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41 Cards in this Set

  • Front
  • Back
T/F regeneration requires an intact connective tissue scaffold.
True.
What happens if healing occurs when there is damage to the ECM?
Scarring
What are labile cells? Stable cells? Permanent cells? Examples?
Labile: constantly dividing; surface epithelium, hematopoietic cells
Stable: divide only in case of injury; liver, endocrine glands, mesenchymal cells
Permanent: cannot divide; neurons, myocardial cells, striated muscle
What does it mean to say that stem cells exhibit asymmetric replication?
With each division, some differentiate and some retain their self-renewing capacity.
Are adult stem cells pluripotent? Explain.
No. They are usually lineage specific, although stem cells in bone marrow seem to have broad differentiation potential. Stem cells are located in niches, which differ among various tissues.
T/F Tissue stem cells can change their differentiation commitment when transplanted into a different tissue.
True.
Where are the stem cells in the liver?
Canals of Hering
How are stem cells in the liver different from stem cells in proliferating tissues?
They function as a reserve compartment for when hepatocyte proliferation is blocked.
Oval cell proliferation and differentiation is prominent in the livers of whom?
Patients recovering from hepatic failure and in some cases, hepatitis and cirrhosis.
How do growth and regeneration happen in skeletal muscle?
Myocytes do not divide even after injury. Rather, growth and regeneration occurs by replication of satellite cells found beneath the myocyte basal lamina.
T/F Satellite cells are present in both skeletal and cardiac muscle.
False. They have not been found in cardiac muscle.
T/F Cell proliferation is usually initiated by growth factors.
True
What are proto-oncogenes?
Genes that regulate the normal cell cycle.
Oncogenes?
Defective proto-oncogenes associated with abnormal proliferation.
Three main types of membrane receptors:
1. Tyrosine-kinase
2. Non-tyrosine-kinase that have to recruit kinase
3. G-protein coupled, seven transmembrane
What happens upon activation of tyrosine-kinase receptors?
Binding of ligand induces dimerization of the receptor, tyrosine kinase autophosphorylation, activation of ras, and so on.
Examples of tyrosine-kinase receptors (2).
Growth factor receptors and insulin receptors.
Receptors without intrinsic catalytic activity:
Cytokine receptors. Inner portion of receptors activates cytosolic tyrosine kinase: Janus kinases (JAK)
Seven transmembrane G-protein coupled receptors:
Largest family of plasma membrane receptors. They transmit signals into cell through trimeric GTP-binding proteins. Binding results in conformational change of receptor.
Give a quick overview of the Ras-mitogen activated protein kinase pathway.
GF binds, and there is autophosphorylation of receptor. Ras-GDP then becomes ras-GTP and binds to Raf, which activates MAPK pathway down to TFs in the nucleus.
The PI3 pathway results in:
inhibition of apoptosis
Phospholipase C
Receptors that activate this pathway are mainly G-protein coupled receptors, but PLC may also be activated by MAP kinase. PLC cleaves a phospholipid, creating DAG and IP3. DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particular calcium channels in the ER. These channels only allow the passage of calcium to move through. This causes the cytosolic concentration of Calcium to increase, causing a cascade of intracellular changes and activity.[
Cyclin B is formed at ____ and binds to ____. This complex is vital for progression to ____.
G2
CDK1
Mitosis
What happens to cyclin B after mitosis?
It is degraded by binding to ubiquitin.
Cyclin E is required for cell cycle transition from ___to___. The cyclinE/cdk complex activates an inhibitor of ____, thus promoting expression of ____, which allows progression into ___ phase.
G1 to S
cyclin D
cyclin A
S
What happens to the cell cycle if there is DNA damage?
p53 is activated, which activates p21 (a cdk inhibitor) and the cycle is then halted for repair or apoptosis
What does p27 do?
p27 is able to bind several different classes of Cyclin and Cdk molecules. It can bind to cyclin D either alone, or when complexed to its catalytic subunit CDK4. In doing so p27 inhibits the catalytic activity of Cdk4, which means that it prevents Cdk4 from adding phosphate residues to its principal substrate, the retinoblastoma (pRb) protein. Increased levels of p27 typically cause cells to arrest in the G1 phase of the cell cycle.
What is the rb protein?
pRb prevents the cell from replicating damaged DNA by preventing its progression along the cell cycle through G1 into S. In the hypophosphorylated state, pRb is active and carries out its role as tumor suppressor by inhibiting cell cycle progression. Phosphorylation inactivates pRb. When it is time for a cell to enter S phase, complexes of CDK and cyclins phosphorylate pRb, inhibiting its activity.
What is EGF/TGFα ?
Epidermal growth factor and transforming growth factor α. Produced by keratinocytes, macrophages, and other inflammatory cells when there is wound healing. EGF binds to receptor with intrinsic tyrosine kinase activity, thereby initiating signal transduction.
What is HGF?
Hepatocyte GF. The receptor for HGF is the product of the proto-oncogene, cMET, which is frequently over-expressed in tumors.
What is VEGF?
Vascular endothelial GF. Potent inducer of blood vessel formation in early development. Is active in repair, and in tumors.
What is PDGF?
Platelet derived GF. Family of several very closely related proteins each consisting of two chains. It is stored in platelet granules and is released upon platelet activation. It causes migration and proliferation of fibroblasts, smooth muscle cells, and monocytes.
What is FGF?
Fibroblast GF. Involved in wound repair, angiogenesis, development, hematopoiesis.
What is TGFβ?
Transforming GF. Epithelial cell and leukocyte inhibitor. It blocks cell cycle by increasing expression of cell-cycle inhibitors. TGFβ has a strong anti-inflammatory effect. Some tumors show loss of TGFβ receptor.
Three main types of proteins in the ECM?
1. Structural proteins: collagen, elastin
2. Adhesive glycoproteins: fibronectin, laminin
3. Proteoglycans
Fibronectin binds to what?
Binds to collagen, fibrin, proteoglycans and cells via integrin receptors.
What is laminin?
The glycoprotein of basement membranes. It binds to cell integrin receptors and to collagen IV. It plays a major role in angiogenesis.
What role do integrin receptors play in the ECM?
They bind fibronectin, laminin, and collagen to cells, and cells to cells. Assist in mediating the transformation of mechanical forces in ECM to gene activation.
Proteoglycans
They consist of a core protein with one or more covalently attached GAG chains. They can be categorized depending upon the nature of their GAG chains. These chains may be: chondroitin sulfate and dermatan sulfate, heparin and heparan sulfate, keratan sulfate
Proteoglycans are a major component of the ECM, as the "filler" substance existing between cells. Here they form large complexes, both to other proteoglycans, to hyaluronan and to fibrous matrix proteins (such as collagen). They are also involved in binding cations (such as sodium, potassium and calcium) and water, and also regulating the movement of molecules through the matrix
What are the stages in repair by connective tissue (fibrosis)?
1. Angiogenesis: promoted by VEGF.
2. ECM deposition and scar formation: TGFβ causes fibroblast migration and proliferation; and inhibition of metalloproteinases, which degrade collagen.
3. Tissue remodeling: transition in composition of ECM, there is both deposition and degradation (metalloproteinases). Connective tissue is restructured.
What are the steps in the healing process?
1. Inflammation with removal of damaged tissue.
2. Proliferation and migration of connective tissue cells.
3. Formation of new blood vessels.
4. Synthesis of ECM proteins and collagen deposition.
5. Tissue remodeling
6. Wound contraction
7. Acquisition of wound strength.