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Gateways of Pathogenic Bacterial Entry into Host Cells—Salmonella
Published in K. Balamurugan, U. Prithika, Pocket Guide to Bacterial Infections, 2019
Balakrishnan Senthilkumar, Duraisamy Senbagam, Chidambaram Prahalathan, Kumarasamy Anbarasu
Caveolae, a 21–24 kDa integral membrane flask-shaped projection in the plasma membrane of endothelial cells, consist of three caveolin proteins named as caveolin 1, 2, and 3. Caveolin 1 and 2 are expressed together as a hetero oligomer in the plasma membrane, and caveolin 3 was expressed only in muscle tissue (Tang et al. 1996; Smart et al. 1999). Caveolin-1, a scaffolding protein expressed within the caveolar membrane, interacts with signaling proteins, such as epidermal growth factor receptor, G-proteins, Src-like kinases, Ha-Ras, insulin receptors, and integrins for regulating their activities (Smart et al. 1999). Caveolar endocytosis is an endocytosis mechanism including nutrients and pathogens in most of the prokaryotes and parasites via endoplasmic reticulum (ER) → golgi → cytoplasm not fuse with lysosome, letting helps the pathogens to escape from lysosomal degradation (Schnitzer et al. 1994).
Pulmonary Endothelium in Health and Viral Infections
Published in Sunit K. Singh, Human Respiratory Viral Infections, 2014
Nikolaos Manitsopoulos, Frantzeska Frantzeskaki, Anastasia Kotanidou, Stylianos E. Orfanos
The transcellular pathway is used by water and molecules with a Mr greater than 3 nm. The former uses channels across the lipid bilayer formed by proteins named aquaporins (Figure 4.1).16 Under normal conditions, the plasma proteins can also be transported through the endothelium via a fluid phase or using a receptor-mediated manner. Additionally, transcellular channels are often formed transiently in order to facilitate protein transportation, such as albumin by caveolae.17 The latter are vesicular carriers established as clusters in the membrane. The major component of caveolae is the protein caveolin-1. It plays an important role in caveolae formation, as well as molecule capture and transcytosis.1,17,18
The Cardiovascular System
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Calvert Louden, David Brott, Chidozie J. Amuzie, Bindu Bennet, Ronnie Chamanza
In mice, targeted gene disruption of caveolin-1 caused impairment of nitric oxide synthase (NOS), NO, and calcium signaling in the cardiovascular system, causing aberrations in endothelium-dependent relaxation, contractility and maintenance of vasculo-myogenic tone (Drab et al. 2001). Functional loss of caveolin-1 was also associated with a 5-fold increase in systemic NO, but no major changes in NOS expression (Drab et al. 2001; Zhao et al. 2002), suggesting that deregulation and/or hyperactivity of NOS was responsible for the massive increase in NO production. Caveolin-1 is expressed within the vascular wall, specifically on the phenotypically anchored primary targets of drug-induced vascular injury, endothelial and smooth muscles cells (Drab et al. 2001; Zhao et al. 2002). Within these cells, caveolin is an important mediator of many signal transduction pathways, including regulation of vascular tone (Martens et al. 2001; Yu et al. 2004). Functionally, caveolae appear to be the focal point for compartmentalizing, organizing and modulating signal transduction activities (Linder et al. 2005; Martens et al. 2001; Yu et al. 2004) for many receptors, such as adenosine, dopaminergic-1, and endothelin, and enzymes, including PDE, nitric oxide synthase (NOS) and adenylyl cyclase (AC) (Table 18.8). Within EC and/or SMC, exaggerated pharmacologic action of these molecules or enzymes that are regulated by caveolin-1, are associated with drug-induced vascular injury. Collectively, these data suggest that caveolin-1 plays an important role in regulating NOS activity and potentially, vascular tone. There is evidence that loss and/or reduced expression of cav-1 in SMC and/or EC is a critical event in drug-induced vascular injury (Brott et al. 2005a; Brott et al. 2005b). In vitro studies have shown that loss of caveolin-1 is an early event that precedes SMC apoptosis. These data suggest that it is possible that drug-induced vascular injury is, in part, mediated through the NO caveolin-1 regulated pathway.
Basic physiology of the blood-brain barrier in health and disease: a brief overview
Published in Tissue Barriers, 2021
Caveolae are characteristic flask-shaped membrane invaginations with a diameter of 50–80 nm, which contain caveolin-1/2 and vesicle-associated membrane protein-2 as well as receptors for certain essential enzymes, hormones, plasma carrier proteins, and cytokines.190,191 Caveolin 1, which is the principal component of caveolae, can also influence the expression of TJ proteins.192 Major Facilitator Superfamily Domain containing 2a (Mfsd2a), a lipid transporter highly expressed in the endothelial cells of brain microvessels, inhibits caveolae production and hence plays an important role in barrier characteristics.196–198 Therefore, brain capillary endothelial cells exhibit few caveolae, whereas arteriolar endothelial cells in which Mfsd2a transcript levels are low display abundant caveolae.199,200 Knock-out of Mfsd2a in mice caused increased caveolae production and transcellular permeability in the brain microvasculature.195,197 On the other hand, the expression of the caveolin-1 is significantly increased in barrier type endothelial cells under several pathological conditions and by aging.193–195 Increase of caveolar vesicles in brain capillary endothelium has been documented in experimental animals with hypertension and during febrile seizures in experimental models of cortical dysplasia, a malformation of the cerebral cortex .96,201
Ultrasonically controlled albumin-conjugated liposomes for breast cancer therapy
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Nahid S. Awad, Vinod Paul, Mohammad H. Al-Sayah, Ghaleb A. Husseini
To internalize molecules from outside the cell, cells use a process called endocytosis. Via this process, cells can take up macromolecules, proteins and ligands [37]. The main endocytic routes are the clathrin-mediated endocytosis and the caveolae-mediated endocytosis. Caveolae are specialized membrane domains enriched in certain lipids cholesterol and proteins [38]. Caveolae can mediate endocytosis through a receptor-dependent or -independent fashion [39]. Caveolin-1 (Cav-1) is one of the main functional components of caveolae and plays an important role in caveolae formation. It expected that to induce tumour formation, rapid proliferation is required, and, therefore, downregulation of caveolin-1 expression may be necessary. The level of caveolin-1 is related to the invasiveness of the tumour [40]. According to Chatterjee et al. [41], nanoparticle conjugate of paclitaxel to HSA exhibits efficacy in pancreatic cancer, non–small cell lung cancer and breast cancer. The study found that Cav-1 protein levels correlated positively with cancer sensitivity to their albumin base nanoparticles and, therefore, caveolae are essential for the cancer uptake of albumin. In general, albumin binds to a cell-surface, 60-kDa glycoprotein (gp60) receptor (albondin). gp60 is localized in the caveolae and binds to caveolin-1 (an intracellular protein) with subsequent formation of the caveolae [42,43].
Caveolae, caveolin-1 and lung diseases of aging
Published in Expert Review of Respiratory Medicine, 2019
Sarah A. Wicher, Y.S. Prakash, Christina M. Pabelick
Due to the variable role of caveolae and specifically caveolin-1 in different airway diseases, it will be important to further explore their beneficial vs. detrimental roles in specific diseases and lung cell types. The current research has identified caveolin-1 as a potential marker for disease as well as therapy. However, new studies involving cavin proteins, their role in lung diseases and their interactions with caveolae and caveolins will make these investigations even more significant. Another area of importance is the use of caveolins or cavins as markers of disease stages within the lung (e.g. inflammation vs. fibrosis). For these investigations to be most successful it needs to be determined where caveolins or cavins should be measured: whole lung, specific tissues, particular cell types, or even blood or bronchoalveolar lavage. Of course, an ideal situation would be for sputum or blood analyses to correlate specific cell types or disease states.