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Plaques, Tangles and Amyloid:
Published in Robert E. Becker, Ezio Giacobini, Alzheimer Disease, 2020
Robert G. Struble, H. Brent Clark
The above observations strongly suggest a non-specific origin of neurites in SP and support the suggestions that some of the classical neuritic changes in AD may represent reactive sprouting (Geddes et al, 1985; Hyman et al, 1987; Struble et al, 1987). Early studies (Ramon y Cajal, 1923) described sprouting in experimentally transected axons which resulted in filopodia that resemble SP neurites. In silver stains of tissue from a case of AD, one of us (RGS) identified an axon displaying filopodia along its length, and was able to trace the axon to a SP. The concept of reactive sprouting should raise questions about possible therapies that would induce or support sprouting because over-stimulation of sprouting could paradoxically increase the progression of one of the classic manifestations of the disease.
Wound healing angiogenesis: An overview on mathematical models
Published in J. Belinha, R.M. Natal Jorge, J.C. Reis Campos, Mário A.P. Vaz, João Manuel, R.S. Tavares, Biodental Engineering V, 2019
A.C. Guerra, J. Belinha, R.M. Natal Jorge
In healthy tissues, mature vessels are in a quiescent state. These blood vessels are composed by a monolayer of endothelial cells surrounded by a basement membrane and coated with smooth muscle cells and pericytes, promoting endothelial cell survival and allowing vessel stability (Carmeliet 2003). However, during wound healing, quiescent vessels are exposed to proangiogenic factors and the angiogenic process is initiated. Therefore, in the region where the new blood vessel will be formed, a previously quiescent endothelial cell is converted into a tip cell. This tip cell forms filopodia, cytoplasmic elongations sensible to the growth factors gradients in the environment, which allows cell migration. The adjacent endothelial cells become stalk cells that start to proliferate and to migrate in the direction of the tip cell, resulting in vessel’s sprouting elongation. Afterwards, blood vessel density increases and the vascular sprout will fuse with another neighbouring vessel. This process is called anastomosis and allows the blood flow’s reestablishment. The unperfused vessels regress by apoptotic processes. Finally, the vasculature returns to a quiescent state, the basement membrane is restored and the new blood vessel is coated by smooth muscle cells and pericytes that stabilize it (Carmeliet, & Jain 2011). If the tissue wound healing was correctly performed, the number of vessels normalizes and returns to a level close to the one observed in uninjured tissue (Yamashita et al. 2014).
Nerve
Published in Manoj Ramachandran, Tom Nunn, Basic Orthopaedic Sciences, 2018
Mike Fox, Caroline Hing, Sam Heaton, Rolfe Birch
The axon proximal to the site of injury forms multiple axon sprouts with a growth cone situated at the tip of each sprout. Filopodia in the growth cone use contact guidance for fibronectin and laminin in the Schwann cell basement lamina to facilitate regeneration. Regeneration of axons can be followed by the presence of an advancing Tinel sign.
Marginal band microtubules are acetylated by αTAT1
Published in Platelets, 2021
Anne-Sophie Ribba, Morgane Batzenschlager, Clotilde Rabat, Thierry Buchou, Sylvie Moog, Saadi Khochbin, Ekaterina Bourova-Flin, Laurence Lafanechère, François Lanza, Karin Sadoul
The functional characterization of αTAT1 deficient platelets revealed only minor consequences of deficient microtubule acetylation. The fact that no significant difference in the spreading capacity was detected between platelets from WT and αTAT1KO mice but a delay in clot retraction may suggest that the absence of tubulin acetylation is less important for early activation events than for subsequent clot retraction. Several publications have shown a role of microtubules in clot retraction [15–17]. Microtubules could be important for the repeated, successive extensions and retractions of filopodia, which bind to fibrin strands to pull them together, thereby retracting the clot [18]. Extension of filopodia might depend on motor driven sliding of microtubules, as it is the case for the extension of proplatelets by megakaryocytes [19]. This, in turn, may be less efficient in αTAT1KO platelets, since microtubule motor actions are less productive on non-acetylated microtubules [3,4]. Alternatively, the effect may be due to deficient acetylation of an additional substrate of αTAT1, such as cortactin [20]. An altered inside-out or outside-in signaling can also not be ruled out.
The molecular basis of platelet biogenesis, activation, aggregation and implications in neurological disorders
Published in International Journal of Neuroscience, 2020
Abhilash Ludhiadch, Abhishek Muralidharan, Renuka Balyan, Anjana Munshi
These interactions of receptor and ligands on platelet surface recruit a signaling cascade that leads to the activation of platelets. For the sake of recognition of receptors by their ligands, change of shape occurs from usual discoidal to spike like filopodia along with the change from non-adhesive to sticky form. Resting platelets have inactive and bent 2+ and a signal which promotes binding of talin to 38]. In resting platelet the microtubules are aligned to the peripheral area (responsible for the discoidal shape) whereas upon activation the microtubules are constricted and changes to a coiled form, giving it a saddle like structure [39]. The actin polymerization leads to the formation of filopodia [38]. Platelet activation affects cytoskeleton system, which adds on to the changed shape. The increased calcium content on activation changes the dynein and kinesin which leads to the sliding of microtubules from marginal area thus aiding the shape change. In contrast to nonactivated platelets, activated platelets changes thier shape in a sequential order upon activation. The cellular shape and filopodia of platelets change in the following order; first filopodia extrusion, blebbing, second filopodia extrusion, shrinkage of cell and detachment [40].
Doxorubicin hydrochloride loaded nanotextured films as a novel drug delivery platform for ovarian cancer treatment
Published in Pharmaceutical Development and Technology, 2020
Gökçen Yaşayan, Pınar Mega Tiber, Oya Orun, Emine Alarçin
Cell adhesion and viability results showed that nanotextured surfaces promote adhesion and viability better in comparison to non-textured 0 nm surfaces, and amongst nanotextured surfaces, these properties were slightly higher for 99 nm films. This difference could be attributed to the better support of focal adhesion formation in 99 nm surfaces compared to other nanotexture diameters due to having lower feature heights. It is well known that extracellular guidance could influence cell behaviour (Berzat and Hall 2010). Cells could sense the environment they are in by lamellipodia and filopodia formation, and response to extracellular environment by activation of intracellular pathways (Lim et al. 2005). Studies in the area often report an increase of cell adhesion and viability in smaller topographical features, and this interaction trigger cellular response in various ways including increases in cellular attachment and viability (Dalby, Gadegaard, et al. 2004; Dalby, Giannaras, et al. 2004; Dalby, Riehle, et al. 2004; Lim et al. 2005; Biggs et al. 2010; Koegler et al. 2012; Skoog et al. 2018). This could be the reason of 99 nm surfaces to be better in increasing cellular adhesion and viability compared to other nanotexture diameters.