Medical Sciences

Special Issue Information

Dear Colleagues,

The caveolin molecule is simply amazing. Understanding how the caveolin family works in the human body is not simple. The caveolin-mediated caveolae, cellular organelles of the cell, regulate the physiology of the human body by communicating with one another, while dysfunctional caveolae lead to pathogenesis. Since the four of us started studying caveolae when we worked at the Whitehead Institute for Biomedical Research of the Massachusetts Institute of Technology (MIT) in Michael P. Lisanti’s laboratory, we have mapped out the caveolin-scaffolding domain (CSD) within the caveolin family molecules and defined the CSD-interacting motifs within multiple lines of receptors involved in signal transduction. We have also established models for studying caveolae (i.e., lipid rafts) genesis. Functionally, we found that the CSD acts as a negative regulator of signal transduction, which inspired the development of therapeutics for diseases. In the past decade or so, we have witnessed the discovery of new regulating networks of caveolae-mediated communication and the dysfunction of caveolae related to pathogenies and cancer. As co-editors of this Special Issue, we invite current researchers in the field to discuss the role of these regulating networks in physiology, how they become impaired in pathology, and how they can be normalized by the development of new therapeutics in disorders. We strive to edit this Special Issue to serve as a unique platform for communicating commentary, original articles, review articles, case studies, letters to editors, rapid communications, and methodology reviews.

Potential Topics (not limited to):

central nervous system caveolae;
central nervous system caveolin-regulated tumors;
autoimmune and caveolae;
cardiovascular caveolae and atherosclerosis;
lung diseases and caveolae;
caveolin-evolved breast cancer;
caveolin-evolved prostate cancer;
Alzheimer’s disease and caveolins;
obesity and diabetes;
caveolin-mediated co-evolution of tumor with its microenvironment.

Dr. Shengwen Calvin Li
Dr. Massimo Sargiacomo
Prof. Jacques Couet
Prof. Eric Kübler
Guest Editors

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Published Papers (2 papers)

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15 pages, 1929 KiB

Open AccessReview

Critical Role of Caveolin-1 Loss/Dysfunction in Pulmonary Hypertension

by Rajamma Mathew

Med. Sci. 2021, 9(4), 58; https://doi.org/10.3390/medsci9040058 - 22 Sep 2021

Cited by 12 | Viewed by 3625

Abstract

Pulmonary hypertension (PH) is a rare disease with a high morbidity and mortality rate. A number of systemic diseases and genetic mutations are known to lead to PH. The main features of PH are altered vascular relaxation responses and the activation of proliferative and anti-apoptotic pathways, resulting in pulmonary vascular remodeling, elevated pulmonary artery pressure, and right ventricular hypertrophy, ultimately leading to right heart failure and premature death. Important advances have been made in the field of pulmonary pathobiology, and several deregulated signaling pathways have been shown to be associated with PH. Clinical and experimental studies suggest that, irrespective of the underlying disease, endothelial cell disruption and/or dysfunction play a key role in the pathogenesis of PH. Endothelial caveolin-1, a cell membrane protein, interacts with and regulates several transcription factors and maintains homeostasis. Disruption of endothelial cells leads to the loss or dysfunction of endothelial caveolin-1, resulting in reciprocal activation of proliferative and inflammatory pathways, leading to cell proliferation, medial hypertrophy, and PH, which initiates PH and facilitates its progression. The disruption of endothelial cells, accompanied by the loss of endothelial caveolin-1, is accompanied by enhanced expression of caveolin-1 in smooth muscle cells (SMCs) that leads to pro-proliferative and pro-migratory responses, subsequently leading to neointima formation. The neointimal cells have low caveolin-1 and normal eNOS expression that may be responsible for promoting nitrosative and oxidative stress, furthering cell proliferation and metabolic alterations. These changes have been observed in human PH lungs and in experimental models of PH. In hypoxia-induced PH, there is no endothelial disruption, loss of endothelial caveolin-1, or enhanced expression of caveolin-1 in SMCs. Hypoxia induces alterations in membrane composition without caveolin-1 or any other membrane protein loss. However, caveolin-1 is dysfunctional, resulting in cell proliferation, medial hypertrophy, and PH. These alterations are reversible upon removal of hypoxia, provided there is no associated EC disruption. This review examined the role of caveolin-1 disruption and dysfunction in PH. Full article

(This article belongs to the Special Issue Beyond Lipid Rafts and Caveolae: Caveolins in Disease)

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13 pages, 1022 KiB

Open AccessReview

The Evolving Role of Caveolin-1: A Critical Regulator of Extracellular Vesicles

by Kareemah Ni, Chenghao Wang, Jonathan M Carnino and Yang Jin

Med. Sci. 2020, 8(4), 46; https://doi.org/10.3390/medsci8040046 - 04 Nov 2020

Cited by 29 | Viewed by 3815

Abstract

Emerging evidence suggests that extracellular vesicles (EVs) play an essential role in mediating intercellular communication and inter-organ crosstalk both at normal physiological conditions and in the pathogenesis of human diseases. EV cargos are made up of a broad spectrum of molecules including lipids, proteins, and nucleic acids such as DNA, RNA, and microRNAs. The complex EV cargo composition is cell type-specific. A dynamic change in EV cargos occurs along with extracellular stimuli and a change in the pathophysiological status of the host. Currently, the underlying mechanisms by which EVs are formed and EV cargos are selected in the absence and presence of noxious stimuli and pathogens remain incompletely explored. The term EVs refers to a heterogeneous group of vesicles generated via different mechanisms. Some EVs are formed via direct membrane budding, while the others are produced through multivesicular bodies (MVBs) or during apoptosis. Despite the complexity of EV formation and EV cargo selection, recent studies suggest that caveolin-1, a well-known structural protein of caveolae, regulates the formation and cargo selection of some EVs, such as microvesicles (MVs). In this article, we will review the current understanding of this emerging and novel role of cav-1. Full article

(This article belongs to the Special Issue Beyond Lipid Rafts and Caveolae: Caveolins in Disease)

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