and renders vessels less resistant to blood flow and pressure changes. Activated microglia enhance inflammation-induced fibrosis. Hypotheses: The COL I/COL III ratio in human and mouse brain arteriovenous malformations (bAVMs) is associated with bAVM hemorrhage, and the depletion of microglia decreases the COL I/COL III ratio and hemorrhage. Method: COL I, COL III, and hemorrhages were analyzed in 12 human bAVMs and 6 control brains, and mouse bAVMs induced in three mouse lines with activin receptor-like kinase 1 (n = 7) or endoglin (n = 7) deleted in the endothelial cells or brain focally (n = 5). The controls for the mouse study were no-gene-deleted litter mates. Mouse bAVMs were used to test the relationships between the Col I/Col III ratio and hemorrhage and whether the transient depletion of microglia reduces the Col I/Col III ratio and hemorrhage. Results: The COL I/COL III ratio was higher in the human and mouse bAVMs than in controls. The microhemorrhage in mouse bAVMs was positively correlated with the Col I/Col III ratio. Transient depletion of microglia reduced the Col I/Col III ratio and microhemorrhage. Conclusions: The COL I/COL III ratio in the bAVMs was associated with bAVM hemorrhage. The depletion of microglia reduced the bAVM Col I/Col III ratio and hemorrhage. Full article

(This article belongs to the Topic Blood Physiology: Molecular Mechanisms of Vascular Wall Functioning, 2nd Volume)

►▼ Show Figures

Figure 1

12 pages, 2561 KiB  

Open AccessArticle

Opposing Roles for the α Isoform of the Catalytic Subunit of Protein Phosphatase 1 in Inside–Out and Outside–In Integrin Signaling in Murine Platelets

by Tanvir Khatlani, Subhashree Pradhan, Kimberly Langlois, Deepika Subramanyam, Rolando E. Rumbaut and K. Vinod Vijayan

Cells 2023, 12(20), 2424; https://doi.org/10.3390/cells12202424 - 10 Oct 2023

Viewed by 1151

Abstract

Platelet activation during hemostasis and thrombosis is facilitated by agonist-induced inside–out and integrin α_IIbβ₃-initiated outside–in signaling via protein kinases and phosphatases. Pharmacological inhibitor studies suggest that the serine/threonine protein phosphatase 1 (PP1) promotes platelet activation. However, since phosphatase inhibitors [...] Read more.

Platelet activation during hemostasis and thrombosis is facilitated by agonist-induced inside–out and integrin α_IIbβ₃-initiated outside–in signaling via protein kinases and phosphatases. Pharmacological inhibitor studies suggest that the serine/threonine protein phosphatase 1 (PP1) promotes platelet activation. However, since phosphatase inhibitors block all the isoforms of the catalytic subunit of PP1 (PP1c), the role of specific PP1c isoform in platelet signaling remains unclear. Here, we employed a platelet-specific PP1cα^−/− mice to explore the contribution of a major PP1 isoform in platelet functions. Loss of PP1cα moderately decreased activation of integrin α_IIbβ₃, binding of soluble fibrinogen, and aggregation to low-dose thrombin, ADP, and collagen. In contrast, PP1cα^−/− platelets displayed increased adhesion to immobilized fibrinogen, fibrin clot retraction, and thrombus formation on immobilized collagen. Mechanistically, post-fibrinogen engagement potentiated p38 mitogen-activated protein kinase (MAPK) activation in PP1cα^−/− platelets and the p38 inhibitor blocked the increased integrin-mediated outside–in signaling function. Tail bleeding time and light-dye injury-induced microvascular thrombosis in the cremaster venules and arterioles were not altered in PP1cα^−/− mice. Thus, PP1cα displays pleiotropic signaling in platelets as it amplifies agonist-induced signaling and attenuates integrin-mediated signaling with no impact on hemostasis and thrombosis. Full article

(This article belongs to the Topic Blood Physiology: Molecular Mechanisms of Vascular Wall Functioning, 2nd Volume)

►▼ Show Figures

Graphical abstract

attachment

Supplementary material:
Supplementary File 1 (ZIP, 2955 KiB)

14 pages, 2057 KiB  

Open AccessArticle

E-Cadherin Is Expressed in Epithelial Cells of the Choroid Plexus in Human and Mouse Brains

by Genta Takebayashi, Yoichi Chiba, Keiji Wakamatsu, Ryuta Murakami, Yumi Miyai, Koichi Matsumoto, Naoya Uemura, Ken Yanase, Gotaro Shirakami, Yuichi Ogino and Masaki Ueno

Curr. Issues Mol. Biol. 2023, 45(10), 7813-7826; https://doi.org/10.3390/cimb45100492 - 26 Sep 2023

Cited by 1 | Viewed by 1724

Abstract

Evidence showing the functional significance of the choroid plexus is accumulating. Epithelial cells with tight and adherens junctions of the choroid plexus play important roles in cerebrospinal fluid production and circadian rhythm formation. Although specific types of cadherin expressed in adherens junctions of [...] Read more.

Evidence showing the functional significance of the choroid plexus is accumulating. Epithelial cells with tight and adherens junctions of the choroid plexus play important roles in cerebrospinal fluid production and circadian rhythm formation. Although specific types of cadherin expressed in adherens junctions of choroid plexus epithelium (CPE) have been examined, they remained uncertain. Recent mass spectrometry and immunolocalization analysis revealed that non-epithelial cadherins, P- and N-cadherins, are expressed in the lateral membrane of CPE, whereas E-cadherin expression has not been confirmed in CPE of humans or mice. In this study, we examined E-cadherin expression in CPE of mice and humans by RT-PCR, immunohistochemical-, and Western blotting analyses. We confirmed, by using RT-PCR analysis, the mRNA expression of E-cadherin in the choroid plexus of mice. The immunohistochemical expression of E-cadherin was noted in the lateral membrane of CPE of mice and humans. We further confirmed, in Western blotting, the specific immunoreactivity for E-cadherin. Immunohistochemically, the expression of E- and N-cadherins or vimentin was unevenly distributed in some CPE, whereas that of E- and P-cadherins or β-catenin frequently co-existed in other CPE. These findings indicate that E-cadherin is expressed in the lateral membrane of CPE, possibly correlated with the expression of other cadherins and cytoplasmic proteins. Full article

(This article belongs to the Topic Blood Physiology: Molecular Mechanisms of Vascular Wall Functioning, 2nd Volume)

►▼ Show Figures

Figure 1

28 pages, 3119 KiB  

Open AccessReview

Biomarkers in Systemic Sclerosis: An Overview

by Giuseppe Di Maggio, Paola Confalonieri, Francesco Salton, Liliana Trotta, Luca Ruggero, Metka Kodric, Pietro Geri, Michael Hughes, Mattia Bellan, Michele Gilio, Selene Lerda, Elisa Baratella, Marco Confalonieri, Lucrezia Mondini and Barbara Ruaro

Curr. Issues Mol. Biol. 2023, 45(10), 7775-7802; https://doi.org/10.3390/cimb45100490 - 25 Sep 2023

Cited by 6 | Viewed by 3612

Abstract

Systemic sclerosis (SSc) is a complex autoimmune disease characterized by significant fibrosis of the skin and internal organs, with the main involvement of the lungs, kidneys, heart, esophagus, and intestines. SSc is also characterized by macro- and microvascular damage with reduced peripheral blood [...] Read more.

Systemic sclerosis (SSc) is a complex autoimmune disease characterized by significant fibrosis of the skin and internal organs, with the main involvement of the lungs, kidneys, heart, esophagus, and intestines. SSc is also characterized by macro- and microvascular damage with reduced peripheral blood perfusion. Several studies have reported more than 240 pathways and numerous dysregulation proteins, giving insight into how the field of biomarkers in SSc is still extremely complex and evolving. Antinuclear antibodies (ANA) are present in more than 90% of SSc patients, and anti-centromere and anti-topoisomerase I antibodies are considered classic biomarkers with precise clinical features. Recent studies have reported that trans-forming growth factor β (TGF-β) plays a central role in the fibrotic process. In addition, interferon regulatory factor 5 (IRF5), interleukin receptor-associated kinase-1 (IRAK-1), connective tissue growth factor (CTGF), transducer and activator of transcription signal 4 (STAT4), pyrin-containing domain 1 (NLRP1), as well as genetic factors, including DRB1 alleles, are implicated in SSc damage. Several interleukins (e.g., IL-1, IL-6, IL-10, IL-17, IL-22, and IL-35) and chemokines (e.g., CCL 2, 5, 23, and CXC 9, 10, 16) are elevated in SSc. While adiponectin and maresin 1 are reduced in patients with SSc, biomarkers are important in research but will be increasingly so in the diagnosis and therapeutic approach to SSc. This review aims to present and highlight the various biomarker molecules, pathways, and receptors involved in the pathology of SSc. Full article

(This article belongs to the Topic Blood Physiology: Molecular Mechanisms of Vascular Wall Functioning, 2nd Volume)

►▼ Show Figures

Figure 1

19 pages, 1427 KiB  

Open AccessReview

Circular RNAs Variously Participate in Coronary Atherogenesis

by Liudmila V. Dergunova, Margarita A. Vinogradina, Ivan B. Filippenkov, Svetlana A. Limborska and Alexander D. Dergunov

Curr. Issues Mol. Biol. 2023, 45(8), 6682-6700; https://doi.org/10.3390/cimb45080422 - 13 Aug 2023

Cited by 5 | Viewed by 1805

Abstract

Over the past decade, numerous studies have shown that circular RNAs (circRNAs) play a significant role in coronary artery atherogenesis and other cardiovascular diseases. They belong to the class of non-coding RNAs and arise as a result of non-canonical splicing of premature RNA, [...] Read more.

Over the past decade, numerous studies have shown that circular RNAs (circRNAs) play a significant role in coronary artery atherogenesis and other cardiovascular diseases. They belong to the class of non-coding RNAs and arise as a result of non-canonical splicing of premature RNA, which results in the formation of closed single-stranded circRNA molecules that lack 5′-end caps and 3′-end poly(A) tails. circRNAs have broad post-transcriptional regulatory activity. Acting as a sponge for miRNAs, circRNAs compete with mRNAs for binding to miRNAs, acting as competing endogenous RNAs. Numerous circRNAs are involved in the circRNA–miRNA–mRNA regulatory axes associated with the pathogenesis of cardiomyopathy, chronic heart failure, hypertension, atherosclerosis, and coronary artery disease. Recent studies have shown that сirc_0001445, circ_0000345, circ_0093887, сircSmoc1-2, and circ_0003423 are involved in the pathogenesis of coronary artery disease (CAD) with an atheroprotective effect, while circ_0002984, circ_0029589, circ_0124644, circ_0091822, and circ_0050486 possess a proatherogenic effect. With their high resistance to endonucleases, circRNAs are promising diagnostic biomarkers and therapeutic targets. This review aims to provide updated information on the involvement of atherogenesis-related circRNAs in the pathogenesis of CAD. We also discuss the main modern approaches to detecting and studying circRNA–miRNA–mRNA interactions, as well as the prospects for using circRNAs as biomarkers and therapeutic targets for the treatment of cardiovascular diseases. Full article

(This article belongs to the Topic Blood Physiology: Molecular Mechanisms of Vascular Wall Functioning, 2nd Volume)

►▼ Show Figures

Figure 1

23 pages, 1652 KiB  

Open AccessReview

Expanding the Horizons of Pre-Transplant Renal Vascular Assessment Using Ex Vivo Perfusion

by Carolina Campos Pamplona, Cyril Moers, Henri G. D. Leuvenink and L. Leonie van Leeuwen

Curr. Issues Mol. Biol. 2023, 45(7), 5437-5459; https://doi.org/10.3390/cimb45070345 - 29 Jun 2023

Cited by 2 | Viewed by 2075

Abstract

Recently, immense efforts have focused on improving the preservation of (sub)optimal donor organs by means of ex vivo perfusion, which enables the opportunity for organ reconditioning and viability assessment. However, there is still no biomarker that correlates with renal viability. Therefore, it is [...] Read more.

Recently, immense efforts have focused on improving the preservation of (sub)optimal donor organs by means of ex vivo perfusion, which enables the opportunity for organ reconditioning and viability assessment. However, there is still no biomarker that correlates with renal viability. Therefore, it is essential to explore new techniques for pre-transplant assessment of organ quality to guarantee successful long-term transplantation outcomes. The renal vascular compartment has received little attention in machine perfusion studies. In vivo, proper renal vascular and endothelial function is essential for maintaining homeostasis and long-term graft survival. In an ex vivo setting, little is known about vascular viability and its implications for an organ’s suitability for transplant. Seeing that endothelial damage is the first step in a cascade of disruptions and maintaining homeostasis is crucial for positive post-transplant outcomes, further research is key to clarifying the (patho)physiology of the renal vasculature during machine perfusion. In this review, we aim to summarize key aspects of renal vascular physiology, describe the role of the renal vasculature in pathophysiological settings, and explain how ex vivo perfusion plays a role in either unveiling or targeting such processes. Additionally, we discuss potentially new vascular assessment tools during ex vivo renal perfusion. Full article

(This article belongs to the Topic Blood Physiology: Molecular Mechanisms of Vascular Wall Functioning, 2nd Volume)

►▼ Show Figures

Figure 1

attachment

Supplementary material:
Supplementary File 1 (ZIP, 377 KiB)

17 pages, 2794 KiB  

Open AccessReview

Heme Interactions as Regulators of the Alternative Pathway Complement Responses and Implications for Heme-Associated Pathologies

by Stefanos A. Tsiftsoglou

Curr. Issues Mol. Biol. 2023, 45(6), 5198-5214; https://doi.org/10.3390/cimb45060330 - 16 Jun 2023

Viewed by 2242

Abstract

Heme (Fe²⁺-protoporphyrin IX) is a pigment of life, and as a prosthetic group in several hemoproteins, it contributes to diverse critical cellular processes. While its intracellular levels are tightly regulated by networks of heme-binding proteins (HeBPs), labile heme can be hazardous [...] Read more.

Heme (Fe²⁺-protoporphyrin IX) is a pigment of life, and as a prosthetic group in several hemoproteins, it contributes to diverse critical cellular processes. While its intracellular levels are tightly regulated by networks of heme-binding proteins (HeBPs), labile heme can be hazardous through oxidative processes. In blood plasma, heme is scavenged by hemopexin (HPX), albumin and several other proteins, while it also interacts directly with complement components C1q, C3 and factor I. These direct interactions block the classical pathway (CP) and distort the alternative pathway (AP). Errors or flaws in heme metabolism, causing uncontrolled intracellular oxidative stress, can lead to several severe hematological disorders. Direct interactions of extracellular heme with alternative pathway complement components (APCCs) may be implicated molecularly in diverse conditions at sites of abnormal cell damage and vascular injury. In such disorders, a deregulated AP could be associated with the heme-mediated disruption of the physiological heparan sulphate–CFH coat of stressed cells and the induction of local hemostatic responses. Within this conceptual frame, a computational evaluation of HBMs (heme-binding motifs) aimed to determine how heme interacts with APCCs and whether these interactions are affected by genetic variation within putative HBMs. Combined computational analysis and database mining identified putative HBMs in all of the 16 APCCs examined, with 10 exhibiting disease-associated genetic (SNPs) and/or epigenetic variation (PTMs). Overall, this article indicates that among the pleiotropic roles of heme reviewed, the interactions of heme with APCCs could induce differential AP-mediated hemostasis-driven pathologies in certain individuals. Full article

(This article belongs to the Topic Blood Physiology: Molecular Mechanisms of Vascular Wall Functioning, 2nd Volume)

►▼ Show Figures

Figure 1

17 pages, 2247 KiB  

Open AccessArticle

Molecular Heterogeneity of the Brain Endothelium

by Nada Alnaqbi, Mohammad G. Mohammad, Rifat Hamoudi, Aloïse Mabondzo and Rania Harati

Curr. Issues Mol. Biol. 2023, 45(4), 3462-3478; https://doi.org/10.3390/cimb45040227 - 16 Apr 2023

Cited by 3 | Viewed by 2342

Abstract

The blood–brain barrier (BBB) is part of a neurovascular structure located in the brain’s micro vessels, that is essential to maintain brain homeostasis, but prevents the brain uptake of most drugs. Because of its importance in neuro-pharmacotherapy, the BBB has been the subject [...] Read more.

The blood–brain barrier (BBB) is part of a neurovascular structure located in the brain’s micro vessels, that is essential to maintain brain homeostasis, but prevents the brain uptake of most drugs. Because of its importance in neuro-pharmacotherapy, the BBB has been the subject of extensive research since its discovery over 100 years ago. Major advances in understanding the structure and function of the barrier have been made. Drugs are re-designed to cross the BBB. However, despite these efforts, overcoming the BBB efficiently to treat brain diseases safely remains challenging. The majority of BBB research studies focus on the BBB as a homogenous structure throughout the different brain regions. However, this simplification may lead to an inadequate understanding of the BBB function with significant therapeutic consequences. From this perspective, we analyzed the gene and protein expression profiles of the BBB in the micro vessels from the brains of mice that were isolated from two different brain regions, namely the cortex and the hippocampus. The expression profile of the inter-endothelial junctional protein (claudin-5), three ABC transporters (P-glycoprotein, Bcrp and Mrp-1), and three BBB receptors (lrp-1, TRF and GLUT-1) were analyzed. Our gene and protein analysis showed that the brain endothelium in the hippocampus exhibits different expression profiles compared to the brain cortex. Specifically, brain endothelial cells (BECs) of the hippocampus express higher gene levels of abcb1, abcg2, lrp1, and slc2a1 compared to the BECs of the cortex regions with a trend of increase for claudin-5, while BECs of the cortex express higher gene levels of abcc1 and trf compared to the hippocampus. At the protein levels, the P-gp expression was found to be significantly higher in the hippocampus compared to the cortex, while TRF was found to be up-regulated in the cortex. These data suggest that the structure and function of the BBB are not homogeneous, and imply that drugs are not delivered similarly among the different brain regions. Appreciation of the BBB heterogeneity by future research programs is thus critical for efficient drug delivery and the treatment of brain diseases. Full article

(This article belongs to the Topic Blood Physiology: Molecular Mechanisms of Vascular Wall Functioning, 2nd Volume)

►▼ Show Figures

Figure 1

21 pages, 1548 KiB  

Open AccessReview

Natural Products for the Treatment of Pulmonary Hypertension: Mechanism, Progress, and Future Opportunities

by Zuomei Zeng, Xinyue Wang, Lidan Cui, Hongjuan Wang, Jian Guo and Yucai Chen

Curr. Issues Mol. Biol. 2023, 45(3), 2351-2371; https://doi.org/10.3390/cimb45030152 - 13 Mar 2023

Cited by 2 | Viewed by 4070

Abstract

Pulmonary hypertension (PH) is a lethal disease due to the remodeling of pulmonary vessels. Its pathophysiological characteristics include increased pulmonary arterial pressure and pulmonary vascular resistance, leading to right heart failure and death. The pathological mechanism of PH is complex and includes inflammation, [...] Read more.

Pulmonary hypertension (PH) is a lethal disease due to the remodeling of pulmonary vessels. Its pathophysiological characteristics include increased pulmonary arterial pressure and pulmonary vascular resistance, leading to right heart failure and death. The pathological mechanism of PH is complex and includes inflammation, oxidative stress, vasoconstriction/diastolic imbalance, genetic factors, and ion channel abnormalities. Currently, many clinical drugs for the treatment of PH mainly play their role by relaxing pulmonary arteries, and the treatment effect is limited. Recent studies have shown that various natural products have unique therapeutic advantages for PH with complex pathological mechanisms owing to their multitarget characteristics and low toxicity. This review summarizes the main natural products and their pharmacological mechanisms in PH treatment to provide a useful reference for future research and development of new anti-PH drugs and their mechanisms. Full article

(This article belongs to the Topic Blood Physiology: Molecular Mechanisms of Vascular Wall Functioning, 2nd Volume)

►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less

Select all

Export citation of selected articles as:

Plain Text BibTeX BibTeX (without abstracts) Endnote Endnote (without abstracts) Tab-delimited RIS

 

Error

Oops... you haven't selected anything for export.

Ok

clear

Displaying articles 1-9