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- 중간섬유는 10나노미터 직경이고, 미세섬유보다 강하게 결합되어 좀더 안정됨.
- 미세섬유처럼, 그들의 기능은 장력에 저항하여 세포 형태의 유지기능.
Microtubules are hollow cylinders about 23 nm in diameter (lumen = approximately 15 nm in diameter), most commonly comprising 13 protofilaments that, in turn, are polymers of alpha and beta tubulin. They have a very dynamic behavior, binding GTP for polymerization. They are commonly organized by the centrosome.
In nine triplet sets (star-shaped), they form the centrioles, and in nine doublets oriented about two additional microtubules (wheel-shaped), they form cilia and flagella. The latter formation is commonly referred to as a "9+2" arrangement, wherein each doublet is connected to another by the protein dynein. As both flagella and cilia are structural components of the cell, and are maintained by microtubules, they can be considered part of the cytoskeleton.
They play key roles in:
세가지 중요한 구조물
- microfilament(actin filaments), intermediate filament, microtubule
They are composed of tension-resistant structures that pull inward and compressive structures that tend to push outward. These are intermediate filaments and cytoskeletal microfilaments that produce tensional force and are balanced by the extracellular matrix (ECM), adhesions, and internal microtubule struts ( Figure 3-1 B). This balancing of forces stabilizes the overaII structure.
- 그것은 장력저항성 구조로 만들어져 안으로 당김 그리고 밖으로 밀어내는 경향을 가진 압박힘으로 이루어짐.
- 중간 필라멘트와 세포골격 미세필라멘트가 있어 장력적 힘을 만들어 내고, 세포외기질, 부착, 미세튜불 연결에 의해서 균형이 만들어짐.
Cells are built, based on a tensegrity model, so as to resist or accommodate for the various external and internal forces acting upon them. So before discussing fascia, this section first takes a few steps back and looks at tensegrity at a molecular level.
- 인체의 세포들은 외부와 내부의 다양한 힘에 축적이나 저항을 위해 장력완전성 모델에 기초하여 만들어짐.
Tensegrity at the Cellular Level
Chapter I revealed microscopic components of fascia and how these components are interconnected to form an uninterrupted system of connections from the inner parts of the cell to the outer ECM and ground substance.
- 이 챕터에서는 기질과 세포외 기질 세포의 내부로부터 단절없이 연결된 형태가 어떻게 연결되었는가와 섬유막의 미세구조를 설명함.
The connections are continuous enough that some studies have shown that applying mechanical stress to integrins (adhesion receptors located on the cell surface that link the ECM on the outside of a cell to the cytoskeleton on the inside of the cell) can affect cellular function, stimulate signal transduction, and affect gene expression (Ingber, 2003).
- 이러한 연결성은 많은 연구에서 보여주는데, 인테그린에 주어진 기계적 힘은 세포기능에 영향을 줄 수 있고, 세포내 전달을 자극하고 유전자 표현에 영향을 줌.
- 인테그린은 세포표면에 존재하는 부착 수용기로서 세포외기질과 연결하는 역할을 함.
참고) 인테그린
Integrins are transmembrane receptors that are the bridges for cell-cell and cell-extracellular matrix (ECM) interactions. When triggered, integrins in turn trigger chemical pathways to the interior (signal transduction), such as the chemical composition and mechanical status of the ECM, which results in a response (activation of transcription) such as regulation of the cell cycle, cell shape, and/or motility; or new receptors being added to the cell membrane. This allows rapid and flexible responses to events at the cell surface, for example to signal platelets to initiate an interaction with coagulation factors.
There are several types of integrins, and a cell may have several types on its surface. Integrins have been found in all animals investigated, from sponges to mammals[citation needed]. Integrins work alongside other receptors such as cadherins, the immunoglobulin superfamily cell adhesion molecules, selectins and syndecans to mediate cell–cell and cell–matrix interaction. Ligands for integrins include fibronectin, vitronectin, collagen, and laminin.
참고) ligand
착물(錯物) 속에서 중심원자에 결합되어 있는 이온 또는 분자의 총칭
Integrins have two main functions:
However, they are also involved in a wide range of other biological activities, including immune patrolling, cell migration, and binding to cells by certain viruses, such as adenovirus, echovirus, hantavirus, and foot and mouth disease viruses.
A prominent function of the integrins is seen in the molecule GPIIbIIIa, an integrin on the surface of blood platelets (thrombocytes) responsible for attachment to fibrin within a developing blood clot. This molecule dramatically increases its binding affinity for fibrin/fibrinogen through association of platelets with exposed collagens in the wound site. Upon association of platelets with collagen, GPIIbIIIa changes shape, allowing it to bind to fibrin and other blood components to form the clot matrix and stop blood loss.
Integrins couple the ECM outside a cell to the cytoskeleton (in particular, the microfilaments) inside the cell. Which ligand in the ECM the integrin can bind to is defined by which α and β subunits the integrin is made of. Among the ligands of integrins are fibronectin, vitronectin, collagen, and laminin. The connection between the cell and the ECM may help the cell to endure pulling forces without being ripped out of the ECM. The ability of a cell to create this kind of bond is also of vital importance in ontogeny.
Cell attachment to the ECM is a basic requirement to build a multicellular organism. Integrins are not simply hooks, but give the cell critical signals about the nature of its surroundings. Together with signals arising from receptors for soluble growth factors like VEGF, EGF, and many others, they enforce a cellular decision on what biological action to take, be it attachment, movement, death, or differentiation. Thus integrins lie at the heart of many cellular biological processes. The attachment of the cell takes place through formation of cell adhesion complexes, which consist of integrins and many cytoplasmic proteins, such as talin, vinculin, paxillin, and alpha-actinin. These act by regulating kinases such as FAK (focal adhesion kinase) and Src kinase family members to phosphorylate substrates such as p130CAS thereby recruiting signaling adaptors such asCRK. These adhesion complexes attach to the actin cytoskeleton. The integrins thus serve to link two networks across the plasma membrane: the extracellular ECM and the intracellular actin filamentous system. Integrin alpha6beta4 is an exception: it links to the keratin intermediate filament system in epithelial cells.
Focal adhesions are large molecular complexes, which are generated following interaction of integrins with ECM, then their clustering. The clusters likely provide sufficient intracellular binding sites to permit the formation of stable signaling complexes on the cytoplasmic side of the cell membrane. So the focal adhesions contain integrin ligand, integrin molecule, and associate plaque proteins. Binding is propelled by changes in free energy.[13] As previously stated, these complexes connect the extracellular matrix to actin bundles. Cryo-electron tomography reveals that the adhesion contains particles on the cell membrane with diameter of 25 +/- 5 nm and spaced at approximately 45 nm.[14] Treatment with Rho-kinase inhibitor Y-27632 reduces the size of the particle, and it is extremely mechanosensitive.[15]
One important function of integrins on cells in tissue culture is their role in cell migration. Cells adhere to a substrate through their integrins. During movement, the cell makes new attachments to the substrate at its front and concurrently releases those at its rear. When released from the substrate, integrin molecules are taken back into the cell by endocytosis; they are transported through the cell to its front by the endocytic cycle, where they are added back to the surface. In this way they are cycled for reuse, enabling the cell to make fresh attachments at its leading front. It is not yet clear whether cell migration in tissue culture is an artefact of integrin processing, or whether such integrin-dependent cell migration also occurs in living organisms.
Integrins play an important role in cell signaling by modulating the cell signaling pathways of transmembrane protein kinases such as receptor tyrosine kinases (RTK). While the interaction between integrin and receptor tyrosine kinases originally was thought of as uni-directional and supportive, recent studies Indicate that integrins have additional, multi-faceted roles in cell signaling. Integrins can regulate the receptor tyrosine kinase signaling by recruiting specific adaptors to the plasma membrane. For example, β1c integrin recruits Gab1/Shp2 and presents Shp2 to IGF1R, resulting in dephosphorylation of the receptor.[16] In a reverse direction, when a receptor tyrosine kinase is activated, integrins co-localise at focal adhesion with the receptor tyrosine kinases and their associated signaling molecules.
The repertoire of integrins expressed on a particular cell can specify the signaling pathway due to the differential binding affinity of ECM ligands for the integrins. The tissue stiffness and matrix composition can initiate specific signaling pathways regulating cell behavior. Clustering and activation of the integrins/actin complexes strengthen the focal adhesion interaction and initiate the framework for cell signaling through assembly of adhesomes.[17]
Depending on the integrin's regulatory impact on specific receptor tyrosine kinases, the cell can experience:
Knowledge of the relationship between integrins and receptor tyrosine kinase has laid a foundation for new approaches to cancer therapy. Specifically, targeting integrins associated with RTKs is an emerging approach for inhibiting angiogenesis.[18]
As mentioned earlier, tensegrity structures are not dependent on gravity. Applying this knowledge at a microscopic level, it is safe to say that cells do not have a gravity-dependent ultrastructure. At a cellular level, gravity is almost nonexistent when compared to local force interactions (Ingber, 1993). The cellular cytoskeleton responds to stresses placed upon it by rearranging itself in a way that does not disrupt the internal cellular structures. Zaner and Val berg's ( 1989) study showed that laboratory constructed, noncontinuous actin filaments that were not prestressed (i.e., not tensegrity based) did not exhibit a stiffening response to applied force (Zaner Et Valberg, 1989).
- 장력완전성 구조는 중력에 의존하지 않음. 미세현미경 레벨에서 이러한 지식을 적용하면 세포는 중력의존성 초미세구조를 가지지 않음. 세포레벨에서 중력은 국소적 힘의 작용과 비교할때 거의 존재하지 않음.
- 세포골격계 구조는 주어진 힘에 반응하여 세포내구조와 단절없는 방식으로 재배열함.
- 자너와 발버그의 연구를 보면 "실험적 구조, 비연속적 액틴 필라멘트는 사전응력을 갖지 않아 적용되는 힘에 반응하여 강화되는 현상을 보이지 않음.
On the other hand, in living cells, the cytoskeletal and nucleus shapes change in an integrated manner (Emerman Et Pitelka,1977). Cellular components such as intermediate filaments are able to couple between integrins and the nucleus.
- 반면에 살아있는 세포에서, 세포골격계와 핵의 형태는 통합된 방식으로 변화함.
- 중간 필라멘트와 같은 세포내 구조는 핵과 인테그린 사이에 짝을 이룰 수 있음.
In addition, they stabilize the microtubules and microfilament networks and thus prevent tearing of the cytoplasm. Local and distant changes occur when mechanical stress is placed on integrin cell receptors. These changes of cytoplasmic realignment and molecular repositioning were observed experimentally (Figure 3-2).
- 게다가, 살아있는 세포는 미세튜블과 미세필라멘트 네트워크를 안정화시켜 세포질의 손상을 막아줌.
- 국소적 distant 변화는 인테그린 세포 수용기에 주어진 기계적 힘이 주어질때 일어남.
- 이러한 세포질 재배열과 분자구조 재위치는 많은 실험에서 보여짐.
Such studies further support the hypothesis that the cellular cytoskeleton is built on the idea of tensegrity, and they give evidence of the importance of molecular components of the framework interconnecting the cell surface and cytoplasm.
- 많은 연구는 세포 골격은 장력완전성에 기초하여 만들어짐을 밝혀냄.
The three components of the cell cytoskeleton include microfilaments, microtubules, and intermediate filaments, as briefly mentioned earlier. What is known is that contractile microfilaments produce forces that create and propagate tension through the cytoskeleton of a cell. On the other hand, microtubules are more representative of the compression resistant struts that oppose tension as already discussed (Lamoureux et aI., 1990).
-세포골격을 위한 세가지 구조물 "미세필라멘트, 미소관, 중간섬유"
- 수축할 수 있는 미세필라멘트는 힘을 만들어 세포의 골격구조를 통해 장력을 전달하고 생성함.
- 반면에 미소관은 압박의 저항에 적합한 구조임.
Intermediate filaments are usually described as the "mechanical integrators" since they are positioned between microfilaments and microtubules. In cells found in the epidermis, intermediate filaments have been known to resist mechanical stress; but in any other cell, these filaments are not associated with cell shape control.
- 중간섬유는 대개 기계적 통합자로 묘사되는데, 중간섬유가 미세필라멘트와 미소관사이에 위치하기 때문임.
- 진피층에서 중간섬유는 기계적 힘에 저항하는 역할을 수행하지만 나머지 세포에서는 그렇지 않음.
Looking more closely at the components of the cytoskeleton under microscopy, microtubules appear curved in nature, particularly near the distal ends(Figure 3-3A).
This provides some evidence that these are indeed more compression-resistant structures. Microfilaments are straight and appear to intersect at 90' and 120' angles, which are the same angles that are seen in tensegrity-based models (Figure 3-38). On the other hand, intermediate filaments resemble a network radiating from the cell nucleus (Figure 3-3C).
- 미세필라멘트는 직선이고 90-120도 각을 이루어 교차하함. 이는 장력안정성에 기초한 모델에서 흔히 보임.
- 반면에 중간섬유는 세포핵으로부터 방사된 네트워크와 비슷함.
There have been numerous theories explaining how exactly cells spread and move under stressful conditions (Ingber, 1993). Using experimental data obtained from studies, along with examination of some of these cell motility theories, certain similarities are revealed.
- 세포가 어떻게 정확히 압박조건하에서 이동하는지를 설명하는 많은 이론이 있음.
- 실험적 데이터를 이용하여 세포이동 이론을 검증함.
First, a cell attaches to the ECM through transmembrane linker glycoproteins, known as integrins. These connections form what are known as focal adhesion complexes (FACs). Interestingly, FACs formed between fibroblasts and the ECM are the most studied. In these studies, fibroblasts appear to be positioned a certain distance from the substratum; but at certain points, this distance is reduced by approximately one-fifth. At these points, the integrin molecule is attached to the ECM components on one side and to actin filaments on the cytoplasmic side of the cell. Thus, FACs act as a bridge connecting the outer ECM environment to the inner cytoskeletal fibers of the cell (Figure 3-4).
- 첫째, 세포는 세포외기질과 연결되어 있는데, 인테그린으로 알려진 세포막 연결고리인 당단백질을 통하여 연결됨. 이러한 연결은 focal adhesion complex(FACs)로알려진 것으로 연결함. FACs는 섬유아세포와 세포외기질을 연결하는데, 많은 연구가 진행됨.
- 섬유아세포는 기층( substratum)으로부터 일정거리 떨어져 위치함. 하지만 어떤 지점에서 이 거리는 1/5로 줄어듬.
- 이러한 지점에서 인테그린 분자는 세포외기질 물질 한쪽면과 부착하고, 세포의 세포질부분에서 액틴 필라멘트와 부착함. 그래서 FAC는 세포의 내측 세포골격부터 세포외기질 외측 환경을 연결하는 역할.
-
However, FACs are not only structural connections. They also act as an information highway, relaying messages from the ECM into the cytoplasm. Phosphorylation of various molecules by kinase proteins, found at the FAC sites, are to some degree controlled by the type of substratum the cell is attached to.
- 하지만 FAC는 단순히 구조적 연결물은 아님. FAC는 정보전달의 고속도로로 작용하고, 세포질에서 세포외기질로 정보를 중계하는 역할을 함.
In fact, cell spreading is controlled by the type of substratum it is attached to. If attached to a flat/planar surface, a cell tends to spread; however, if a cell is not attached or is attached to a malleable substratum, then it becomes spherical in shape (Volokh, 2003; Volokh, Vilnay, Et Belsky,2000).
- 사실상, 세포확산은 기층의 형태가 부착된 것에 의해서 조절됨.
- 만약 편평한 면에 부착되면 세포는 펴지는 경향이지만 세포가 부착되지 않거나 펼수 있는 기층에 부착되면, 형태가 둥근모양이 됨.
참고) cell spreading(세포확산)
동물세포가 기질에 접착한 후, 세포질을 기질면에 얇게 펴서 넓히는 과정. 세포가 기질에의 세포부착을 완료한 상태라고도 할 수 있다. 많은 정상세포는 기질에 접착하여 신전하지 않으면 증식할 수 없다. 이를 기반의존성이라고 한다. 암세포, 혈액세포, 부유세포는 여기에 속하지 않는다. 세포확산은 세포표면 상의 세포부착수용체인 인테그린이 기질 상의 세포부착성 단백질 등을 인식하여 접착함으로써 일어난다. 그 접착 정보가 세포 내에 전해져 그 결과로서 세포골격이 배향하여 세포질이 기질면에 얇게 넓혀진다고 생각된다. 세포확산은 충분하게 일어나 다검체측정을 할 수있기 때문에 이 계는 세포부착성 단백질이나 인테그린의 세포확산 활성의 측정에 자주 사용된다. 생체 내에서의 역할은 세포와 기질간의 접착 그 자체이고, 세포의 식작용이나 세포이동에도 관계한다. 보통은 세포의 접착 후 계속 신전되기 때문에 세포부착이라는 용어에 세포확산의 개념을 포함해서 쓰는 경우가 많다. 조건에 따라 세포부착만 일어나고, 세포확산이 일어나지 않을 때도 있어 정확하게 구별하여 사용해야 된다.
This latter phenomenon occurs because tensegrity models (such as fibroblasts) always try to be in a structure of minimal stress. Phosphorylation reactions are important in cell growth, movement, and differentiation. Therefore, the ECM environment of a cell is important in regulating cell activity.
- 후자의 현상은 장력완전성 모델은 항상 작은 자극의 구조에서 시도됨.
- 인산화 반응은 세포성장, 움직임, 분화에 중요함. 그래서 세포외기질 환경은 세포 활동성을 조절하는데 중요한 역할.
Consequently, any abnormalities in ECM composition can affect fibroblast activity and, in the end, can alter connective tissue and fascia properties and function.
- 세포외기질 조성에서 어떤 비정상은 섬유아세포 활성화에 영항을 미치고, 결국에는 결합조직과 섬유막조성과 기능을 변화시킴.
Once the FAC is attached to the ECM, Lotz, Burdsal, Erikson, and McClay ( 1989) discovered that tension is exerted by the cells onto the FACs within 20 minutes of FAC creation. If tension is continuous (the basis of tensegrity models), microfilaments restructure themselves into linear bundles, better known as "stress fibers," and the cells flatten out (Kreis Et Birchmeiser, 1980). Stress fibers are prominent components of the cytoskeleton of fibroblasts and are an example of a temporary contractile bundle of actin filaments and myosin II type fibers.
- 일단 FAC가 세포외기질에 부착하면, 로츠 등은 장력이 FAC 생성의 20분이내에 FAC로 세포에 의해 exerted됨.
- 만약 장력이 연속되면 미세필라멘트는 stress fiber로 알려진 직선 다발을 재구성하고 세포는 flatten out됨.
- stress fiber는 섬유아세포의 세포골격의 우세한 구성물임. 그리고 액틴과 미오신의 일시적 수축다발의 사례가 됨.
At one end they insert onto the FAC; at the other, they are either attached to another FAC or to intermediate filaments that surround the nucleus. Stress fibers are created as a result of tensional forces and are dissolved if this tension is eliminated (this occurs either when the cell detaches from the substratum or by breaking the connection of the stress fiber with the FAC).
- stress fiber는 장력힘의 결과로 만들어지고, 만약 장력이 제거되면 사라짐.
This situation is true for micro filaments directly attached to the FAC. Microfilaments within the same cell that are far removed from the FAC also undergo structural modifications. These filaments instead form triangular structures referred to as "actin geodomes" (Heuser Et Kirschner, 1980).
- 이런 상황은 FAC에 부착하는 미세필라멘트를 위한 것으로 볼때 맞는 현상임.
- 같은 세포내에서 미세필라멘트는 FAC로부터 떨어지고.. 이러한 필라멘트는 액틴 geodomes로 언급되는 삼각형구조를 만듬.
Actin geodomes appear to be important to cellular motility. Obviously, cellular motility and cellular spreading are not the same thing. The vertices of these actin geodomes function as sites of actin polymerization during lamellipodia organization. What are lamellipodia? Let us look at cell motility much more closely.
- 액틴 geodomes는 세포 움직임에 중요함. 분명하게 세포 움직임과 세포확산은 같은 현상이 아님.
- 액틴 geodomes기능의 정점은 ....
The Actin Filament and Cell Motility
As mentioned earlier in this chapter, actin filaments are the tension-resistant structures of the cell. It is these molecules that give cells their tensegrity properties, so that they can change their shape in response to stress or movement.
- 액틴 필라멘트는 세포에서 장력저항구조임.
- 액틴필라멘트분자가 세포에게 장력적 특성을 제공하여, 힘 또는 움직임에 반응하여 그들의 형태를 변형시킬 수 있음.
In a fibroblast, half the actin molecules are arranged in filaments; the other half exist as monomers. Several proteins associated with the plasma membrane are bound to monomer actin molecules, thus preventing them from binding to actin filaments.
- 섬유아세포에서 액틴 분자의 절반은 필라멘트로 배열됨. 나머지 절반은 mononer로 존재함.
- 세포벽과 관련있는 몇가지 단백질은 단위체(monomer) 액틴 분자에 부착하여, 액틴필라멘트에 부착하는 것을 억제함.
One such monomer-binding protein, profilin, is known to accelerate ATP exchange and to play a part in stimulating actin polymerization during cellular movement. When a cell moves, its leading edge produces flat distensions or processes known as lamellipodia. The actin filaments in a lamellipodium are well organized and project outward, forming the actin geodomes already mentioned.
- 프롤린은 ATP교환을 촉진하는 물질로 세포가 이동하는 동안 액틴 중합반응을 자극하는 역할을 함.
- 세포가 움직일때, ... 액틴필라멘트는 잘 조직화되고 밖으로 투사되고 위에서 설명한 액틴 Geodomes를 형성함.
At this leading edge of the cell, it appears the actin is continuously polymerized; near the core of the cell, however, the actin continuously depolymerizes. The rapid assembly of actin filaments within the lamellipodium requires release of monomer-binding proteins from actin monomers. Actin polymerization appears to be regulated by extracellular signals binding to cell surface receptors that act through G proteins. It is clear that actin forms the basis of cell motility.
- 세포의 leading edge에서 액틴은 지속적으로 중합되는 것처럼 보임. 하지만 실제 액틴은 지속적으로 해중합됨.
- 액틴 필라멘트의 빠른 모음은 액틴단위체로부터 monomer-binding 단백질 분비를 필요로 함.
- 액틴 중합은 세포외 신호에 의해서 조절됨.
- 액틴이 세포이동의 기초를 만드는 것은 분명함
In general terms, three stages have been identified in the movement of a cell: protrusion, attachment, and traction. Protrusion is a function of the leading edge of the cell. This stage involves the actin polymerization just described. Next, the actin filaments attach to the substratum through FAC creation. These focal complexes are temporary; as the cell moves, its FACs repeatedly are broken and made again. Finally, traction is the movement of the back of the cell forward. The mechanism for this action is still not completely understood. One theory is that movement generated at the leading edge of the cell drags the rear end of the cell with it.
- 일반적으로 세포이동은 세단계로 설명됨. protrusion, attachment, traction
- protrusion은 세포의 leading edge의 기능임. 이 단계에서 액틴 중합이 관여함.
- 다음에 FAC 만듬을 통해 기층에 액틴필라멘트 부착단계. FAC는 일시적이고 세포가 이동함에 따라 반복적으로 만들어지고 부서짐.
- 마지막으로 traction은 세포가 움직이는 단계임. 이 단계에서 액틴의 기전이 명확히 밝혀지지 않음. 하나의 이론은 ...
Cellular Tensegrity and Mechanotransduction
Mechanotransduction is the cell's ability to convert a mechanical signal into a biochemical one. First, cells contain mechanosensitive ion channels that are activated, or deactivated, by mechanical stimulation of the cell membrane. In addition, G-protein activation, release of chemical second messengers (cyclic AMP), protein phosphorylation, secretion of growth factors, remodeling of cell-ECM adhesions, and changes in gene expression also occur within seconds to minutes following mechanical perturbation (Ingber, 1993).
- 역학형질도입은 기계적 신호를 생화학적 신호로 변화시키는 능력을 말함.
- 첫째, 모든 세포는 기계적민감 이온채널을 함유하여 세포벽의 기계적 자극에 의해 활성화 또는 불활성화됨.
- 게다가 G-protein 활성화는 주기 AMP를 분비, 단백질 인산화, 성장인자 분비, 세포외기질유착의 재구성, 유전자 표현의 변화가 몇초에서 몇분동안 일어남.
However, it is interesting to note that many of these reactions can take place without stimulation of mechanosensitive ion channels. Therefore, mechanotransduction must be explained using the internal structural framework that exists within cells (Ingber, 1993). This internal structural organization is of course based on the tensegrity model, as discussed already.
- 이러한 많은 반응이 기계적민감성 이온채널의 자극없이 일어난다는 것은 흥미로운 일임.
- 그래서 역학형질도입은 세포내에서 존재하는 내부구조적 틀에서 설명되어야 함.
- 이러한 내부구조 조직화는 이미 언급한 장력완전성 모델에 기초함.
The chemical reactions mediating protein synthesis, RNA transport, glycolysis, and DNA synthesis all appear to involve channeling of sequestered substrates and products from along the cytoskeletal filaments and nuclear matrix scaffolds (Ingber, 1993). Signal transduction may be similarly regulated since it has been demonstrated that multiple signaling molecules that are activated by integrins and growth factors become physically associated with the cellular framework of the FAC (Ingber, 1993). Because these signaling molecules lie in the main path for mechanical force transfer, the FAC represents a potential site for translating the mechanical stresses into a biochemical response. This is supported by the finding that mechanical stretch increases phosphorylation of the focal adhesion protein, tyrosine kinase (Ingber, 1993).
- 단백질합성, RNA transport, 당분해(glycolysis), DNA합성을 매개하는 화학반응은 sequestered 효소의 채널과 연관되고 nuclear matrix scaffold와 골격 필라멘트를 따라서 생성함.
-인테그린과 성장인자가 FAC의 세포틀과 연관됨에 의해서 다중신호분자가 활성화되어 signal transduction은 유사하게 조절될 수 있음. ....
- 이러한 신호분자가 기계적 힘전달을 위한 주요길에 놓여지기 때문에, FAC는 기계적 힘이 생화학적 반응으로 변화하는 부위를 보여줌.
- 이것은 다음과 같은 사실에 의해서 지지됨. 기계적 스트레치는 국소유착 단백질, 타이로신 키나제의 인산화를 증가시킴.
Thus, mechanical disturbances in cell shape definitely affect cellular biochemistry and behavior. Changing the tension placed on a cell will change cellular and-on a higher level-tissue tone. Stiffening of the cell can potentially alter not only cellular mechanics but also vibrational frequencies, which in turn affect reaction rates. Obviously, cellular changes produce a cumulative effect that will be expressed at the tissue level. For example, look at how bone responds to stress. If an area of an osseous structure is stressed, more bone will be deposited in that area.
- 그래서 세포형태에서 기계적 혼란은 세포의 생화학과 행위에 영향을 미침.
- 장력변화는 세포변화와 High level tisue tone를 변화시킴.
- 세포의 stiffening은 세포역학을 바꿀뿐 아니라 진동 주파수를 바꾸어 반응속도에 영향을 줌.
- 분명하게, 세포변화는 조직 level에서 축적효과를 생성함.
- 예를들어 뼈가 압박힘에 어떻게 반응하는가를 보자. 만약 뼈의 구조에 힘이 주어지면 뼈는 좀더 많은 축적이 일어남.
This theory is better known as Wolf's law.
Tensegrity and Myofascia
Organs and tissues are dynamic structures that change in response to variations in pressure or stress. The restructuring obviously occurs at the cellular level and is grossly seen at a tissue level. Individual cells change shape and orientation, and they move to adapt to changing environments and forces placed upon them. The changes occurring within each cell, as well as through the ECM and into the next cell, are seen and felt by a trained practitioner when examining connective tissue and fascia integrity.
- 기관과 조직은 압력이나 장력에 다양성에 반응하여 변화하는 동적구조임.
- 세포단위에서 재구성은 명백하게 일어나고 조직단위에서 grossly(극도로) 보여짐.
- 개별의 세포는 형태와 방향을 바꾸고, 외부환경변화에 적응하기 위해 움직임.
- 이 변화는 각각의 세포내에서 발생하고 세포외기질을 통할 뿐아니라 다음 세포를 통함. 섬유막과 결합조직 완전성을 검사할때 전문치료사에 의해서 느껴질 수 있음.
Ingber ( 1993) stated that only tensegrity can explain how every time that you move your arm, your skin stretches, your ECM extends, your cells distort, and the interconnected molecules that constitute the internal framework of the cell feel the pull-all without any breakage or discontinuity:'
- 잉버는 오직 장력완전성이 당신의 팔을 움직일때마다 어떻게 당신의 피부가 늘어나는지, 당신의 세포외기질이 확장되는지, 당신의 세포가 비틀리는지를 설명할 수 있다고 말함.
Thus, we can extrapolate this tensegrity model as seen at the cellular level to a more macroscopic level. The musculoskeletal system as a whole demonstrates components of tensegrity. The skeletal system (bones) can be envisioned as the compressive struts described earlier, while myofascia (muscles, ligaments, tendons) represents the tension components of the model.
- 그래서 우리는 세포단위에서 장력완전성 모델을 추론할 수 있음. 근골격계는 장력완전성의 구조를 보여줌. 뼈는 압박요소로서 인정되고, 근막(근육, 인대, 힘줄)은 장력완전성 모델의 장력 요소로 인정됨.
As explained, tensegrity models depend on a balance between these two components: tension structures and compression struts. If there is balance between the two, then the body can function effectively and injury. Applying a force to one area of a tensegrity structure will resull in restructuring of the whole in order to accommodate.
- 앞에서 설명한바와 같이 장력완전성 모델은 장력구조와 압박구조 두가지의 균형에 의존함. 만약 두개의 균형이 깨지면 인체는 효과적으로 기능하지 못하고 손상을 당함.
- 장력 완전성 구조의 한 부분에 힘이 주어짐은 다른 부위에 축적된 힘을 재구성함.
Again, quoting Donald Ingber ( 1993), An increase in tension of one of the members results in increased tension in members throughout the structure, even ones on the opposite side. This situation can be compared to that of the spider web. If something gets caught within one end of the spider web, the whole web shifts, or is pulled, to that side. Tension occurs even in areas far removed from the snag in the web.
- 장력 구조와 압박 구조 중 하나의 장력이 증가하면 전체 구조를 통틀어 장력 증가를 초래하고, 심지어 반대편도 마찬가지.
- 이 상황은 마치 거미줄 같이 비교될 수 있음
- 만약 어떤 물질이 거미줄 내에 걸리면, 전체 거미줄이 이동하거나 한쪽으로 당겨짐
- 장력은 거미줄에서의 문제가 제거되어도 발생됨
All this research points to a holistic role for the mechanical distribution of strain in the body that goes far beyond dealing with localized tissue pain. Creating an even tone across the myofascial meridians, and further across the entire fascial net, could have profound implications for health-both cellular and general. Very simply, transmission of tension through a tensegrity array provides a means to distribute forces to all interconnected elements, and at the same time to couple or tune the whole system mechanically as one. This role for manual and movement therapy of tuning the entire fascial system could have long-term effects in immunological health, as well as in an individual's sense of self integrity.
- 모든 이러한 연구는 국소적인 조직 통증을 다루는 인체에 주어지는 긴장의 역학적인 분포의 전체적인 역할을 가리킴
- 매우 간단하게 장력 완전성 구조 배열을 통한 장력의 전달은 모든 상호연결된 계체들의 힘(force)의 분포와 동시에 역학적으로 전체 시스템을 조절를 제공
- 전체 근막시스템을 조절하는 수기치료와 운동치료의 이러한 역할은 면역학적인 건강과 개인의 통합적 감각의 장기적효과를 자김
첫댓글 TENSEGRITY, THIXOTROPY, AND SOMATIC RECALL
장력완전성, 점탄성완전성, 조직기억(유전자 기억)
WHAT IS TENSEGRITY?
The concept of tensegrity was first introduced in 1961 by the architect Buckminster Fuller. Tensegrity is the union of two words: tension and integrity. Tensegrity is the property certain structures possess of maintaining their integrity as a result of continuous tensile integrity, rather than continuous compressive integrity (Pienta Et Coffey, 1991). This concept is used to explain how various cells and tissues are built and to explain how fascia is structured. The ideas presented in this chapter lay the foundation for some of the discussions found later in this book.
1961년 버크민스터 풀러가 만든개념.
- tension과 integrity의 조합어.
- 장력완전성은 연속적인 압박 완전성을 의미하기 보다는 연속적인 장력완전성의 결과를 유지하는 구조를 설명하는 용어임.
Tensegrity-based structures are composed of a continuous series of tension-resistant components and a series of discontinuous compression-resistant (struts) elements. This is the only requirement of the tensegrity model: tension must be continuous, and compression must be localized. The tensegrity structure was visualized by Kenneth Snelson through his sculpture of stainless steel bars held in place by tension cables (Figure 3-IA).
- 완전성에 기초한 구조는 장력-저항구조의 연속물과 끊이지 않는 압박-저항 요소가 조합되어 있음.
- 장력완전성 모델의 필요조건 : 장력은 연속적이어야 하고, 압박은 국소