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COD Matrix biology Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

Describe the ECM

A

Highly specialised
Composed of fibrillar and non-fibrillar molecules
Reciprocally influences cellular function
Modulates normal tissue homeostasis and progression of disease

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2
Q

Give an example of some molecules found in the ECM

A 
Collagens
Structural proteins
Proteoglycans
Glycosaminoglycans
Glycoproteins
Proteinases
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3
Q

Describe collagens

A

Most abundant and widespread distribution in tissues
28 different collagen types
Construct fibers, networks and filaments in the ECM
Formed from polypeptide alpha chains
These create homo or hetero trimeric triple helices
Typical collagenous domains within alpha chains consist of repeat triplets of amino acids Gly-X-Y
Fibrillar is the most common
FACIT and MACIT
Anchoring and Beaded fillaments are self assembled forming

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4
Q

What are MACIT and FACIT collagens?

A

MACIT - membrane associated collagens with interrupted triple helices
FACIT - Fibril associated collagens with interrupted triple helices

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5
Q

What are some subclasses of collagen types?

A 
Fibrillar
Network forming
FACIT
MACIT
Anchoring filaments
Beaded filaments
Multiplexin
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6
Q

What are heterotypic fibrils

A

A mixture of different collagen types
Dermis, tendon and bone - Type I,III,V
Cartilage and Vitreous - Type II,IX,XI

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7
Q

What is Elastin used for?

A

Structural protein

Lends elasticity and resilience to tissues

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8
Q

What are laminins used for?

A

Structural protein

Cell-cell assembly

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9
Q

What are fibronectins used for?

A

Structural protein

A receptor that binds to other ECM molecules

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10
Q

What are the 4 types of glycosaminoglycans?

A 
Carbohydrate attached to a protein core
Chondroitin sulphate
Dermatan sulphate
Heparan sulphate
Keratan sulphate
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11
Q

Describe the glycosaminoglycan Hyaluronan

A

Synthesised and assembled on the plasma membrane
Non-Sulphated
Not attached to a protein core
Found in joint synovial fluids to facilitate joint movement

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12
Q

Describe the glycosaminoglycan Heparin

A

Prevents clotting
Synthesised and stored in mast cells
Used as an anticoagulant in medicine

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13
Q

Describe glycoproteins

A

Non structural
Modulate cell function
By interacting with cell surface receptors, hormones, proteases, structural matrix proteins (collagens)

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14
Q

What are some enzyme components of the ECM?

eg heparanases

A 
Matrix Metalloproteinases (MMP)
ADAM and ADAMTS proteinases
Serine proteases
Cathepsins
HA-degrading enzymes (Hyaluronidases)
Heparanases
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15
Q

Tissues requiring high tensile strength are enriched in what?

A

Fibrillar collagens eg tendons, bone, ligaments

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16
Q

Tissues requiring compressive properties are enriched in what?

A

Proteoglycans and hyaluronan eg cartilage

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17
Q

Tissues requiring elastic properties and recoil are enriched in what?

A

Elastin, eg skin, ligaments, connective tissue of lungs/blood vessels

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18
Q

Matrix stored chemical signals include what?

A

Growth factors

Cytokines

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19
Q

Where is the mutation in Ehlers-Danlos Syndrome?

A

Collagen
MMP gene that play key roles in regulating
collagen organization

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20
Q

Describe Ehlers-Danlos Syndrome

A

Elastic skin
Hyper flexible joints
Valvular heart disease

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21
Q

Invertebral disc disease IVD is a disorder of aging. What impact does this have and what is it attributed to?

A 
Impacts mobility
Decreased workplace productivity
Attributed to loss of glycosaminoglycans through the loss of aggrecan
Decreased hydration
Reduced compressibility
Increased risk of disc herniation
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22
Q

What are the changes in cell behaviour in IVD disease?

A

Hypoxia (O2)
Inflammation
Autophagy (Self eating)

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23
Q

Describe fibrosis

A

Damaging
Can occur as a result of excess formation of
connective tissue in response to injury
Due to a combination of factors such as a disproportionate activity of
matrix enzymes responsible for matrix degradation and reorganization
Hyperactive ligand-mediated receptor signaling via TGF-ß
Activity of mesenchymal cells

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24
Q

Name some common diseases that exhibit fibrosis

A

Pulmonary fibrosis
Hepatic fibrosis
Renal scarring

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25
Q

Describe osteoarthritis

A

Bone ends rub together

Thinned cartilage

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26
Q

Describe rheumatoid arthritis

A

Bone erosion

Swollen inflamed synovial membrane

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27
Q

What is the structure of the knee joint?

A 
Synovial membrane
Articular cartilage
Fibrous joint capsule
Joint cavity filled with synovial fluid
Ligaments
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28
Q

Describe the bio mechanical function of articular cartilage

A

Composite of collagens, proteoglycans and water
Allows tissue to withstand load
Provides a near frictionless surface for joint articulation
Tension, compression, shear, lubrication

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29
Q

What is the morphology of articular cartilage?

A 
No lymphatics
Avascular
Aneural
Hypocellular
No basement membrane
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30
Q

Articular cartilage is highly hydrated with water accounting for WHAT% of its wet weight

A

65 - 85%

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31
Q

What are chondrocytes?

A

Resident cells

Produce collagen, proteogylcans and enzymes

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32
Q

What are type II collagens?

A

Major collagen

Provides a cartilaginous framework and tensile strenght

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33
Q

What proteoglycans?

eg aggrecan

A

Major proteoglycan

Gives cartilage compressive stiffness

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34
Q

What is the chondrocyte morphology?

eg what are the zones

A

Superficial zone
Middle (intermediate) zone
Deep zone
Calcified zone

35
Q

Describe the zones of chondrocytes

eg superficial, intermediate, deep, calcified

A

Superficial - 600um. Cells flat, collagen Fibrils parallel to articular surface
Intermediate - 1500um. Cells round, collagen fibrils diagonal to articular surface
Deep - Cells round, collagen fibrils perpendicular to articular surfaces
Calcified - 300um, cells round, collagen fibrils perpendicular to articular surface

36
Q

What are aggrecan aggregates composed of?

A 
30-50 aggrecan monomers
1 Hyaluronan Glycosaminoglycan
30 - 50 Link proteins that stabilise the aggrecan interactions
All of these interactions are
non-covalent
37
Q

Describe the glycosaminoglycans charge

A

Negative charges
Create strong charge repulsive forces
Charge repulsion stiffens proteoglycans in the collagen network
And give cartilage compressive stiffness

38
Q

Load bearing properties of cartilage are provided by the tensile properties of WHAT?

A

Of the collagen fiber network and

The osmotic swelling pressure of the high concentration of aggrecan

39
Q

Aggrecan is immobolised within the matrix by forming WHAT aggrecates with hyaluronan and link protein?

A

Supramolecular

40
Q

What 2 phases are there in the biomechanical behaviour of cartilage?

A

Fluid and solid phase

41
Q

Describe the fluid phase in the biomechanical behaviour of cartilage

A

Is under high interstitial fluid pressurisation

Allows for the transmission of load in cartilage

42
Q

Describe the solid phase in the biomechanical behaviour of cartilage

A

Low permeability
This is because the proteoglycans PGs resist fluid flow
They are also restricted by the collagen fibril network

43
Q

WHAT are the major proteinases responsible for matrix turnover in cartilage?

A

Metalloproteinases

44
Q

Is cartilage turnover relatively slow or fast in adults?

A

Slow

45
Q

MMP (Metalloproteinases) and ADAMTS (A Disintegrin And Metalloproteinase with ThromboSpondin motif) are enzymes that require what for their activity?

A

Zinc OR
Calcium
(metal ions)

46
Q

True or false

Matrix proteinases are proteolytic enzymes

A

True

47
Q

Collagenases (MMPs) and gelatinases (MMPs) degrade WHAT

A

The collagen fibers

48
Q

Aggrecanases (ADAMTS4 and ADAMTS5) degrade WHAT

A

Aggrecan

49
Q

Stromelysins (MMP3 and MMP10) degrade WHAT

A

Non- collagenous matrix proteins

50
Q

Collagenases (MMP-1 & MMP-13) - degrade WHAT
Gelatinases (MMP-2 & MMP-9) - degrade WHAT
Stromelysins (MMP-3 & MMP-10)-degrade WHAT

A

triple helical collagens
denatured collagens
non-collagenous matrix proteins (not aggrecan)

51
Q

What are the 2 classifications of OA?

A

Primary

Secondary

52
Q

Describe primary OA

A

Idiopathic (no known cause)

53
Q

Describe secondary OA

A 
Post traumatic
Metabolic
Endocrine disorders
Congenital (present at birth)
Malposition
54
Q

What are some risk factors associated with OA?

A 
Age
Sex 
Hereditary
Ethnicity
Overweight
Lifestyle
Post menopausal
Resective joint surgery
55
Q

What are symptoms of OA?

A

Limited movement
Pain
Crepitation (crackling/rattling sound)
Sensitivity to damp or cold

56
Q

How do you diagnose OA?

A

X-ray

57
Q

What is the main hallmark of OA?

A

Matrix degradation of the articular cartilage

Results in loss of tissue function

58
Q

In OA, chondrocyte metabolism is altered. Explain how

A

Mechanical forces (through mechano and osmo sensors embedded in the chrondrocyte plasma membrane)
Inflammatory mediators (cytokines, chemokines, reactive oxygen species, nitric oxide)
Increased synthesis and activation of aggrecanases and MMP through NF kappa signalling pathway
Increased degradation of aggrecan and collagen

59
Q

What is catabolism?

A

Hallmark of OA

Loss of cartilage

60
Q

Aggrecanase activity is defined by the
specific cleavage between a Glutamate (E)
and an Alanine (A) peptide bond in the
WHAT of Aggrecan

A

Interglobular Domain (IGD)

61
Q

The cleavage in the IGD of Aggrecan
allows the WHAT
attachment domains of Aggrecan to
be released from the cartilage

A

glycosaminoglycan (GAG)

62
Q

Loss of aggrecan results in the loss of WHAT and the ability to imbibe water
Net loss of compressive properties

A

glycosaminoglycans

63
Q 
True or false
Loss of collagen results in the
breakdown of the framework of
cartilage and the tensile strength
of the tissue.
Collagen loss is reversible
A

FALSE

Collagen loss is irreversible

64
Q

Name some treatments for OA

A

Steroids
Non steroidal anti-inflammatory drugs (NSAIDs)
Anti-cytokine antibodies
Neutraceuticals
Joint replacement surgery
Autologous chondrocyte or mesenchymal repair
Future- specific drugs to target enzyme activity

65
Q

Human adults can regenerate only some organs. Give an example

A

Skin

Liver

66
Q

Give an example of human tissues that do not regenerate

A

Cartilage

Nerve tissue

67
Q

What is tissue engineering?

A

Involves the practice of combining scaffolds, cells and biologically active molecules into functional tissues

68
Q 
Tissue engineering
Give an example of:
Structural replacement
Functional replacement
Wound healing
A

Cosmetic reconstruction
Musculoskeletal tissues
Autologous skin grafts in burn patients

69
Q

What is regenerative medicine?

A

Research field that includes tissue engineering but also research on self-healing
This is where the body uses its own systems,
Sometimes with the help of foreign biological material
To recreate cells and rebuild tissues and organs

70
Q

What are ‘key ingredients’ of tissue engineering?

A

Cell precursors
Autologous, heterologous (allogeneic) or
xenogeneic cells derived from healthy or
pathological tissue
Source of cells (skin biopsy, bone marrow)
Types/origins of cells (embryonic stem cells/mesenchymal stem cells)
Bioactive molecules (enzymes, growth factors,interleukins)

71
Q

What are cell precursors?

A

Produce ECM
and/or
synthesis and release bioactive molecules (growth factors)

72
Q

In tissue engineering, what is used to make ‘scaffolds’?

Natural products

A 
Purified collagens (usually Type I) 
Fibronectin 
Fibrin 
Hyaluronan
Silk 
Plant polysaccharides e.g. cellulose 
Animal polysaccharides e.g. Chitin
73
Q

In tissue engineering, what is used to make ‘scaffolds’?
Synthetic biomaterials
Composites

A 
Polylactic acid (PLA) biodegradable
• Polyglycolic acid (PGA) biodegradable
• Carbon fibres
• PLA/Elastin
• PLGA/Hyaluronan
74
Q

What are some common knee sport injuries?

A

Meniscal Cartilage Tears
Collateral Ligament injuries
Cartilage lesions- e.g.Osteochondritis Dissecans

75
Q

Describe Osteochondritis Dissecans OCD

A

Inflammation of bone and cartilage
Results in the formation of loose fragments
Occurs in 15-29 of 100,000 patients
More common in males than females ( between 2:1 and 3:1)
Most common aged 10-20
Common in young athletes
Idiopathic focal joint disorder affecting the subchondral
bone
Knee is the commonly affected joint
A Fragment of cartilage and subchondral bone separates from the articular surface
Due to a lack of blood supply (osteonecrosis) in the underlying bone
Decalcification of the trabecular bone matrix
Left untreated, OCD can lead to the development of degenerative arthritis

76
Q

What are they symptoms of Osteochondritis Dissecans OCD?

A 
Pain
Inflammation
Swelling
Edema
Soreness in the joint
Catching and locking in the joint during movement
Reduced range of motion
Crepitus
77
Q

How do you diagnose Osteochondritis Dissecans OCD?

A

Radiographic examination

MRI

78
Q

Describe simply a chondrocyte transplantation in the right femoral condyle

A

A lesion in the right femoral condyle is made
There is a biopsy of the healthy cartilage
There is enzymatic digestion
These are cultivated for between 11-21 days
They are treated with trypsin
Suspension of cells
There is an injection of the cultured chondrocytes under the lap in the lesion
A periosteal flap is taken from the medial tibia and sutured over the lesion

79
Q

When doing a chondrocyte transplantation, how many mgs of cartilage is harvested from low weight bearing region?

A

300-500mg

80
Q

Describe Autologous matrix-induced chondrogenesis (MACI)

eg cell precursors and scaffold

A

Cell precursors- bone marrow and constituents

Scaffold- hydrogel

81
Q

Describe first generation ACI

A

Cell precursors- autologous chondrocytes

Scaffold-none- but use of periosteal flap/collagen membrane

82
Q

Describe second generation ACI (also known as MACI)

A

Cell precursors: autologous chondrocytes

Scaffolds: hydrogels, fibrous scaffolf, decelluarised ECM

83
Q

Describe third generation ACI

A

Cell precursors: allogenic stem cells, autologous stem cells
Scaffolds:hydrogel, fibrous scaffold, decelluraised ECM,
or composite

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