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Cell Adhesion in Animal Cell Culture: Physiological and Fluid-Mechanical Implications
Published in Martin A. Hjortso, Joseph W. Roos, Cell Adhesion, 2018
Manfred R. Koller, Eleftherios T. Papoutsakis
Close contacts are characterized by a 30–50-nm spacing between the cell surface and the substratum and are broad areas that are often found surrounding sites of focal adhesion. A meshwork of actin microfilaments that stains positively for α-actinin is often seen subtending the membrane at these sites. All close-contact sites stain moderately for fibronectin, but are negative for vinculin, suggesting that they are similar to the more predominant type of ECM contact discussed above. In early culture, close contacts were numerous in forming 50% of the cell-substratum contacts, but this number declined sharply to 10% in late culture. Close contacts were found to comprise 40% of the cell-cell contacts in late culture, making close contacts the most abundant type of cell-cell contact between fibroblasts.
Genetic polymorphisms related to muscular strength and flexibility are associated with artistic gymnastic performance in the Japanese population
Published in European Journal of Sport Science, 2023
Hiroshi Kumagai, Tomoko Kaneko, Yuko Shintake, Eri Miyamoto-Mikami, Hiroyuki Tomita, Makoto Fukuo, Wataru Kawai, Mutsumi Harada, Naoki Kikuchi, Nobuhiro Kamiya, Kosuke Hirata, Hirofumi Zempo, Seiji Maeda, Naokazu Miyamoto, Noriyuki Fuku
Higher physical fitness, including muscular strength, cardiorespiratory fitness, and flexibility, is associated with better competition levels in athletes as well as the prevention of chronic diseases in the general population (Blair et al., 1989; Komatsu et al., 2017; Leong et al., 2015; Yamamoto et al., 2009). The R577X polymorphism in the α-actinin-3 gene (ACTN3) and I/D polymorphism in the angiotensin-converting enzyme (ACE) are the most studied physical fitness-related genetic polymorphisms (Montgomery et al., 1998; Yang et al., 2003). The α-actinin-3 protein is a major component of the Z-line in muscles and is only expressed in fast-twitch fibers. The ACTN3 R577X polymorphism, a common nonsense mutation in ACTN3, causes α-actinin-3 deficiency (North et al., 1999), and X allele carriers show reduced muscle strength by regulating skeletal muscle fiber composition (Kumagai et al., 2018; Vincent et al., 2007). Although the detailed mechanisms have not been elucidated, it has been suggested that the D and I alleles of the ACE I/D polymorphism contribute to muscular strength-and endurance-related performances, respectively (Montgomery et al., 1998; Nazarov et al., 2001). The associations between these genetic polymorphisms and physical performances have been validated by a meta-analysis (Ma et al., 2013). However, although the heritability estimates of flexibility are 50% (Schutte, Nederend, Hudziak, de Geus, & Bartels, 2016), flexibility-related genetic polymorphisms are poorly understood.
The stiffness response of type IIa fibres after eccentric exercise-induced muscle damage is dependent on ACTN3 r577X polymorphism
Published in European Journal of Sport Science, 2019
Siacia Broos, Laurent Malisoux, Daniel Theisen, Ruud Van Thienen, Marc Francaux, Martine A. Thomis, Louise Deldicque
In addition, α-actinin-3 deficiency may influence susceptibility to exercise-induced muscle damage. The α-actinin proteins are the main building blocks of the Z-disc, which is the most vulnerable structure of the sarcomere for exercise-induced muscle damage (Cheung, Hume, & Maxwell, 2003). Normally, α-actinin-3 is expressed in fast twitch fibres, while α-actinin-2 is present in all fibre types (North & Beggs, 1996). As XX genotypes do not express α-actinin-3 in their muscles, the Z-discs of their fast muscle fibres are composed only of α-actinin-2. The different build-up of fast fibre Z-discs between RR and XX genotypes could influence the susceptibility for exercise-induced muscle damage.