Specialized Membrane Structures Research Articles

Mesenchymal stem cell-derived extracellular vesicles in periodontal bone repair.

Periodontitis is a chronic inflammatory disease that destroys tooth-supporting structures and poses significant public health challenges due to its high prevalence and links to systemic health conditions. Traditional treatments are effective in reducing the inflammatory response and improving the clinical symptoms of periodontitis. However, these methods are challenging to achieve an ideal treatment effect in alveolar bone repair. Mesenchymal stem cells (MSCs) represent a potential alternative for the treatment of periodontal bone defects due to their self-renewal and differentiation capabilities. Recent research indicates that MSCs exert their effects primarily through paracrine mechanisms. Mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) serve as pivotal mediators in intercellular communication, transferring microRNAs (miRNAs), messenger RNAs (mRNAs), proteins, and cytokines to recipient cells, thereby emulating the therapeutic effects of MSCs. In periodontitis, MSC-EVs play a pivotal role in immunomodulation and bone remodeling, thereby facilitating periodontal bone repair. As a cell-free therapy, MSC-EVs demonstrate considerable clinical potential due to their specialized membrane structure, minimal immunogenicity, low toxicity, high biocompatibility, and nanoscale size. This review indicates that MSC-EVs represent a promising approach for periodontitis treatment, with the potential to overcome the limitations of traditional therapies and offer a more effective solution for bone repair in periodontal disease. In this review, we introduce MSC-EVs, emphasizing their mechanisms and clinical applications in periodontal bone repair. It synthesizes recent advances, existing challenges, and future prospects to present up-to-date information and novel techniques for periodontal regeneration and to guide the improvement of MSC-EV therapy in clinical practice.

Mechanism, structural and functional insights into nidovirus-induced double-membrane vesicles.

During infection, positive-stranded RNA causes a rearrangement of the host cell membrane, resulting in specialized membrane structure formation aiding viral genome replication. Double-membrane vesicles (DMVs), typical structures produced by virus-induced membrane rearrangements, are platforms for viral replication. Nidoviruses, one of the most complex positive-strand RNA viruses, have the ability to infect not only mammals and a few birds but also invertebrates. Nidoviruses possess a distinctive replication mechanism, wherein their nonstructural proteins (nsps) play a crucial role in DMV biogenesis. With the participation of host factors related to autophagy and lipid synthesis pathways, several viral nsps hijack the membrane rearrangement process of host endoplasmic reticulum (ER), Golgi apparatus, and other organelles to induce DMV formation. An understanding of the mechanisms of DMV formation and its structure and function in the infectious cycle of nidovirus may be essential for the development of new and effective antiviral strategies in the future.

#897 Peritoneal inflammation in PD-related peritonitis induces systemic eryptosis: in vitro and in vivo assessments

Abstract Background and Aims Erythrocytes (RBCs) have a highly specialized and organized membrane structure and undergo programmed cell death, known as eryptosis ( = stress-induced RBC death mechanism). Triggers of eryptosis include oxidative stress, inflammation and several uremic toxins. Our preliminary data show a significant increase of eryptosis during peritoneal dialysis (PD) -associated peritonitis in PD patients. The aims of this study were: assessment of incrementation of eryptosis in PD patients with peritonitis, evaluation of the relationship between systemic eryptosis in peritonitis and specific peritonitis biomarkers in PD effluent (PDE), and confirmation of the induction of eryptosis by peritonitis in a vitro setting. Method We enrolled 34 PD patients in stable condition (without systemic inflammation nor PD-related peritonitis in the last 3 months), 31 PD patients with acute peritonitis, and 17 healthy subjects (CTR). For PD stable patients, blood samples for eryptosis evaluation were drawn during the regular outpatient. For PD patients with peritonitis, blood samples and PDE samples were collected at the time of peritonitis diagnosis. PDE samples were used for peritoneal White Blood Cell count (pWBC), peritoneal Neutrophil Gelatinase-associated Lipocalin (pNGAL) and peritoneal cytokines levels (IL-1β and IL-6) measurements. For in vitro study, healthy RBCs were exposed to plasma of 31 PD patients with peritonitis and plasma of CTR group for 2, 4 and 24 hours. Morphological markers of eryptosis (cell membrane scrambling, cell shrinkage) and eryptosis percentage (based on PS exposure at RBC surface and AnnexinV-binding) were evaluated by flow cytometric analyses in vivo and in vitro. Results Totally, 65 chronic PD patients were included in this study. 57% of patients were treated with continuous ambulatory PD (CAPD) and 43% with automated PD (APD). The median PD vintage was 38 months (IQR 3.6–124.9 months). Table 1 reports clinical data for our PD population (Table 1). The percentage of AnnexinV-binding RBCs was significantly higher in PD patients than in CTR (2.7%; IQR 1.6–3.9 vs CTR: 0.8; IQR 0.7–1.3 P < .05). Eryptosis levels did not differ significantly between PD pts with and without diabetes, with and without hypertension, with and without cardiovascular disease. Eryptosis showed no significant differences between patients treated by CAPD/APD, and with Kt/Vurea values ≤ 1.7 and > 1.7. Generally, RBCs of all 65 PD patients were dramatically deranged in their morphology. In particular, RBCs from PD patients with peritonitis were characterized by dramatically deranged morphology and increased median cell volume in comparison with PD stable patients (P < .001). The percentages of AnnexinV-binding RBCs were significantly increased in the PD-associated peritonitis group (9.6%; IQR 4.2–16.7 versus 2.7%; IQR 1.6–3.9) (P<.0001) (Fig. 1). The percentage of AnnexinV-binding RBCs was significantly higher in PD patients with peritonitis than in healthy CTR (P < .001). We confirmed these in vivo data by in vitro results: healthy RBCs incubated with plasma from PD patients with peritonitis demonstrated a significant increase of eryptosis compared to healthy RBCs exposed to plasma from control group at all times (Fig. 2). Furthermore, significant positive strong correlations were observed between eryptosis level and all analysed peritoneal biomarkers of peritonitis (Spearman's rho pWBC = 0.77, P<.001, Spearman's rho pNGAL = 0.64, P = .001, Spearman's rho IL-6 = 0.61, P = .003 and Spearman's rho IL-1β = 0.64, P = .001,) (Fig. 3). Conclusion We investigated a potential connection between systemic eryptosis and peritoneal biomarkers of peritonitis. In particular, we theorized that the eryptosis enhancement is directly connected with peritonitis, and, based on the results, we hypothesized that the peritoneal membrane injury could be related to eryptosis. Upregulation of inflammatory markers could explain the increased rate of systemic eryptosis during PD-related peritonitis. In particular, we corroborated this point with our observations about in vitro induction of eryptosis by plasma from PD patients on the first day of peritonitis.

Peritoneal Inflammation in PD-Related Peritonitis Induces Systemic Eryptosis: In Vitro and In Vivo Assessments.

Erythrocytes (RBCs) have a highly specialized and organized membrane structure and undergo programmed cell death, known as eryptosis. Our preliminary data show a significant increase in the eryptosis during peritoneal dialysis (PD)-associated peritonitis. The objectives of the present study were assessment of the incrementation of eryptosis in PD patients with peritonitis, evaluation of the relationship between systemic eryptosis in peritonitis and specific peritonitis biomarkers in PD effluent (PDE), and confirmation of the induction of eryptosis by peritonitis in a vitro setting. We enrolled 22 PD patients with peritonitis and 17 healthy subjects (control group, CTR). For the in vivo study, eryptosis was measured in freshly isolated RBCs. For the in vitro study, healthy RBCs were exposed to the plasma of 22 PD patients with peritonitis and the plasma of the CTR group for 2, 4, and 24 h. Eryptosis was evaluated by flow cytometric analyses in vivo and in vitro. PDE samples were collected for biomarkers analysis.The percentage of eryptotic RBCs was significantly higher in PD patients with peritonitis than in CTR (PD patients with peritonitis: 7.7; IQR 4.3-14.2, versus CTR: 0.8; IQR 0.7-1.3; p < 0.001). We confirmed these in vivo results by in vitro experiments: healthy RBCs incubated with plasma from PD patients with peritonitis demonstrated a significant increase in eryptosis compared to healthy RBCs exposed to plasma from the control group at all times. Furthermore, significant positive correlations were observed between eryptosis level and all analyzed peritoneal biomarkers of peritonitis. We investigated a potential connection between systemic eryptosis and peritoneal biomarkers of peritonitis. Up-regulation of inflammatory markers could explain the increased rate of systemic eryptosis during PD-related peritonitis.

Biogenesis of Rab14-positive endosome buds at Golgi–endosome contacts by the RhoBTB3–SHIP164–Vps26B complex

Early endosomes (EEs) are crucial in cargo sorting within vesicular trafficking. While cargoes destined for degradation are retained in EEs and eventually transported to lysosomes, recycled cargoes for the plasma membrane (PM) or the Golgi undergo segregation into specialized membrane structures known as EE buds during cargo sorting. Despite this significance, the molecular basis of the membrane expansion during EE bud formation has been poorly understood. In this study, we identify a protein complex comprising SHIP164, an ATPase RhoBTB3, and a retromer subunit Vps26B, which promotes the formation of EE buds at Golgi–EE contacts. Our findings reveal that Vps26B acts as a novel Rab14 effector, and Rab14 activity regulates the association of SHIP164 with EEs. Depletion of SHIP164 leads to enlarged Rab14+ EEs without buds, a phenotype rescued by wild-type SHIP164 but not the lipid transfer-defective mutants. Suppression of RhoBTB3 or Vps26B mirrors the effects of SHIP164 depletion. Together, we propose a lipid transport-dependent pathway mediated by the RhoBTB3–SHIP164–Vps26B complex at Golgi–EE contacts, which is essential for EE budding.

A Review of Gap Junction Protein and its Potential Role in Nervous System-Related Disease.

Gap junction (GJ) is a special cell membrane structure composed of connexin. Connexin is widely distributed and expressed in all tissues except differentiated skeletal muscle, red blood cells, and mature sperm cells, which is related to the occurrence of many genetic diseases due to its mutation. Its function of regulating immune response, cell proliferation, migration, apoptosis, and carcinogenesis makes it a therapeutic target for a variety of diseases. In this paper, the possible mechanism of its action in nervous system-related diseases and treatment are reviewed.

Cerebrospinal fluid sulfatide isoforms lack diagnostic utility in separating progressive from relapsing-remitting multiple sclerosis.

Multiple sclerosis (MS) is an immune-mediated demyelinating disorder of the central nervous system. The glycosphingolipid sulfatide, a lipid particularly enriched in the myelin sheath, has been shown to be involved the maintenance of this specific membrane structure. Sulfatide in cerebrospinal fluid (CSF) may reflect demyelination, a dominating feature of MS. We investigated the diagnostic utility of CSF sulfatide isoform levels to separate different courses or phenotypes of MS disease. This was a mono-center, cross-sectional study of relapsing-remitting MS (RRMS) (n=45) and progressive MS (PMS) (n=42) patients (consisting of primary PMS (n=17) and secondary PMS (n=25)) and healthy controls (n=19). In total, 20 sulfatide isoforms were measured in CSF by liquid chromatography-mass spectrometry. CSF total sulfatide concentrations, as well as CSF sulfatide isoform distribution, did not differ across the study groups, and their levels were independent of disease course/phenotype, disease duration, time to conversion to secondary PMS, age, and disability in MS patients. CSF sulfatide isoforms lack diagnostic and prognostic utility as a biomarker for progressive MS.

Caveolae and Bin1 form ring-shaped platforms for T-tubule initiation.

Excitation-contraction coupling requires a highly specialized membrane structure, the triad, composed of a plasma membrane invagination, the T-tubule, surrounded by two sarcoplasmic reticulum terminal cisternae. Although the precise mechanisms governing T-tubule biogenesis and triad formation remain largely unknown, studies have shown that caveolae participate in T-tubule formation and mutations of several of their constituents induce muscle weakness and myopathies. Here, we demonstrate that, at the plasma membrane, Bin1 and caveolae composed of caveolin-3 assemble into ring-like structures from which emerge tubes enriched in the dihydropyridine receptor. Bin1 expression lead to the formation of both rings and tubes and we show that Bin1 forms scaffolds on which caveolae accumulate to form the initial T-tubule. Cav3 deficiency caused by either gene silencing or pathogenic mutations results in defective ring formation and perturbed Bin1-mediated tubulation that may explain defective T-tubule organization in mature muscles. Our results uncover new pathophysiological mechanisms that may prove relevant to myopathies caused by Cav3 or Bin1 dysfunction.

Characterization of Cellulose Acetate Membrane at Different Thicknesses on Sucrose Concentration by Forward Osmosis

Forward osmosis (FO) requires a specific membrane structure for applications like juice concentration. The phase inversion method was used to make cellulose acetate (CA) FO membranes. The solvents used were acetone and 1,4-dioxane. Additives included polyvinylpyrrolidone (PVP), methanol, and maleic acid were used in the preparation of CA membrane, which make it easier to improve a FO membrane's permeability. The performance of fabricated FO membrane and their morphology were evaluaed with different casting thicknesses of 150, 200, and 250 µm. Experiment works begins with an hour of membrane flux testing, deionized water was used as feed solution and 1 M NaCl as draw solution. The membrane was then used to concentrate 0.5 M sucrose with NaCl for 240 minutes (2 M). Contact angle, porosity, and scanning electron miscroscopy (SEM) were used to characterize membrane properties and morphology. High water flux (2.25 L/m2hr) and high porosity (75.86%) were found at 200 µm casting thickness. Water permeability of sucrose concentration at 200 µm casting thickness had the highest flux (2.39 L/m2hr). The results also show that flux values vary with membrane thickness. All membranes were hydrophilic with contact angles below 90°. A 200 µm casting thickness produces a membrane with smooth and evenly distributed pores, according to morphology analysis. Structural parameter (S) values had a proportional relationship with the FO membrane thickness, which thinner membrane potentially reduces the internal concentration polarization (ICP).

Alternating exosomes and their mimetics as an emergent strategy for targeted cancer therapy.

Exosomes, a subtype of the class of extracellular vesicles and nano-sized particles, have a specific membrane structure that makes them an alternative proposition to combat with cancer through slight modification. As constituents of all most all the primary body fluids, exosomes establish the status of intercellular communication. Exosomes have specific proteins/mRNAs and miRNAs which serve as biomarkers, imparting a prognostic tool in clinical and disease pathologies. They have efficient intrinsic targeting potential and efficacy. Engineered exosomes are employed to deliver therapeutic cargos to the targeted tumor cell or the recipient. Exosomes from cancer cells bring about changes in fibroblast via TGFβ/Smad pathway, augmenting the tumor growth. These extracellular vesicles are multidimensional in terms of the functions that they perform. We herein discuss the uptake and biogenesis of exosomes, their role in various facets of cancer studies, cell-to-cell communication and modification for therapeutic and diagnostic use.

Separation of NaCl and humic substances in anion exchange spent brine with electrodialysis

The advanced treatment process of anion exchange can be an effective approach for removing dissolved organic matter in the drinking water, but the production of anion exchange spent brine is a main drawback. Herein, electrodialysis (ED) was used to separate high-concentration NaCl and humic substances (HSs) from anion exchange spent brine. The composition and characteristics of anion exchange spent brine were systematically studied, and the impacts of ion exchange membrane type, volume ratio of initial concentrate to dilute (Vc,0/Vd,0) and flow rate on the performance of lab-scale and pilot-scale ED were investigated. Our results demonstrated the cost-effective membrane pair was TWEDC1/TWEDA1 to treat anion exchange spent brine with high degree of aromaticity and plentiful oxygen-containing functional groups, because of its special membrane structure and membrane properties. High current efficiency of 90.60% and low energy consumption of 0.91 kW h/kg NaCl were achieved by ED with TWEDC1/TWEDA1. When Vc,0/Vd,0 was 1:4, 15% (w/w) recovery NaCl solution concentrated by lab-scale first-stage ED could be used as resin regeneration agent. Furthermore, lab-scale and pilot-scale two-stage ED were simultaneously verified to effectively separate NaCl and HSs in the anion exchange spent brine.

Fabrication of mixed matrix membranes blending with the TiO2/Bi3O4Cl 2D/2D heterojunction for photocatalytic degradation of tetracycline

The photocatalytic composite membranes had becoming potential functional material for wastewater treatment because of facile separation of solid liquid phases after-treatment process. In this study, the 2D/2D TiO2/Bi3O4Cl heterojunctions were designed as a functional photocatalyst to prepare a series of PVDF photocatalytic membranes through phase inversion method. This tight-contact 2D/2D heterostructure results in shorter migration distance of photo-generated carriers to the surface of the 2D/2D TiO2/Bi3O4Cl heterojunctions, so that it can faster participation in photocatalytic degradation. Moreover, the 2D/2D heterostructure can improve the pore structure of membrane, which will enhance the porosity and mean pore size, and then providing more photocatalytic active sites for degradation process. As a result, under optimal conditions, the TiO2/Bi3O4Cl/PVDF membranes exhibited a higher tetracycline (TC) degradation rate of 88.85% in comparison with pure PVDF membranes. The cyclic degradation experiment proved that the TiO2/Bi3O4Cl/PVDF membranes showed good stability after several cycles. This work highlights the construction of 2D/2D heterojunction and the improvement of the photocatalyst property by special membrane structure and their application in wastewater treatment.

Shear stress triggered circular dorsal ruffles formation to facilitate cancer cell migration

Circular dorsal ruffles (CDRs) are a kind of special ring-shaped membrane structure rich in F-actin, it is highly involved in the invasion-metastasis of tumor. Shear stress is one of the biophysical elements that affects the fate of tumor cells. However, how shear stress contributes to the CDRs formation is still unclear. In this study, we found that shear stress stimulated the formation of CDRs and promoted the migration of human breast MDA-MB-231 carcinoma cells. Integrin-linked kinase (ILK) mediated the recruiting of ADP-ribosylation factors (ARAP1/Arf1) to CDRs. Meanwhile, the transfection of ARAP1 or Arf1 mutant decreased the number of cells with CDRs, the CDRs areas and perimeters, thus blocked the cancer cell migration. This indicated that the ARAP1/Arf1 were necessary for the CDRs formation and cancer cell migration. Further study revealed that shear stress could stimulate the formation of intracellular macropinocytosis (MPS) thus promoted the ARAP1/Arf1 transportation to early endosome to regulate cancer cell migration after the depolymerization of CDRs. Our study elucidates that the CDRs formation is essential in shear stress-induced breast cancer cell migration, which provides a new research target for exploring the cytoskeletal mechanisms of breast cancer malignance.

Do human sinoatrial node cells have t-tubules?

Every heartbeat is generated by spontaneously depolarizing specialised nodal cells that make up the sinoatrial node (SN). The SN's unique properties depend on two complex mechanisms - the membrane-voltage and the Ca2+ clocks, regulated by strictly defined expression of ion channels, connexins and Ca2+-handling proteins. In the working myocardium these proteins are accumulated in specialised membrane structures– the transverse tubules (t-tubules). It is well known that small mammals do not exhibit t-tubules in their atrium, but such structures are observed in the atria of bigger mammals such as sheep. No information on t-tubules in the human SN is present yet. The aim of our study was to determine if t-tubules are present in the human SN, as well as surrounding atrial myocardium. Dystrophin (cytoplasmic protein connecting the muscle fibres to the surrounding extracellular membrane), Na+-Ca2+ exchanger (NCX1), sarcoplasmic-endoplasmic reticulum calcium adenosine triphosphatase (SERCA2a), α-actinin, and ryanodine receptor 2 (RyR2) were investigated. Staining with wheat germ agglutinin (WGA, specific marker of t-tubules) demonstrated that human RA cells contain t-tubules, but these structures are very sparse in the SN. Experiments in single nodal cells from rat and mouse showed no expression of t-tubular network, but striated pattern of expression of RyR2 was obtained similar to the human sections, suggesting its manner of organization is dependent on α-actinin colocalization.

Differentiation of Trafficking Pathways at Golgi Entry Core Compartments and Post-Golgi Subdomains.

Eukaryotic cells have developed specialized membrane structures called organelles, which compartmentalize cellular functions and chemical reactions. Recent improvements in microscopy and membrane compartment isolation techniques are now sophisticating our view. Emerging evidences support that there are distinct sub-populations or subdomains, which are spatially and/or temporally segregated within one type of organelle, contributing to specify differential sorting of various cargos to distinct destinations of the cell. In plant cells, the Golgi apparatus represents a main trafficking hub in which entry occurs through a Golgi Entry Core Compartment (GECCO), that remains to be further characterized, and sorting of cargos is mediated through multiple transport pathways with different sets of regulator proteins at the post-Golgi compartment trans-Golgi network (TGN). Both GECCO and TGN are differentiated sub-populations as compared to the rest of Golgi, and moreover, further subdomain formation within TGN is suggested to play a key role for cargo sorting. In this review, we will summarize recent findings obtained on organelle subdomains, and their relationship with cargo entry at and exit from the Golgi apparatus.

Ion Transport of Biohybrid Asymmetric Membranes by pH and Light‐Cooperative Modulation

AbstractBacteriorhodopsin (bR) is an excellent light‐driven proton pump and plays a vital role in chemical and biological analytical processes, such as maintaining osmotic balance, intracellular acidity, and participating in photosynthesis. Inspired by the special membrane structure with 75% bR and 25% lipid forming a purple membrane (PM) embedded on the Halobacterium salinarum cell membrane, an asymmetric membrane is fabricated by covering an anodic aluminum oxide (AAO) with a mixture of PM and poly(vinyl alcohol) (PVA) and ion transport modulation is achieved via coordination of pH and light stimuli. The rectification ratio of the PM‐doped asymmetric membrane is increased from 2 to 14.43 under costimulation of pH and light. Because bR is a conventional proton pump, the mechanism of this device may shed light on the design of other ionic asymmetric membranes (e.g., Na+, Cl−) via homologs of bR.

Dietary lipids and cardiometabolic health: a new vision of structure-activity relationship.

The impact of dietary lipids on cardiometabolic health was mainly studied considering their fatty acid composition. This review aims to present the recent change in paradigm whereby the food matrix, the molecular and supramolecular structures of dietary lipids modulate their digestive fate and cardiometabolic impact. Epidemiological studies have reported that the metabolic impact of full-fat dairy products is better than predictable upon saturated fatty acid richness. Milk polar lipid supplementation reduced adiposity and inflammation in rodents by modulating gut microbiota and barrier, and decreased lipid markers of cardiovascular disease risk in humans by lowering cholesterol absorption. The metabolic importance of the structure of lipid molecules carrying omega-3 (molecular carrier) has also been documented. Plant lipids exhibit specific assemblies, membrane and molecular structures with potential health benefits. Lipid emulsifiers used to stabilize fats in processed foods are not mere bystanders of lipid effects and can induce both beneficial and adverse health effects. These findings open new clinical research questions aiming to further characterize the cardiometabolic fate of lipids, from digestion to bioactive metabolites, according to the food source or molecular carrier. This should be useful to elaborate food formulations for target populations and personalized dietary recommendations.

The novel zebrafish model pretzel demonstrates a central role for SH3PXD2B in defective collagen remodelling and fibrosis in Frank-Ter Haar syndrome.

ABSTRACTFrank-Ter Haar syndrome (FTHS, MIM #249420) is a rare skeletal dysplasia within the defective collagen remodelling spectrum (DECORS), which is characterised by craniofacial abnormalities, skeletal malformations and fibrotic soft tissues changes including dermal fibrosis and joint contractures. FTHS is caused by homozygous or compound heterozygous loss-of-function mutation or deletion of SH3PXD2B (Src homology 3 and Phox homology domain-containing protein 2B; MIM #613293). SH3PXD2B encodes an adaptor protein with the same name, which is required for full functionality of podosomes, specialised membrane structures involved in extracellular matrix (ECM) remodelling. The pathogenesis of DECORS is still incompletely understood and, as a result, therapeutic options are limited. We previously generated an mmp14a/b knockout zebrafish and demonstrated that it primarily mimics the DECORS-related bone abnormalities. Here, we present a novel sh3pxd2b mutant zebrafish, pretzel, which primarily reflects the DECORS-related dermal fibrosis and contractures. In addition to relatively mild skeletal abnormalities, pretzel mutants develop dermal and musculoskeletal fibrosis, contraction of which seems to underlie grotesque deformations that include kyphoscoliosis, abdominal constriction and lateral folding. The discrepancy in phenotypes between mmp14a/b and sh3pxd2b mutants suggests that in fish, as opposed to humans, there are differences in spatiotemporal dependence of ECM remodelling on either sh3pxd2b or mmp14a/b. The pretzel model presented here can be used to further delineate the underlying mechanism of the fibrosis observed in DECORS, as well as screening and subsequent development of novel drugs targeting DECORS-related fibrosis.This paper has an associated First Person interview with the first author of the article.

Self-assembled vesicles of sodium oleate and chitosan quaternary ammonium salt in acidic or alkaline aqueous solutions

Fatty acids are anionic surfactants under their deprotonated forms, which have biodegradability and biocompatibility. The fatty acid self-assembled aggregates exhibit many potential applications. Fatty acid vesicles are the most representative because of their special hollow double-layer membrane structure. However, their application is hindered by a poor stability against variations in pH, salt, and temperature. In this work, the anionic surfactant sodium oleate (SO) and the polycationic hydroxypropyltrimethyl ammonium chloride chitosan (HACC) were mixed to form complex vesicles in a wider pH scale. The formation of vesicles was proved through TEM, fluorescence spectroscopy, and DLS; meanwhile, the intermolecular force–formed vesicles were verified through FT-IR and zeta potential analyses. The effect of electrolyte and temperature on the stability of the vesicle was also studied. The experimental results showed that with the aid of H-bonding and the electrostatic attraction separately, amphiphilic molecules were formed and they self-assembled into vesicles in both acidic and alkaline aqueous solutions.

Abnormal Excitation-Contraction Coupling and Calcium Homeostasis in Myopathies and Cardiomyopathies

Muscle contraction requires specialized membrane structures with precise geometry and relies on the concerted interplay of electrical stimulation and Ca2+ release, known as excitation-contraction coupling (ECC). The membrane structure hosting ECC is called triad in skeletal muscle and dyad in cardiac muscle, and structural or functional defects of triads and dyads have been observed in a variety of myopathies and cardiomyopathies. Based on their function, the proteins localized at the triad/dyad can be classified into three molecular pathways: the Ca2+ release complex (CRC), store-operated Ca2+ entry (SOCE), and membrane remodeling. All three are mechanistically linked, and consequently, aberrations in any of these pathways cause similar disease entities. This review provides an overview of the clinical and genetic spectrum of triad and dyad defects with a main focus of attention on the underlying pathomechanisms.