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Developmental Diseases of the Nervous System
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
James H. Tonsgard, Nikolas Mata-Machado
The majority of primitive neurons migrate radially or upward along glial fibers that extend from the VZ to the outer molecular layer. However, some neurons move tangentially or laterally within the VZ and SVZ, and intermediate zone (the future white matter [WM]). Radial and tangential movements are determined by characteristics of the radial glial fibers as well as a number of molecules (BLBP, ErbB4 receptor, and Notch receptors). The molecules that contribute to movement include cytoskeletal proteins (filamin A, doublecortin, Lis 1, ARFGEF2), signaling molecules (reelin), molecules modulating glycosylation that provide stop signals, neurotransmitters, neural cell adhesion molecules, and growth factors. Toxins such as alcohol and cocaine may also affect this process. Migration of neurons primarily occurs between the 12th and 24th fetal weeks.
Plaques, Tangles and Amyloid:
Published in Robert E. Becker, Ezio Giacobini, Alzheimer Disease, 2020
Robert G. Struble, H. Brent Clark
In sum, NFT, GVD and HB all represent apparent disorganization of the cytoskeleton. However, documenting the presence of cytoskeletal abnormalities does not necessarily imply that cytoskeletal dysfunction is the cause of AD. Rather, abnormalities of cytoskeletal proteins could be a secondary response to some unknown primary cause.
Ultra-Structural Analysis of the Intrahepatic Bile Duct System
Published in Gianfranco Alpini, Domenico Alvaro, Marco Marzioni, Gene LeSage, Nicholas LaRusso, The Pathophysiology of Biliary Epithelia, 2020
Luca Marucci, Anne Marie Jezequel, Antonio Benedetti
Alteration of specific cytoskeletal proteins may also have substantial impact on the cellular structure and function. Recently, Fitz and co-authors29 have demonstrated that during warm liver ischemia, cholangiocyte membrane structure appears altered both in vivo and in vitro after ATP depletion. Lateral interdigitations are gready reduced after 120 minutes of ischemia or ATP depletion, and apical microvilli appear to increase in length but become progressively less abundant. In a time course that paralleled the loss of microvilli, the actin membrane linking protein ezrin, progressively dissociated from the microvillar cytoskeleton, suggesting the role of alteration in the membrane-cytoskeletal interactions at the early stages of these events. These studies indicate that the initial cellular response to metabolic inhibition involves early and characteristic changes in the membrane-cytoskeleton and secondary structures of the plasma membrane. Although cell viability and epithelial barrier function remained largely intact, the profound loss of membrane organization and surface area may negatively impair the secretory capacity of intrahepatic bile duct until the membrane domains are re-established.
Role of exosomes and its emerging therapeutic applications in the pathophysiology of non-infectious diseases
Published in Biomarkers, 2022
Gauresh G. Shivji, Rajib Dhar, Arikketh Devi
It has been observed that the protein content of exosomes can be affected by the depletion of the specific ESCRT family proteins and also the rate of exosomes release from cells may be hindered. The proteins which form a part of ESCRT independent mechanism include the biogenesis proteins, such as Alix and TSG101, exosomal membrane proteins and adhesion molecules like the TSPAN domains of CD9, CD63, CD81, TSPAN8 and integrins. Membrane transport and fusion proteins, such as Ras associated binding (Rab) proteins, annexins and Guanosine triphosphate (GTPases) and heat shock proteins (HSPs), such as HSP 70 and HSP 90 are also part of the exosomes and all these proteins play a role in cancer immunity. Cytoskeletal proteins, such as actin, tubulin and cofilin have also been identified in exosomes (Figure 1) (Vanlandingham and Ceresa 2009).
Ser69 phosphorylation of TIMAP affects endothelial cell migration
Published in Experimental Lung Research, 2021
Nikolett Király, Csilla Csortos, Anita Boratkó
Endothelium regulates vascular function. It has a central role in hemostasis, inflammation, vasoregulation, angiogenesis, and vascular growth. Endothelial cells (EC) form a barrier between blood and the underlying tissue and its integrity is critical to proper tissue and organ function. . EC integrity depends on the structure of the cytoskeleton and cell-cell junctions. Organization of the cytoskeletal elements is flexible, it is highly adapted to extra- and intracellular signals which affect the phosphorylation state and eventually the actual conformation of cytoskeletal proteins. Equilibrium between contractile and tethering forces determines the actual shape, and the actual interactions of the cell with neighboring cells.1 Regulation of the phosphorylation level of adherent or tight junction, furthermore cytoskeleton and cytoskeleton-associated proteins is greatly clinically relevant, as these proteins are crucial in the EC barrier function.1–3 Both Ser/Thr and Tyr phosphorylation play a regulatory role in EC junction and cytoskeletal structures, and eventually, influence paracellular permeability.4
Synergistic effect of glucocorticoids and IGF-1 on myogenic differentiation through the Akt/GSK-3β pathway in C2C12 myoblasts
Published in International Journal of Neuroscience, 2020
Xiao-Bo Fang, Zu-Biao Song, Meng-Shu Xie, Yan-Mei Liu, Wei-Xi Zhang
Duchenne muscular dystrophy (DMD), with an X-linked recessive genetic mode, is among the most prevalent fatal muscular dystrophies, influencing approximately 15.9–19.5 individuals per 100000 male births [1,2]. DMD is caused by dystrophin gene mutations resulting in deficient dystrophin, a cytoskeletal protein that supports muscle cell membrane integrity. This deficiency leads to progressive necrosis, excessive inflammation, fibrosis and impaired muscle regeneration. To date, there is no cure for DMD, and except for multidisciplinary management, glucocorticoids are the only therapeutics that have been proven to delay DMD progression, manifested as improved muscle strength and respiratory function as well as increased ambulation time [3–5]. The effect of glucocorticoids on differentiated skeletal muscle has been clearly elaborated. However, whether glucocorticoids can promote myogenic differentiation in addition to stabilizing membranes, decreasing muscle necrosis and fibrosis, modulating inflammation, and improving regeneration is still controversial. Several studies have revealed that the effect of glucocorticoids on myogenic differentiation is dose dependent, as low-dose glucocorticoids can enhance myogenic differentiation, while high-dose glucocorticoids restrict differentiation [6–9]. Given that younger children benefit from low-dose glucocorticoid treatment more than adults, we hypothesized that low-dose glucocorticoids may enhance myogenic differentiation in the myoblast stage due to the presence of sufficient satellite cells.