Skeletal Muscle Cells

Skeletal Muscle Structure.The cells of skeletal muscles are long fiber-like structures. They contain many nuclei and are subdivided into smaller structures called myofibrils. Myofibrils are composed of 2 kinds of myofilaments. The thin filaments are made of 2 strands of the protein actin and one strand of a regulatory protein coiled together. The thick filaments are staggered arrays of myosin molecules.

What are the different levels of organization of a muscle down to myofilaments? What is a “sarcomere” and how are its proteins organized?

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Serves as the cell 's skeleton. It is an interior protein system that gives the cytoplasm quality and adaptability. The cytoskeleton of all cells is made of microfilaments, halfway fibers, and microtubules. Muscle cells contain these cytoskeletal parts in addition to thick fibers. The fibers and microtubules of the cytoskeleton frame a dynamic system whose ceaseless rearrangement influences cell shape and capacity.

Muscle fibres, as shown in Diagram 1, consist of myofibrils, which contain the proteins, actin and myosin, in specific arrangements . The diagram illustrates how a muscle is made up of many fascicles, which in turn are made up of many endomysiums, and within them, many muscle fibres. Each muscle fibre is made up of many myofibrils that consist of sarcomeres bound end on end . Actin is a thin filament, about 7nm in diameter, and myosin is a thick filament, about 15nm in diameter , both of which reside in the sarcomere. They are held together by transverse bands known as Z lines . Diagram 2 shows actin and myosin filaments within a sarcomere, and the Z lines that connect them.

Myofibrils are made up of long proteins that include myosin, titin, and actin while other proteins bind them together. These proteins are arranged into thin and thick filaments that are repetitive along the myofibril in sectors known as sarcomeres. The sliding of actin and myosin filaments along each other is when the muscle is contracting. Dark A-bands and light I-bands reappear along myofibrils. The alignment of myofibrils causes an appearance of the cell to look banded or striated. A myofibril is made up of lots of sarcomeres. As the sarcomeres contract individually the muscle cells and myofibrils shorten in length. The longitudinal section of skeletal muscle exhibits a unique pattern of alternating light and dark bands. The dark staining, A-bands possess a pale region in the middle called the H-zone. In the middle of the H-zone the M-line is found, that displays filamentous structures that can join the thick filaments. The light-staining bands also known as I-bands are divided by thin Z-line. These striated patterns appear because of the presence of myofibrils in the sarcoplasm (IUPUI, 2016).

The nervous system is made up of three vital parts; the brain, spinal cord and nerves. This system controls everything we do from breathing, to running to making our heartbeat fast or slow. The nervous system is very complicated although it can be broken down into smaller components.

Different types of muscles. Smooth muscle cells are shaped in spindles with single nucleus, have involuntary movement through the body and do not have any striation. Smooth muscle can be found in digestive system, urinary tract. Muscular cells are found as bundles, with striation and are multiple nucleus found along the membrane surface. Cardiac muscle cells are only found in the heart, the cells short, branched with a centrally located, single nucleus and are striated with intercalated disc found between to speed up the electrical conduct of the heart rhythm without external stimulus.

1.a) Contractile protein molecules that are seen in skeletal muscle fibres are actin (thin filaments) and myosin (thick filaments). Together, they produce the force of muscle contractions by forming cross bridges, and moving via a power stroke. The regulatory proteins that are seen within a skeletal muscle are troponin and tropomyosin. These proteins play a role in starting or stopping muscle contractions. When a muscle fibre is relaxed, there are no contractions because actin is unable to bind with the cross bridge. This is because tropomyosin covers the myosin binding sites on the actin proteins. In addition, troponin is not bound to calcium when a muscle fibre is relaxed, thus keeping the tropomyosin in its blocking position. When calcium enters the muscle fibres, it binds with troponin. This binding causes the tropomyosin to move away

The skeletal muscles are one of three major muscles types. As the name implies, these muscles are attached to bones by bundles o collagen fibers that are known as tendons. Skeletal muscles are made up of individual components that are known as muscle cells. These muscles have the appearance of long cylinders. The basic function is responsible for skeletal muscles to

The contractile unit of a muscle cell is the sarcomere. Sarcomeres are mostly comprised of actin and myosin which pull and slide upon each other. These contractile units are linked end to end, like a chain, throughout the length of any given muscle. Certain proteins link the ends of these chains to the cell membrane. When a normally healthy individual exercises, some of these fibers, both in the sarcomere and at the connections to the cell wall, will be broken down due to damage (Leyva, 2013). Associated with this process includes the rebuilding of these fibers, in which the body builds back what was damaged stronger than before the damage occurred (Leyva, 2013). One of these end proteins is dystrophin. The purpose of this paper is to explore the implications of insufficient production of dystrophin, as in DMD.

They include muscle proteins, which are found in other cells and tissues. These proteins are involved in contractile events in the cytoplasm, abling the muscles to move and fix the cells together. Actin is a thin filament and myosin is a thick filament. These are protein filaments that cause contraction of muscles when the filaments slide over each other in a series of repetitive events. This is called the sarcomere. Sarcomere shortens when a myosin heads and a thick myofilaments form cross bridges with actin molecules. A bond with calcium causes troponin to change shape and tropomyosin moves away from the myosin binding site on actin allowing the myosin head to bind actin. This is continuous causing muscle

Skeletal muscle plays a pivotal role in regulating systemic glucose homeostasis in part through the conserved cellular energy sensor AMP-activated protein kinase (AMPK). AMPK activation increases glucose uptake, lipid oxidation and mitochondrial biogenesis, thereby enhancing muscle insulin sensitivity and whole-body energy metabolism. Here we show that the H19 long noncoding RNA (lncRNA) post-transcriptionally increases expression of the atypical dual-specificity phosphatase 27 (DUSP27) which forms complexes with and activates AMPK in muscle. Consistent with decreased H19 expression in muscle of insulin resistant human subjects and rodents, mice with genetic H19 ablation exhibit musclesystemic insulin resistance and altered whole-body

Skeletal muscles are highly complex and heterogeneous tissues, serving a multitude of functions in different organisms. The process of generating muscle myogenesis can be divided into several distinct phases [40]. Ubiquitin-mediated protein degradation is one of the main mechanisms for controlling proteolysis, which is crucial for muscle development and maintenance. Recently notch signaling has appeared as a key player in skeletal muscle development and regeneration. Simply stated, Notch signaling inhibits differentiation. Accordingly, fine-tuning the pathway is essential for proper muscle homeostasis.Less is known regarding the functions of ASB proteins in muscle development, although various ASB proteins are found to be expressed in the skeletal

Other types of leukocytes, such as lymphocytes and mast cells, also accumulate in the subendothelial space.10 The cross-talk between monocytes, macrophages, foam cells, and T-cells results in cellular and humoral immune responses, and ultimately in a chronic inflammatory state with the production of several proinflammatory molecules.11,12 This process continues with the migration of smooth muscle cells from the medial layer of the artery into the intima, resulting in the transition from a fatty streak to a more complex lesion.5 Once smooth muscle cells are in the intima media, they produce extracellular matrix molecules, creating a fibrous cap that covers the original fatty streak. Foam cells inside the fibrous cap die and release lipids that