Cell Bio Lecture 11 - Cell-cell, cell-matrix interactions Flashcards

1
Q

Describe the structure of a proteoglycan.

A

Hyaluronan backbone (its a carb), core proteins branch the backbone, with complex carb branches off the core proteins. The carb branches are usually GAGs.

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2
Q

What are three functions of proteoglycans?

A

They are extracellular matrix proteins that do the following:

  1. Regulate hydration states of tissues, esp. cartilage
  2. Provide resistance to impact in cartilage
  3. Act as reservoirs for growth factors and cytokines
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3
Q

What are the causes of chondrodysplasias?

A
  1. Defective chondroitin sulfate proteoglycans.

2. Defective collagen II (found in cartilage exclusively)

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4
Q

Where are matricellular proteins found?

A

Outside the cell but STILL BOUND to the membrane.

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5
Q

Name three examples of matricellular proteins.

A
  1. Fibronectin
  2. Laminin
  3. CCN proteins
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6
Q

What type of protein is fibronectin and where is it found?

A

It is a matricellular protein found in the connective tissue matrix.

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7
Q

What type of protein is laminin and where is it found?

A

It is a matricellular protein found in the epithelial cell matrix (basal lamina, basement membrane)

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8
Q

What are integrins and what two things do they bind?

A

They are a type of matricellular protein. The STRONGLY bind the actin cytoskeleton inside the cell and STRONGLY bind matrix proteins extracellularly.

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9
Q

What is the defect in patients with Glanzmann’s Thrombasthenia?

A

Defective integrin, which binds to fibrinogen for clotting.

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10
Q

Where is elastin found?

A

Lungs, skin, artery walls.

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11
Q

What is the basic structure of artery wall proteins?

A

Elastin linked together with fibrillin.

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12
Q

What is the defect in Marfan’s syndrome?

A

Defective fibrillin cross-links.

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13
Q

What do matrix metalloproteases (MMPs) do? What is an example of their use?

A

They are extracellular matrix-degrading enzymes. Used for angiogenesis (notably in cancer metastasis).

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14
Q

How does atherosclerosis develop?

A

Chronic injury to the endothelial cells creates a non-thrombogenic surface that attacts leukocytes. The leukocytes infiltrate the smooth muscle underneath, and cytokines initiate proliferation. Leukocytes take up cholesterol, forming foam cells. Large plaques can develop their own blood supply, which are often unstable and burst, causing massive clotting suddenly.

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15
Q

What are the paracellular links in desmosomes made of?

A

Cadherin proteins. Defects can cause blistering diseases.

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16
Q

Describe leukocyte-endothelium adhesion.

A

Weak interactions between P-selectins on endothelium and the ligands on the leukocytes slow leukocytes and cause them to roll. If damage is present to endothelium, PAF and more P-selectin is expressed. Once PAF is bound to the endothelial receptor, the leukocyte integrin is activated, which binds to ICAM 1 (a STRONG binding interaction).