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Biochem BLOCK 4 > The extracellular Matrix > Flashcards

The extracellular Matrix Flashcards

1
Q

Major constituents of the ECM

A
  1. Collagen fibers
  2. Elastic fibers
  3. Proteogylcans and hyaluronic acid
  4. Glycoproteins
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2
Q

What gives the tissue tensile strength?

A

Collagen fibers

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3
Q

What gives the elasticity to the tissue?

A

Elastic fibers

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4
Q

Gel like or slimy, the major constituents of the amorphous ground substance

A

Proteoglycans and hyaluronic acid

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5
Q

The glue that holds the fibers and cells together

A

Glycoproteins

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6
Q

_________ + __________ = ECM

A

Fibers + ground substance

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7
Q

Where is ECM very abundant in the eye?

A
  • Bruch’s membrane
  • sclera
  • cornea
  • lens
  • vitreous humor
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8
Q

What is the most abundant protein in the human body?

A

Collagen

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9
Q

Structure of collagen

A

Long, rigid structure in which three polypeptides (a chains) are wound around one another in a rope-like triple helix

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10
Q

What are the three a chains of collagen stabilized by?

A

Interchain hydrogen bonds

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11
Q

How many types of collage are there?

A

More than 25, as well as additional proteins that have collagen like domains

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12
Q

What are the groups of collagen

A

Fibril forming
Network forming
Fibril associated

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13
Q

What type of collagen is in the cornea?

A

Type I and VIII

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14
Q

What type of collage is in the vitreous body

A

Type II

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15
Q

What type of collage is in the corneal and vascular endothelium?

A

Type VIII

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16
Q

Collage is a fibrous porcine composed of ______________

A

a chains forming triple stranded helix

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17
Q

What is collagen rich in?

A

Proline and glycine every 3 AA

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18
Q

Collagen contains ____________ and ___________ formed by post translational hydrozxylation of proline and lysin residues

A

Hydroxyproline and hydroxylysine

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19
Q

What are the enzymes that form hydroxyproline and hydroxylysine in collagen?

A

Prolyl hydroxylase and lysyl hydroxylase

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20
Q

What do the enzymes prolyl hydroxylase and lysyl hydroxylase require to form hydroxyproline and hydroxylysine?

A

O2, Fe2+, and ASCO RBI acid (vit C) as reducing equivalents

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21
Q

What is Vitamin C required for in collagen?

A

As a cofactors for the enzymes involved in hydroxylation of proline and lysin residues in collagen

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22
Q

Lack of proline and lysine hydroxylation lead to what?

A

Impairment of the interchain H bond formation which prevents the formation of a stable triple helix and affects proper cross linking

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23
Q

What greatly decreases the tensile strength of the assembled collagen fiber in scurvy?

A

Lack of proline and lysine hydroxylation lead to impairment of the interchain H bond formation which prevents the formation of a stable triple helix and affects proper cross linking

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24
Q

Symptoms of scurvy

A
  • easy bruising
  • loose teeth and bleeding gums (1st sign)
  • poor wound healing
  • poor bone development
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25
Q

Crosslinking of collagen fibers occurs __________

A

Extracellulary

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26
Q

Crosslinking of collagen occurs by the enzyme

A

Lysyl oxidase

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27
Q

Crosslinking of collagen happens how?

A

Oxidative deamination of reactive aldehydes that condense to form cross-linking

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28
Q

What happens when there is a deficiency of copper for crosslinking?

A

X-linked Menkes disease

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29
Q

What happens when there is a copper overload during crosslinking?

A

Wilson disease

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30
Q

________ is a defect in any of the synthetic steps of collagen

A

Collagenopathies

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31
Q

Degradation of collagen

A

Half life is several years, degraded by collagenases

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32
Q

Menkes syndrome is a mutation in the ________ leading to a lack of ______

A
  • ATP7A gene

- Cu2+

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33
Q

Menkes syndrome is inherited in an _____________ pattern.

A

X-linked recessive pattern

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34
Q

Menkes syndrome symptoms

A

Weak muscle tone (hypotonia), sagging facial features, seizures, intellectual disability, and developmental delay. The patients have brittle hair (kinky hair disease)

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35
Q

Wilson’s disease is an autosomal recessive condition due to the mutaiton in the ________ gene leading to _________.

A
  • ATP7B gene

- too much Cu2+

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36
Q

Symptoms of Wilson’s disease in the liver

A

Vomiting, weakness, fluid build up in the abdomen, swelling of the legs, yellowish skin

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37
Q

Symptoms of Wilson’s disease in the brain

A

Tremors, muscle stiffness, trouble speaking, personality changes, anxiety, and seeing or hearing things

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38
Q

What can you see in the eye that is indicative of Wilson’s disease?

A

Kayser-Fleischer Rings

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39
Q

Which type of osteogenesis imperfecta is more severe?

A

Type II

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40
Q

Type I osteogenesis imperfecta

A

Less severe, may be mistaken for child abuse

-decreased production of certain forms of collagen

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41
Q

Type II osteogenesis imperfecta

A

Fatal in uterus or in the neonatal period.
-caused by mutations in the collagen genes, mose common of which are substitutions of an AA with a bulky R group (Gly-X-Y)

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42
Q

Common characteristics of osteogenesis imperfecta

A
  • multiple bone fractures
  • skeletal deformities
  • blue sclera
  • hearing loss
  • dental imperfections
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43
Q

Why does the sclera appear blue in osteogenesis imperfecta?

A

Due to thinning tissue hair allows underlying pigment to show through

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44
Q

Ehlers-Danlos syndrome (EDS)

A
  • defective collagen genes or collagen processing enzymes with multiple mutation types
  • severity and symptoms depend on which collagen type is affected
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45
Q

Characteristics of EDS

A
  • hyperextensible skin
  • hypermobile joints
  • easy bleeding/bruising
  • may have blue sclera
  • most severe forms have potentially lethal vascular problems due to defective collagen in the arteries
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46
Q

Which diseases can cause blue sclera?

A

Osteogenesis imperfecta

EDS

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47
Q

Composition of elastic fibers

A
  • an inner core of amorphous elastin

- 10nm microfibrils surrounding the elastin composed of the proline fibrilin

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48
Q

What is the most abundant protein in arteries?

A

Amorphous elastin

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49
Q

What are elastic fibrils composed of in short?

A

Elastin and microfibrils (fibrilin)

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50
Q

Elastin structure

A

Connective tissue protein with rubber like properties, can be stretched to several times their normal length but recoil to their original shape when the stretching force is relaxed

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51
Q

Elastin is an insoluble protein polymer synthesized from a precursor ___________

A

Tropoelastin

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52
Q

What is the main difference between collagen and elastin

A

Elastin is rich in proline and lysine but contains SCANT hydroxyproline and hydroxylysine

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53
Q

Production of elastin

A

Lysyl oxidase modifies lysyl side chains in tropoelastin forming a desmosine cross linking which produces elastin

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54
Q

Extensively interconnected, rubbery network that can stretch and bend in any direction when stressed, giving connective tissue elasticity

A

Elastin

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55
Q

Cause of marfan syndrome

A

Mutations in the fibrillin-1 protein

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56
Q

Marfan syndrome is a rare ___________ condition

A

Dominantly inherited

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57
Q

Apapearance of patients with Marfan syndrome

A

Tall, with long, spidery fingers, lens displacement, media of large arteries is usually weak.

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58
Q

What do patients with Marfan syndrome usually die of?

A

Die suddenly in midlife after rupture of their dilated aorta

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59
Q

What disease would you see a dislocated lens?

A

Marfan syndrome

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60
Q

Large complexes of heteropolysaccharide chains associated with a small amount of protein

A

Proteoglycans

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61
Q

Protein with a variable but typically small amount of carbohydrate

A

Glycoproteins

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62
Q

Function of proteoglycans

A
  • produce gel like matrix
  • form basis of the body’s ground substance
  • serve as flexible support for ECM
  • sieve influencing the movement of materials through the ECM
  • contributes to the viscous, lubricating properties of mucous secretions
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63
Q

What produces a gel like matrix and forms the basis of the body’s ground substance?

A

Proteoglycans

64
Q

What serves as a flexible support for the ECM and acts as a sieve influencing the movement of materials through the ECM?

A

Proteoglycans

65
Q

What contributes to the viscous, lubticating properties of mucous secretions

A

Proteoglycans

66
Q

Proteoglycan aggregates are composed of

A
  1. Proteoglycan monomers
  2. Hyaluronic acid
  3. Link protein
67
Q

What is a proteoglycan monomer made of?

A
  • glycosaminoglycans (GAGS)

- a core protein

68
Q

what do proteoglycan monomers resemble?

A

Bottle brush

69
Q

Long unbranched, heteropolysaccharide chains composed of a repeating disaccharide unit [acidic sugar-amino sugar]n

A

glycosaminoglycans (GAGS)

70
Q

How many different types of proteoglycans are there in glysoaminoglycans (GAGS?

A

6 different types divided according to the monomeric compositions, type of glycosidic linkage and degree an location of sulfate units

71
Q

Where are glycoaminoglycans (GAG) found?

A

Always found external to the cytosol: inside an organelle or exterior of the cell

72
Q

What is linked to a serine residue with >100 monosaccharides/chain extending out from it?

A

A core protein

73
Q

How many families of core protein are there?

A

4

74
Q

A specific glycosaminoglycan not covalently attached to a core protein

A

Hyaluronic acid

Anchor point

75
Q

Small protein that stabilizes the association between the core protein and the hyaluronic acid

A

Link protein

76
Q

Large complexes of negatively charges heteropolysaccharide chains

A

Glycosaminoglycans (GAGs)

77
Q

Characteristics of glycosaminoglycans

A
  • unbranched

- repeating disaccharide units [acidic sugar-amino sugar]n

78
Q

Characteristics of the amino sugar of the glycosaminoglycan

A
  • D-glucosamine

- D-galactosmine

79
Q

The amino group of the glysoaminoglycan is usually _____________

A

Acetylated

-elimates the + charge

80
Q

Amino sugars on the glysoaminoglycans can be __________

A

Sulfate

-enhancing the - charge

81
Q

Acid sugar of the glycosaminoglycans

A
  • D-glucuronic acid

- L-iduronic acid (C-5) epimer

82
Q

The acidic sugars of the glysoaminoglycans have a _______ that has a - charge at physiological pH

A

Carboxyl group

83
Q

GAGs have a strong (-) charge due to ____________ and __________

A

Carboxyl groups and sulfate groups

84
Q

Why are glysoaminoglycans (GAGs) extended in solution, repel each other, and develop mydriatic spheres?

A

Due to a larger number of negative charges

85
Q

When GAGs are compressed together, they ‘slip’ past each other…

A

-have repulsive interactions and release water

86
Q

Decompression of the GAGs results in

A

Reestablishment of their extended and hydrated nature

87
Q

What does the extended and hydrated nature of GAGs contribute to?

A
  • hydraulic absorption and resilience of synovial fluid and vitreous humor of the eye
  • lubricating effect of mucous and synovial fluid
88
Q

What are the classifications of GAG’s divided according to?

A
  • monomeric composition
  • type of glycosidic linkages
  • degree and location of sulfate units
89
Q

most abundant GAGs in the body, found in cartilage, tendons, filaments and aorta

A

Chondroitin 4- and 6-sulfate

90
Q

Most heterogeneous GAGs, and type I is found in corenas; type II found in loose connective tissue proteoglycan aggregates with chondroitin sulfate.

A

Keratin sulfate (KS) I and II

91
Q

What is the only GAG not attached to a core protein?

A

Hyaluronic acid (hyaluronate)

92
Q

This is not covalently attached to a protein, and only GAG not limited to animal tissue, but also found in bacteria

A

Hyaluronic acid (hyaluronte)

93
Q

What is the only GAG not sulfate?

A

Hyaluronic acid

94
Q

This GAG is foundin skin, blood vessels and heart valves

A

Dermatan sulfate

95
Q

only GAG that is intracellular and a component of mast cells. Serves as an anticoagulant

A

Heparin

96
Q

This GAG is acetylated and there are fewer sulfate groups than other GAGs. It is an extracellular GAG found in BM and as a ubiquitous component of cell surfaces

A

Heparan sulfate

97
Q

Which is larger, heparin or heparan sulfate?

A

Heparan sulfate

98
Q

Synthesis of the core protein

A
  • translated into the ER lumen by ER associated ribosomes

- trafficked to the golgi where it can be glycosylated by glycosyltranferases to form short carbohydrate linkage region

99
Q

Synthesis of carbohydrate chain (synthesis of proteoglycans)

A

-synthesis and elongation by sequential addition of alternating acidic and amino sugars by a family of specific glycosyltranferases

100
Q

Addition of sulfate groups (synthesis of proteoglycans)

A

Sulfotransferases transfersulfate groups to specific sites on the growing carbohydrate chain

101
Q

What are the steps of proteoglycan synthesis

A
  1. Synthesis of the core protein
  2. Synthesis of the carbohydrate chain
  3. Addition of sulfate groups
102
Q

A defect in the sulfation of the growing GAG chains results in one of several disorders that affect the proper development and maintenance of the skeletal system

A

Chondrodystrophy

103
Q

Characteristics of chondrodystrophy

A
  • autosomal recessive

- dwarfism

104
Q

Degradation of GAGs

A

Extracellular GAGs enters into the cell by phagocytosis and end up in the lysosomes

105
Q

Once the GAG is in the lysosomes for degradation

A

Hydrologic enzymes degrade the GAGs which require large number of acid hydrolases for complete digestion

106
Q

Half life of GAGs

A

Varies

  • keratin sulfate > 120 days
  • others range from about 3 days to about 10 days
107
Q

Deficiency of any one of the lysosomal hydrolyses involved in heparin sulfate and/or dermatan sulfate degradation leads to _________________

A

Mucopolysaccharidoses

108
Q

Progressive disorders characterized by GAGs accumulating in the lysosomes of various tissues results in oligosaccharides in the urine

A

Mucopolysaccharidoses

109
Q

Diagnoses of mucopolysaccharidoses

A
  • the specific mucopolysaccharidoses is determined by identifying the structure present at the non-reducing end of the oligosaccharide
  • diagnosis is confirmed by measuring the patients cellualr level of lysosomal hydrolases
110
Q

Symptoms of mucopolysaccharidoses

A
  • apparently normal at birth, gradually deteriorate, severe cases may result in childhood mortality
  • a range of skeletal and extracellular matrix deformities and mental retardation
111
Q

What are the 4 mucopolysaccharidoses diseases?

A
  • Hurler syndrome
  • hunter syndrome
  • sanfilippo syndrome
  • sly syndrome
112
Q

Hurler syndrome (MPS 1 H) is a ___________ deficiency

A

Alpha-L-iduronidase deficiency (degradation of dermatan and heparin sulfate deficiency)

113
Q

Symptoms of Hurler syndrome

A
  • corneal clouding
  • meant all retardation, dwarfing
  • coarse facial features
  • upper airway obstruction
  • deposition in coronary artery leads to ischemia and early death
114
Q

Treatments for hurler syndrome (MPS 1 H)

A
  • bone marrow or cord blood transplant

- enzyme replacement

115
Q

What is the most severe form of MPS?

A

Hurler syndrome

116
Q

Hunter syndrome (MPS II) is a deficiency of what?

A

Iduranate sulfatase deficiency (dermatan and heparan sulfate)

117
Q

What kind of genetic disorder is Hunter syndrome?

A

X linked

118
Q

Symptom of hunter syndrome

A
  • NO corneal clouding
  • physical deformity
  • mental retardation
  • coarse facial features
  • growth deficiency
119
Q

Treatments for hunter syndrome

A

-enzyme replacement therapy

120
Q

Symptoms of sanfilippo syndrome types A-D (MPS III)

A
  • nervous system disorder

- Neumann retardation

121
Q

What is Sly syndrome deficient in

A

Beat-glucuronidase deficient (dermatan sulfate and heparan sulfate deficiency)

122
Q

What MPS is extremely rare?

A

Sly syndrome (MPS VII)

123
Q

Symptoms of sly syndrome

A
  • corneal clouding
  • depressed nasal bridge, epicanthic folds
  • long philtrum, thin upper lip
  • hypertrichosis (abnormal hair growth)
124
Q

Treatments for Sly syndrome

A

No approved specific treatments

125
Q

Which MPS diseases cause corneal clouding?

A

Hurler syndrome and Sly syndrome

126
Q

What are the functions of membrane bound glycoproteins

A
  • cell surface recognition by other cels, hormones, and viruses
  • cell surface antigenicity (blood group antigens)
  • formation of the ECM and mucins of the GI and uritogenital tracts. Biological lubricants
127
Q

Function of non membrane bound glycoproteins

A
  • almost all globular proteins secreted in the plasma are glycoproteins
  • many of the lysosomal proteins are glycoproteins
128
Q

Where are glycoproteins found

A

Outer surface of the plasma membrane or inside an organelle. Not in the cytoplasm

129
Q

Structure of the carbohydrate chain in the glycoproteins oligosaccharide

A
  • relatively short
  • do not have serial repeats
  • often branched
  • may or may not be negatively charges
  • highly variable
130
Q

Examples of how variable the composition of carbohydrates are in glycoproteins

A
  • immunoglobulin IgG has < 4% carbs

- gastric glycoproteins (mucin) has >80% carbs

131
Q

Structure of the linkage between carbohydrate and protein

A

-an N- or an O-glycosidic link between the oligosaccharide and the protein

132
Q

N-glycosidic link of the linkage between the carbohydrate and the protein in the glycoprotein

A

The sugar chain is attached to the amine group of an asparagine side chain

133
Q

O-glycosidic link between the carbohydrate and the protein of the glycoproteins

A

The sugar chain is attached to the hydroxyl group of either a serine or threonine R-group

134
Q

What kind of linkages do glycoproteins have?

A

They might contain only one type of glycosidic linkage (N- or 0- linked), or it may have both O- and N- linked

135
Q

O-linked oligosaccharides (glycoproteins)

A
  • Diverse sugars
  • may have one or more of a wide variety of sugars arranged in either a linear or branched pattern (usually branched)
  • found on extracellular glycoproteins and membrane glycoproteins
136
Q

This like of linked oligosaccharide may have one or more of a wide variety of sugars arranged in either a linear or branched pattern

A

O-linked

137
Q

This type of linked oligosaccharide can be found on extracellular glycoproteins or membrane glycoproteins

A

O-linked

138
Q

What helps provide the ABO blood group determinants?

A

O-linked oligosaccharides on the surface of RBCs help proved the ABO blood group determinant s

139
Q

What are the two broad classes of N-linked oligosaccharides

A
  • complex oligosaccharides

- high mannose oligosaccharides

140
Q

What do both classes of N-linked oligosaccharides contain?

A

The same core pentasaccharide but the complex oligosaccharides contain a diverse group of additional sugars

141
Q

Complex oligosacharides additional sugars

A
  • GlcNAc
  • Fuc
  • NANA
142
Q

High mannose oligosacharides diverse sugars

A

Contain primarily mannose

143
Q

Glycoproteins destined for cellular membranes,m lysosomes, or to be exported from the cell as secretory:

A
  • Synthesized On ribosomes attached to the RER
  • N-terminus hydrophobic sequence
  • extruded into the ER lumen
  • proteins transported via secretory vesicles to golgi which acts as sorting center that gives molecular address labels
144
Q

Where does the O linkage happen for glycoproteins

A

Golgi only

145
Q

Where does N-linkage occur?

A

In the ER, additional sugars and/or modifications may be added in the golgi

146
Q

How do soluble glycoproteins get distributed?

A

In the golgi they are packaged into vesicles that fuse with the cell membrane and release their contents

147
Q

How do membrane glycoproteins get distributed

A

Integrated into the ER membrane, pass through the golgi, and are packaged into vesicles for delivery to the cell membrnae

148
Q

Enzymes destined for the lysosomes

A
  • Nlinked glycoproteins can be phosphorylated at specific mannose residues
  • mannose-6-phosphate receptors located in the golgi membrane bind the target phosphorylated glycoproteins, concentrates them into vesicles and traffics them to the lysosomes
149
Q

What is I cell disease a deficiency of

A

In the ability to phosphorylate mannose

150
Q

What does the disability to phosphorylate mannose cause for I-cell disease?

A

Accumulation of large lysosomal inclusion bodies composed of missing hydrolase substrate

151
Q

What kind of disease is I-cell disease

A

Lysosomal storage disease

152
Q

Symptoms of I cell disease

A

Skeletal abnormalities, restricted joint movements, coats dysmorphic facial features, severe psychomotor impairment
-death likely prior to 8 years old

153
Q

Where does degradation of glycoproteins occur?

A

In the lysosomes

154
Q

What happens when there is a hydrolase enzyme missing in the lysosomes for degradation of glycoproteins?

A

Other expenses cannot participate in continued component degradation
-lead to accumulation of partially degraded structures in the lysosomes

155
Q

Deficiencies in the hydrolase enzymes of the lysosomes are what kind of disorder?

A

Autosomal recessive

Biochem BLOCK 4 (11 decks)

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