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Physiology 1 > Extracellular Matrix > Flashcards

Extracellular Matrix Flashcards

1
Q

Functions of ECM

A
  • cellular division
  • motility
  • differentiation
  • adhesion
  • structure
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2
Q

Components of ECM

A
  • Structural Proteins = collagens and elastins (strength and flexibility)
  • Proteoglycans =protein-polysaccharides complexes (matrix for collagen and elastins to be embedded in)
  • Adhesive Glycoproteins = Fibronectins and Laminins (attach cells to matrix)
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3
Q

Collagens

A
  • Structural Proteins
  • Most Abundant Protein in vertebrates (25% - 30% of total body protein)
  • Abundant in tendons and ligaments
  • Secreted by several connective tissue cells (ex-fibroblasts)
  • Rigid Triple Helix structure with polypeptide chains high in glysine, hydroxylysine, and hydroxyproline
  • Have incredible strength
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4
Q

Collagen Cross Linking

A

When Produced: Collagen bundles cross-linked which strengthens collagen bundle and helps withstand high stress

With Aging:
Abnormal Crosslinking which leads to loss of joint function

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5
Q

hypermobility

A

deficiency in collagen synthesis or assembly (collagenase)

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6
Q

Elastin provides….

A
  • flexibility

- elasticity

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7
Q

What is elastin?

A
  • proteins rich in glycine and proline

- molecules of elastin are crosslinked BETWEEN lysines

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8
Q

Why is elastin flexible?

A
  • can form variety of confirmations
  • the tension in it allows for stretching
  • no tension when relaxed so no stretching
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9
Q

Why does skin become wrinkled and joints become inflexible as we age?

A

Elastins are lost as we age

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10
Q

What is supravalvular aortic stenosis (SVAS)?

A
  • inherited obstructive vascular diesease that affects the aorta, carotid, coronary and pulmonary arteries
  • Mutation in elastin gene disrupts elastin protein synthesis and result in narrowing of aorta or pulmonary vessels
  • This can lead to a heart murmur and ventricular hypertrophy
  • Not frequently seen
  • defect is located just above the aortic valve
  • Affects some large dog breeds = Newfoundland, Golden Retriever, Boxer, and Rottweiler
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11
Q

Proteoglycans

A
  • Make up Gel-like network that surrounds collagen and elastin
  • Proteoglycans are glycoproteins
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12
Q

What are glycoproteins?

A
  • Protein with glycoaminogylcans

- Up to 95% carbohydrate

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13
Q

Functions of Proteoglycans

A
  • Receptors
  • Filtration
  • Shock Absorption
  • Trap water = >50% Times Their Weight
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14
Q

Hyaluronate

A
  • Proteoglycan that acts as the backbone in cartilage
  • also acts a free molecule

Function

  • lubricates any place with friction = joints
  • found on suface of migrating cells
    - disappears upon cell-to-cell contact
    • facilitate cell migration by making matrix more water-soluble
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15
Q

T/F: Hyaluronan is quite large in comparison to other ECM components

A

True.

Hyaluronan is much larger than other ECM components.

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16
Q

Glycosaminoglycan Side Chains can be used for classification. What are the 3 types and their uses?

A
  • Chondroitin Sulfate = cartilage/ osteoarthritis
  • Keratan Sulfate = cornea, cartilage, bone, cushion
  • Heparin/ Heparin Sulfate = Anticoagulant, bind growth factors, important role in inflammation, entry of virus into cells (herpes, rabies)
17
Q

Heparin/ Heparan Sulfate

A
  • Heparan Sulfate is found in every cell of body and has side chains made of D-glucosamine/ L-iduronic acid
  • Heparin is one member of the Heparan Sulfate Family and serves as an anticoagulant
  • Other Family Members bind growth factors, play an important role in inflammation, and entry of viruses into cell like herpes and rabies
18
Q

Fibronectin

A
  • widely distributed
  • most common adhesive glycoprotein
  • can be soluble, insoluble, or partialy soluble (can be from same gene due to alternative splicing)
19
Q

Roles of Fibronectin

A
  • maintains cell shape
  • possible role in cancer
  • blood clotting
  • wound healing
  • cell movement
20
Q

Fibronectins Role in Cancer

A
  • Many carcinomas are unable to synthesize fibronectins, lose normal shape, and cells detach from ECM
  • Give fibronectin and cells revert to normal shape, bind to ECM, and are no longer malignant
21
Q

How does fibronectin connect into blood clotting?

A

-recognizes fibrin (blood clotting protein) that is attached to blood platelets

22
Q

What does fibronectin do in wound healing?

A

guides immune cells to wound

23
Q

Where are laminins mainly located?

A

Basal Laminae

24
Q

Basal Laminae

A
  • Thin sheet of EC material (approx. 50nm thick)
  • underlies epithelial cells
  • separates ECM from epi cells
  • Surrounds muscle cells, fat cells, and Schwann cells
25
Q

Properties of Basal Lamina

A
  • Structural Support
  • Permeability Barrier = kidney -> can let in small proteins, but not blood into urine
  • Cell Migration
26
Q

T/F: When ECM has been damaged and is remodeled, it is laid down in the same pattern as it was originally.

A

False.

ECM is initially very well organized and structured. After damage and remodeling, it is not well organized and structured.

27
Q

Why is ECM constantly being remodeled?

A
  • growth
  • changes in mechanical forces
  • heal
28
Q

Synthesis Of ECM

A
  • Under Transcriptional (genesis) Control by parent cell types
  • osteoblasts
  • chondrocytes
  • fibrocytes
  • Cells respond to:
  • paracrine signaling by growth factors
  • physical (lack of) contact with other cells and ECM
29
Q

Degrading ECM

A

-Accomplished by enzymes = metalloproteinases and serine proteases

30
Q

What does metalloproteinases need for ECM?

A
  • require Zinc or Calcium

- usually specific for 1 ECM Component

31
Q

How do serine proteases play into degrading ECM?

A
  • cleave protein sequences at serine residues

- work with metalloproteinases

32
Q

How can ECM degradation be stopped?

A
  • Tissue Inhibitors of Metalloproteinases (TIMP1, 2 ,3, and 4) that form high affinity complexes with metalloproteinases that are irreversible
  • Serine Protease Inhibitors that inactivate serine proteases
33
Q

Alpha 1-antitrypsin deficiency

A
  • Alpha 1-antitrypsin is produced in liver and macrophages = protects lungs from neutrophil elastase enzyme, which can disrupt connective tissue
  • Deficiency caused by defective production of alpha 1-antitrypsin
  • Emphysema/COPD and liver disease (cirrhosis) can result
  • Treatment is IV infusions of alpha 1-antitrypsin
34
Q

Panniculitis

A
  • alpha 1-antitrypsin deficiency in dogs leading to rare skin condition
  • characterized by hardened skin with painful lumps or patches
  • can vary in severity
  • can occur at any age

Physiology 1 (27 decks)

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